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anti-cxcl10 neutralizing mab clone 1f11  (Bio X Cell)


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    Bio X Cell anti-cxcl10 neutralizing mab clone 1f11
    Neutralization of <t>CXCL10</t> does not inhibit the effector function of CD8 + immune T cells to eliminate T. gondii cysts from the brains of chronically infected SCID mice following the adoptive transfer of T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) bradyzoite (cyst)-specific BAG1, ( B ) cyst-specific CST-1, and ( C ) bradyzoite-specific SAG2C were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.
    Anti Cxcl10 Neutralizing Mab Clone 1f11, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+cxcl10+neutralizing+mab/cxcl10+blocking+antibody/pmc11596037-47-12-17
    Average 90 stars, based on 1 article reviews
    anti-cxcl10 neutralizing mab clone 1f11 - by Bioz Stars, 2026-10
    90/100 stars

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    1) Product Images from "The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice"

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice

    Journal: Microorganisms

    doi: 10.3390/microorganisms12112172

    Neutralization of CXCL10 does not inhibit the effector function of CD8 + immune T cells to eliminate T. gondii cysts from the brains of chronically infected SCID mice following the adoptive transfer of T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) bradyzoite (cyst)-specific BAG1, ( B ) cyst-specific CST-1, and ( C ) bradyzoite-specific SAG2C were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.
    Figure Legend Snippet: Neutralization of CXCL10 does not inhibit the effector function of CD8 + immune T cells to eliminate T. gondii cysts from the brains of chronically infected SCID mice following the adoptive transfer of T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) bradyzoite (cyst)-specific BAG1, ( B ) cyst-specific CST-1, and ( C ) bradyzoite-specific SAG2C were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Techniques Used: Neutralization, Infection, Adoptive Transfer Assay, Control, Purification, Injection, Negative Control, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    Neutralization of CXCL10 does not inhibit recruitment of CD8 + immune T cells into the brain and their cytotoxic activity in this organ following the adoptive transfer of the T cells into T. gondii -infected SCID mice. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. The date from two independent experiments were combined. * p < 0.05, ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.
    Figure Legend Snippet: Neutralization of CXCL10 does not inhibit recruitment of CD8 + immune T cells into the brain and their cytotoxic activity in this organ following the adoptive transfer of the T cells into T. gondii -infected SCID mice. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. The date from two independent experiments were combined. * p < 0.05, ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Techniques Used: Neutralization, Activity Assay, Adoptive Transfer Assay, Infection, Control, Purification, Injection, Negative Control, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    Blocking of CXCL10 activity by a neutralizing mAb does not increase the mRNA levels for this chemokine to compensate for the neutralization of the activity of this chemokine in the brains of T. gondii -infected SCID mice following adoptive transfer of CD8 + immune T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of these two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group of infected SCID mice was injected with isotype control Ab in the same manner. As a negative control, one group of infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. The cerebral mRNA levels for CXCL10 were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.
    Figure Legend Snippet: Blocking of CXCL10 activity by a neutralizing mAb does not increase the mRNA levels for this chemokine to compensate for the neutralization of the activity of this chemokine in the brains of T. gondii -infected SCID mice following adoptive transfer of CD8 + immune T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of these two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group of infected SCID mice was injected with isotype control Ab in the same manner. As a negative control, one group of infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. The cerebral mRNA levels for CXCL10 were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Techniques Used: Blocking Assay, Activity Assay, Neutralization, Infection, Adoptive Transfer Assay, Control, Purification, Injection, Negative Control, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii rather enhances the elimination of cerebral tissue cysts of the parasite after receiving an adoptive transfer of CD8 + immune T cells from chronically infected WT mice. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. ( A ) Cerebral mRNA levels for the cyst (bradyzoite)-specific BAG1 were measured by RT-PCR. ( B ) Decreases in BAG1 mRNA levels by the transfer of CD8 + immune T cells were measured by calculating differences in the mean value of BAG1 mRNA levels in the control mice with no T-cell transfer and the BAG1 mRNA level of the mice that had received CD8 + T cells in each of RAG1 −/− and RAG1 −/− CXCL10 −/− groups. There were 4 mice in each experimental group. * p < 0.05, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.
    Figure Legend Snippet: The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii rather enhances the elimination of cerebral tissue cysts of the parasite after receiving an adoptive transfer of CD8 + immune T cells from chronically infected WT mice. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. ( A ) Cerebral mRNA levels for the cyst (bradyzoite)-specific BAG1 were measured by RT-PCR. ( B ) Decreases in BAG1 mRNA levels by the transfer of CD8 + immune T cells were measured by calculating differences in the mean value of BAG1 mRNA levels in the control mice with no T-cell transfer and the BAG1 mRNA level of the mice that had received CD8 + T cells in each of RAG1 −/− and RAG1 −/− CXCL10 −/− groups. There were 4 mice in each experimental group. * p < 0.05, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Techniques Used: Infection, Adoptive Transfer Assay, Control, Purification, Injection, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii does not affect the recruitment of adoptively transferred CD8 + immune T cells into the brain but enhances the GzmB mRNA expression in their brains. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.
    Figure Legend Snippet: The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii does not affect the recruitment of adoptively transferred CD8 + immune T cells into the brain but enhances the GzmB mRNA expression in their brains. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Techniques Used: Infection, Expressing, Control, Purification, Injection, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    Related Articles

    Infection:

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice.
    Article Snippet: .. Infected and sulfadiazine-treated SCID mice were injected intraperitoneally with 100 μg of anti-CXCL10 neutralizing mAb (clone 1F11, BioXcell, Lebanon, NH, USA) every other day beginning at one day before the transfer of CD8+ immune T cells. .. As a control, another group of the infected SCID mice were injected with isotype control Ab (BioXcell) in the same manner.

    Injection:

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice.
    Article Snippet: .. Infected and sulfadiazine-treated SCID mice were injected intraperitoneally with 100 μg of anti-CXCL10 neutralizing mAb (clone 1F11, BioXcell, Lebanon, NH, USA) every other day beginning at one day before the transfer of CD8+ immune T cells. .. As a control, another group of the infected SCID mice were injected with isotype control Ab (BioXcell) in the same manner.



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    Neutralization of <t>CXCL10</t> does not inhibit the effector function of CD8 + immune T cells to eliminate T. gondii cysts from the brains of chronically infected SCID mice following the adoptive transfer of T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) bradyzoite (cyst)-specific BAG1, ( B ) cyst-specific CST-1, and ( C ) bradyzoite-specific SAG2C were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.
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    Neutralization of CXCL10 does not inhibit the effector function of CD8 + immune T cells to eliminate T. gondii cysts from the brains of chronically infected SCID mice following the adoptive transfer of T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) bradyzoite (cyst)-specific BAG1, ( B ) cyst-specific CST-1, and ( C ) bradyzoite-specific SAG2C were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Journal: Microorganisms

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice

    doi: 10.3390/microorganisms12112172

    Figure Lengend Snippet: Neutralization of CXCL10 does not inhibit the effector function of CD8 + immune T cells to eliminate T. gondii cysts from the brains of chronically infected SCID mice following the adoptive transfer of T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) bradyzoite (cyst)-specific BAG1, ( B ) cyst-specific CST-1, and ( C ) bradyzoite-specific SAG2C were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Article Snippet: Infected and sulfadiazine-treated SCID mice were injected intraperitoneally with 100 μg of anti-CXCL10 neutralizing mAb (clone 1F11, BioXcell, Lebanon, NH, USA) every other day beginning at one day before the transfer of CD8 + immune T cells.

    Techniques: Neutralization, Infection, Adoptive Transfer Assay, Control, Purification, Injection, Negative Control, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    Neutralization of CXCL10 does not inhibit recruitment of CD8 + immune T cells into the brain and their cytotoxic activity in this organ following the adoptive transfer of the T cells into T. gondii -infected SCID mice. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. The date from two independent experiments were combined. * p < 0.05, ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Journal: Microorganisms

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice

    doi: 10.3390/microorganisms12112172

    Figure Lengend Snippet: Neutralization of CXCL10 does not inhibit recruitment of CD8 + immune T cells into the brain and their cytotoxic activity in this organ following the adoptive transfer of the T cells into T. gondii -infected SCID mice. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of those two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group was injected with isotype control Ab in the same manner. As a negative control, one group of the infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. The date from two independent experiments were combined. * p < 0.05, ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Article Snippet: Infected and sulfadiazine-treated SCID mice were injected intraperitoneally with 100 μg of anti-CXCL10 neutralizing mAb (clone 1F11, BioXcell, Lebanon, NH, USA) every other day beginning at one day before the transfer of CD8 + immune T cells.

    Techniques: Neutralization, Activity Assay, Adoptive Transfer Assay, Infection, Control, Purification, Injection, Negative Control, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    Blocking of CXCL10 activity by a neutralizing mAb does not increase the mRNA levels for this chemokine to compensate for the neutralization of the activity of this chemokine in the brains of T. gondii -infected SCID mice following adoptive transfer of CD8 + immune T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of these two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group of infected SCID mice was injected with isotype control Ab in the same manner. As a negative control, one group of infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. The cerebral mRNA levels for CXCL10 were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Journal: Microorganisms

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice

    doi: 10.3390/microorganisms12112172

    Figure Lengend Snippet: Blocking of CXCL10 activity by a neutralizing mAb does not increase the mRNA levels for this chemokine to compensate for the neutralization of the activity of this chemokine in the brains of T. gondii -infected SCID mice following adoptive transfer of CD8 + immune T cells. SCID mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into two groups of chronically infected SCID mice at 3 weeks after infection. One of these two groups of infected SCID mice was injected intraperitoneally with anti-CXCL10 mAb (100 μg) every other day beginning at one day before the CD8 + T-cell transfer. Another group of infected SCID mice was injected with isotype control Ab in the same manner. As a negative control, one group of infected SCID mice did not receive any T cells or any Ab treatment. Their brains were obtained at 7 days after the T-cell transfer. The cerebral mRNA levels for CXCL10 were measured by RT-PCR. There were 4 mice in each experimental group. The date from two independent experiments were combined. ** p < 0.01, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Article Snippet: Infected and sulfadiazine-treated SCID mice were injected intraperitoneally with 100 μg of anti-CXCL10 neutralizing mAb (clone 1F11, BioXcell, Lebanon, NH, USA) every other day beginning at one day before the transfer of CD8 + immune T cells.

    Techniques: Blocking Assay, Activity Assay, Neutralization, Infection, Adoptive Transfer Assay, Control, Purification, Injection, Negative Control, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii rather enhances the elimination of cerebral tissue cysts of the parasite after receiving an adoptive transfer of CD8 + immune T cells from chronically infected WT mice. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. ( A ) Cerebral mRNA levels for the cyst (bradyzoite)-specific BAG1 were measured by RT-PCR. ( B ) Decreases in BAG1 mRNA levels by the transfer of CD8 + immune T cells were measured by calculating differences in the mean value of BAG1 mRNA levels in the control mice with no T-cell transfer and the BAG1 mRNA level of the mice that had received CD8 + T cells in each of RAG1 −/− and RAG1 −/− CXCL10 −/− groups. There were 4 mice in each experimental group. * p < 0.05, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Journal: Microorganisms

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice

    doi: 10.3390/microorganisms12112172

    Figure Lengend Snippet: The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii rather enhances the elimination of cerebral tissue cysts of the parasite after receiving an adoptive transfer of CD8 + immune T cells from chronically infected WT mice. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. ( A ) Cerebral mRNA levels for the cyst (bradyzoite)-specific BAG1 were measured by RT-PCR. ( B ) Decreases in BAG1 mRNA levels by the transfer of CD8 + immune T cells were measured by calculating differences in the mean value of BAG1 mRNA levels in the control mice with no T-cell transfer and the BAG1 mRNA level of the mice that had received CD8 + T cells in each of RAG1 −/− and RAG1 −/− CXCL10 −/− groups. There were 4 mice in each experimental group. * p < 0.05, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Article Snippet: Infected and sulfadiazine-treated SCID mice were injected intraperitoneally with 100 μg of anti-CXCL10 neutralizing mAb (clone 1F11, BioXcell, Lebanon, NH, USA) every other day beginning at one day before the transfer of CD8 + immune T cells.

    Techniques: Infection, Adoptive Transfer Assay, Control, Purification, Injection, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

    The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii does not affect the recruitment of adoptively transferred CD8 + immune T cells into the brain but enhances the GzmB mRNA expression in their brains. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Journal: Microorganisms

    Article Title: The Absence of CXCL10 Activity Does Not Affect the Capability of CD8 + T Cells to Migrate and Eliminate the Tissue Cysts of Toxoplasma gondii from the Brains of Chronically Infected Mice

    doi: 10.3390/microorganisms12112172

    Figure Lengend Snippet: The absence of the CXCL10 gene in T cell-deficient RAG1 −/− mice infected with T. gondii does not affect the recruitment of adoptively transferred CD8 + immune T cells into the brain but enhances the GzmB mRNA expression in their brains. RAG1 −/− and RAG1 −/− CXCL10 −/− mice were infected with 10 cysts and treated with sulfadiazine beginning at 7 days after infection to control tachyzoite proliferation and maintain chronic infection in their brains. CD8 + T cells purified from the spleens of chronically infected WT mice were injected (2 × 10 6 cells/mouse) intravenously into one group of each of the chronically infected RAG1 −/− and RAG1 −/− CXCL10 −/− mice at 3 weeks after infection. Another group of each of these two strains of infected mice did not receive the T cells as a control. Their brains were obtained at 7 days after the T-cell transfer. Cerebral mRNA levels for ( A ) CD8β, ( B ) perforin, and ( C ) GzmB were measured by RT-PCR. Relative ratios of ( D ) perforin mRNA levels to CD8β mRNA levels and ( E ) GzmB mRNA levels to CD8β mRNA levels were also calculated. There were 4 mice in each experimental group. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 by Student’s t test or Mann–Whitney U test. The latter was used when the variations in data within the experimental group significantly differed between the two groups compared. N.S.: Not significant.

    Article Snippet: Infected and sulfadiazine-treated SCID mice were injected intraperitoneally with 100 μg of anti-CXCL10 neutralizing mAb (clone 1F11, BioXcell, Lebanon, NH, USA) every other day beginning at one day before the transfer of CD8 + immune T cells.

    Techniques: Infection, Expressing, Control, Purification, Injection, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY