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Figure 3. <t>RvCXCL1</t> Induces Migration of Naive NK Cells (A) Transwell migration assays of freshly isolated NK cells toward increasing concentrations of rvCXCL1 (indicated on the x axis). RhFck and rhIL8 were used as positive controls. Percent of migrating cells was calculated out of total input cells. Data are presented as mean ± SEM (n = 4). (B) Freshly isolated NK cells were incubated for 1 hr with mAb against vCXCL1 or isotype-matched control. RvCXCL1 was placed in the bottom chamber, and migration was performed for 3 hr at 37C. The numbers of migrated cells was determined by FACS following 3 hr of incubation at 37C. The basal migration rate of NK cells toward medium that did not contain rvCXCL1 was set as 1 and the results presented as fold increase (FI). *p < 0.05. **p < 0.005.

Rvcxcl1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 2 article reviews

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1) Product Images from "HCMV vCXCL1 Binds Several Chemokine Receptors and Preferentially Attracts Neutrophils over NK Cells by Interacting with CXCR2."

Article Title: HCMV vCXCL1 Binds Several Chemokine Receptors and Preferentially Attracts Neutrophils over NK Cells by Interacting with CXCR2.

Journal: Cell reports

doi: 10.1016/j.celrep.2016.04.042

Figure 3. RvCXCL1 Induces Migration of Naive NK Cells (A) Transwell migration assays of freshly isolated NK cells toward increasing concentrations of rvCXCL1 (indicated on the x axis). RhFck and rhIL8 were used as positive controls. Percent of migrating cells was calculated out of total input cells. Data are presented as mean ± SEM (n = 4). (B) Freshly isolated NK cells were incubated for 1 hr with mAb against vCXCL1 or isotype-matched control. RvCXCL1 was placed in the bottom chamber, and migration was performed for 3 hr at 37C. The numbers of migrated cells was determined by FACS following 3 hr of incubation at 37C. The basal migration rate of NK cells toward medium that did not contain rvCXCL1 was set as 1 and the results presented as fold increase (FI). *p < 0.05. **p < 0.005.

Figure Legend Snippet: Figure 3. RvCXCL1 Induces Migration of Naive NK Cells (A) Transwell migration assays of freshly isolated NK cells toward increasing concentrations of rvCXCL1 (indicated on the x axis). RhFck and rhIL8 were used as positive controls. Percent of migrating cells was calculated out of total input cells. Data are presented as mean ± SEM (n = 4). (B) Freshly isolated NK cells were incubated for 1 hr with mAb against vCXCL1 or isotype-matched control. RvCXCL1 was placed in the bottom chamber, and migration was performed for 3 hr at 37C. The numbers of migrated cells was determined by FACS following 3 hr of incubation at 37C. The basal migration rate of NK cells toward medium that did not contain rvCXCL1 was set as 1 and the results presented as fold increase (FI). *p < 0.05. **p < 0.005.

Techniques Used: Migration, Isolation, Incubation, Control

Figure 4. RvCXCL1 Induces Naive NK Cell Migration via CX3CR1 and CXCR1 (A) Freshly isolated NK cells were incubated with and without 0.1 mg and 1 mg (indicated on the left side of the ﬁgure) of rhIL8 (red histograms, left), rhFck (blue histograms, middle), or rvCXCL1 (green histograms, right), at 37C for 1 hr. Next, cells were stained with anti-CX3CR1 (two upper rows) or with anti-CXCR1 (two lower rows). Open gray histograms show the staining of the chemokine receptors on untreated cells. Filled gray histograms show staining of the untreated NK cells with an isotype control. The backgrounds of the treated cells were similar to the untreated cells and are not shown in the ﬁgure. See also Table S2. (B) Binding of vCXCL1-Ig to 293T-CX3CR1 transfectant (black open histogram) or to the 293T parental cells (gray open histogram). Filled gray histogram is the staining of the control fusion protein (control-Ig) on the 293T-CX3CR1-transfected cells. Staining of the parental 293T cells with control-Ig was similar to the 293T- CX3CR1-transfected cells and is not shown in the ﬁgure. (C) Freshly isolated NK cells were incubated for 1 hr with and without the proteins indicated on the x axis. RvCXCL1 was placed in the bottom chamber, and migration was performed for 3 hr at 37C. Migrating cells were counted by FACS. NK cell migration toward rvCXCL1 without pre-blocking was set as 100%, and the results are presented as % of migration. *p < 0.05. NS, not signiﬁcant. Figure shows one representative experiment out of three performed.

Figure Legend Snippet: Figure 4. RvCXCL1 Induces Naive NK Cell Migration via CX3CR1 and CXCR1 (A) Freshly isolated NK cells were incubated with and without 0.1 mg and 1 mg (indicated on the left side of the ﬁgure) of rhIL8 (red histograms, left), rhFck (blue histograms, middle), or rvCXCL1 (green histograms, right), at 37C for 1 hr. Next, cells were stained with anti-CX3CR1 (two upper rows) or with anti-CXCR1 (two lower rows). Open gray histograms show the staining of the chemokine receptors on untreated cells. Filled gray histograms show staining of the untreated NK cells with an isotype control. The backgrounds of the treated cells were similar to the untreated cells and are not shown in the ﬁgure. See also Table S2. (B) Binding of vCXCL1-Ig to 293T-CX3CR1 transfectant (black open histogram) or to the 293T parental cells (gray open histogram). Filled gray histogram is the staining of the control fusion protein (control-Ig) on the 293T-CX3CR1-transfected cells. Staining of the parental 293T cells with control-Ig was similar to the 293T- CX3CR1-transfected cells and is not shown in the ﬁgure. (C) Freshly isolated NK cells were incubated for 1 hr with and without the proteins indicated on the x axis. RvCXCL1 was placed in the bottom chamber, and migration was performed for 3 hr at 37C. Migrating cells were counted by FACS. NK cell migration toward rvCXCL1 without pre-blocking was set as 100%, and the results are presented as % of migration. *p < 0.05. NS, not signiﬁcant. Figure shows one representative experiment out of three performed.

Techniques Used: Migration, Isolation, Incubation, Staining, Control, Binding Assay, Transfection, Blocking Assay

$Figure 5. RvCXCL1 Induces Neutrophil Migration via CXCR1 and CXCR2 (A) Freshly isolated neutrophils were stained with mAb against CD16 and CEACAM1 (left dot plot). The double positive fraction (red square) was stained with speciﬁc antibodies against the chemokine receptors CXCR1, CXCR2, and CX3CR1. (B) Transwell migration assays were performed using freshly isolated neutrophils toward the recombinant proteins indicated on the x axis (rhFck, rhIL8, or rvCXCL1). The number of migrating cells was quantiﬁed by FACS, following a 30-min incubation period, at 37C. Percent of migrating cells out of total input cells was calculated. Data are presented as mean ± SEM (n = 6). (C) Freshly isolated neutrophils were incubated with and without 0.1 mg and 1 mg (indicated in the left of the ﬁgure) of rhIL8 (red histograms, left) or rvCXCL1 (green histograms, right) for 10 min at 37C, followed by staining with anti-CXCR1 (two upper rows) or anti-CXCR2 (two lower rows). Open gray histograms show chemokine receptors staining of the untreated cells. Filled gray histograms represent staining of the untreated cells with an isotype control. The backgrounds of the treated cells were similar to the untreated cells and are not shown in the ﬁgure. (D) Freshly isolated neutrophils were incubated at 37C for 10 min with or without the proteins indicated on the x axis. RvCXCL1 was placed in the bottom chamber, and the migrating neutrophils were counted using FACS following 30 min incubation at 37C. Neutrophil migration toward rvCXCL1 after pre-blocking with rhFck was set as 100%, and the results are presented as % of migration. *p < 0.05. **p < 0.005. Figure shows one representative experiment out of three performed. See also Table S3.$
Figure Legend Snippet: Figure 5. RvCXCL1 Induces Neutrophil Migration via CXCR1 and CXCR2 (A) Freshly isolated neutrophils were stained with mAb against CD16 and CEACAM1 (left dot plot). The double positive fraction (red square) was stained with speciﬁc antibodies against the chemokine receptors CXCR1, CXCR2, and CX3CR1. (B) Transwell migration assays were performed using freshly isolated neutrophils toward the recombinant proteins indicated on the x axis (rhFck, rhIL8, or rvCXCL1). The number of migrating cells was quantiﬁed by FACS, following a 30-min incubation period, at 37C. Percent of migrating cells out of total input cells was calculated. Data are presented as mean ± SEM (n = 6). (C) Freshly isolated neutrophils were incubated with and without 0.1 mg and 1 mg (indicated in the left of the ﬁgure) of rhIL8 (red histograms, left) or rvCXCL1 (green histograms, right) for 10 min at 37C, followed by staining with anti-CXCR1 (two upper rows) or anti-CXCR2 (two lower rows). Open gray histograms show chemokine receptors staining of the untreated cells. Filled gray histograms represent staining of the untreated cells with an isotype control. The backgrounds of the treated cells were similar to the untreated cells and are not shown in the ﬁgure. (D) Freshly isolated neutrophils were incubated at 37C for 10 min with or without the proteins indicated on the x axis. RvCXCL1 was placed in the bottom chamber, and the migrating neutrophils were counted using FACS following 30 min incubation at 37C. Neutrophil migration toward rvCXCL1 after pre-blocking with rhFck was set as 100%, and the results are presented as % of migration. *p < 0.05. **p < 0.005. Figure shows one representative experiment out of three performed. See also Table S3.

Techniques Used: Migration, Isolation, Staining, Recombinant, Incubation, Control, Blocking Assay

Figure 6. Neutrophils Migrate Faster and More Efﬁciently Than NK Cells in Response to rvCXCL1 (A) A transwell migration assay was performed using rvCXCL1, rhIL8, or rhFck as the chemoattractant with either freshly isolated neutrophils (gray triangles) or NK cells (black squares) placed in the upper chamber for 10, 20, and 30 min at 37C. Migration of untreated neutrophils and NK cells at the beginning of the experiment was set as 1, and the results are presented as FI. Figure shows one representative experiment out of two performed. (B) Diagram that describes competitive transwell migration assay in which NK cells and neutrophils were incubated together at the upper chamber and their ability to migrate toward rvCXCL1 (lower chamber) is determined. (C) Competitive transwell migration assays described in (B) was performed for 30 min (left panel) and 3 hr (right panel). Percent of migrating cells out of total input cells was calculated separately for neutrophils (gray) and NK cells (black). Data are presented as mean ± SEM (n = 3). *p < 0.05. **p < 0.005. ***p < 0.0005.

Figure Legend Snippet: Figure 6. Neutrophils Migrate Faster and More Efﬁciently Than NK Cells in Response to rvCXCL1 (A) A transwell migration assay was performed using rvCXCL1, rhIL8, or rhFck as the chemoattractant with either freshly isolated neutrophils (gray triangles) or NK cells (black squares) placed in the upper chamber for 10, 20, and 30 min at 37C. Migration of untreated neutrophils and NK cells at the beginning of the experiment was set as 1, and the results are presented as FI. Figure shows one representative experiment out of two performed. (B) Diagram that describes competitive transwell migration assay in which NK cells and neutrophils were incubated together at the upper chamber and their ability to migrate toward rvCXCL1 (lower chamber) is determined. (C) Competitive transwell migration assays described in (B) was performed for 30 min (left panel) and 3 hr (right panel). Percent of migrating cells out of total input cells was calculated separately for neutrophils (gray) and NK cells (black). Data are presented as mean ± SEM (n = 3). *p < 0.05. **p < 0.005. ***p < 0.0005.

Techniques Used: Transwell Migration Assay, Isolation, Migration, Incubation

Figure 7. Reduced Neutrophil and NK Cell Migration in the Absence of UL146 during HCMV Infection (A) Freshly isolated neutrophils were incubated with increasing concentrations (indicated in the x axis) of rvCXCL1 (gray circles) for 30 min at 37C, followed by staining with anti-CXCR2. MFI of CXCR2 expression without blocking was set on 100%, and the residual CXCR2 expression was calculated. Estimated levels of vCXCL1 following infection of HFF cells with WT HCMV are shown as blue square on the graph. (B) HFFs were infected (MOI of 0.5) with WT HCMV (blue circles) or DUL146 (red circles), and supernatants containing progeny viruses were harvested at the indicated hours postinfection (x axis). The plaque-forming units (PFU) were determined using a standard plaque assay on HFF monolayers. (C and D) HFF cells were infected with WT HCMV or with HCMV DUL146 at a MOI of 1. Three days postinfection, cell supernatants were collected and used for transwell migration assays with either neutrophils (C) or NK cells (D). Neutrophils and NK cell migration toward supernatants from mock-infected HFF was set as 1, and the results are presented as FI. (E and F) Freshly isolated neutrophils were incubated at 37C for 30 min with or without the proteins indicated on the x axis. Transwell migration assays were performed with neutrophils (E) or NK cells (F) toward supernatant from mock-infected or WT-HCMV-infected HFFs. Neutrophils and NK cell migration toward supernatants from mock-infected cells was set as 1, and the results are presented as FI. *p < 0.05. **p < 0.005. ***p < 0.0005. (G) HCMV-infected endothelial cells secrete vCXCL1 (1) and recruit both neutrophils and NK cells to the infection site (2). Migration of NK cells is dependent on CXCR1 and CX3CR1 receptors, whereas neutrophil migration is dependent on CXCR2 and CXCR1. Neutrophils migrate faster and more efﬁciently in comparison to NK cells due to their CXCR2 receptor (3). Therefore, neutrophils reach the infection site early and can disseminate the virus while proceeding to travel throughout the body (4). This enables the virus to maintain a pool of HCMV-infected cells. NK cells that migrate toward vCXCL1 will get to the infection site at a later time point (5) and will be subverted by HCMV-immune evasion tactics.

Figure Legend Snippet: Figure 7. Reduced Neutrophil and NK Cell Migration in the Absence of UL146 during HCMV Infection (A) Freshly isolated neutrophils were incubated with increasing concentrations (indicated in the x axis) of rvCXCL1 (gray circles) for 30 min at 37C, followed by staining with anti-CXCR2. MFI of CXCR2 expression without blocking was set on 100%, and the residual CXCR2 expression was calculated. Estimated levels of vCXCL1 following infection of HFF cells with WT HCMV are shown as blue square on the graph. (B) HFFs were infected (MOI of 0.5) with WT HCMV (blue circles) or DUL146 (red circles), and supernatants containing progeny viruses were harvested at the indicated hours postinfection (x axis). The plaque-forming units (PFU) were determined using a standard plaque assay on HFF monolayers. (C and D) HFF cells were infected with WT HCMV or with HCMV DUL146 at a MOI of 1. Three days postinfection, cell supernatants were collected and used for transwell migration assays with either neutrophils (C) or NK cells (D). Neutrophils and NK cell migration toward supernatants from mock-infected HFF was set as 1, and the results are presented as FI. (E and F) Freshly isolated neutrophils were incubated at 37C for 30 min with or without the proteins indicated on the x axis. Transwell migration assays were performed with neutrophils (E) or NK cells (F) toward supernatant from mock-infected or WT-HCMV-infected HFFs. Neutrophils and NK cell migration toward supernatants from mock-infected cells was set as 1, and the results are presented as FI. *p < 0.05. **p < 0.005. ***p < 0.0005. (G) HCMV-infected endothelial cells secrete vCXCL1 (1) and recruit both neutrophils and NK cells to the infection site (2). Migration of NK cells is dependent on CXCR1 and CX3CR1 receptors, whereas neutrophil migration is dependent on CXCR2 and CXCR1. Neutrophils migrate faster and more efﬁciently in comparison to NK cells due to their CXCR2 receptor (3). Therefore, neutrophils reach the infection site early and can disseminate the virus while proceeding to travel throughout the body (4). This enables the virus to maintain a pool of HCMV-infected cells. NK cells that migrate toward vCXCL1 will get to the infection site at a later time point (5) and will be subverted by HCMV-immune evasion tactics.

Techniques Used: Migration, Infection, Isolation, Incubation, Staining, Expressing, Blocking Assay, Plaque Assay, Comparison, Virus

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Journal: Cell reports

Article Title: HCMV vCXCL1 Binds Several Chemokine Receptors and Preferentially Attracts Neutrophils over NK Cells by Interacting with CXCR2.

doi: 10.1016/j.celrep.2016.04.042

Figure Lengend Snippet: Figure 3. RvCXCL1 Induces Migration of Naive NK Cells (A) Transwell migration assays of freshly isolated NK cells toward increasing concentrations of rvCXCL1 (indicated on the x axis). RhFck and rhIL8 were used as positive controls. Percent of migrating cells was calculated out of total input cells. Data are presented as mean ± SEM (n = 4). (B) Freshly isolated NK cells were incubated for 1 hr with mAb against vCXCL1 or isotype-matched control. RvCXCL1 was placed in the bottom chamber, and migration was performed for 3 hr at 37C. The numbers of migrated cells was determined by FACS following 3 hr of incubation at 37C. The basal migration rate of NK cells toward medium that did not contain rvCXCL1 was set as 1 and the results presented as fold increase (FI). *p < 0.05. **p < 0.005.

Article Snippet: Filters were then plated in bottomwells containing 600 ml migrationmedium (RPMI 1640with 1% fetal calf serum [FCS]) supplemented with either rvCXCL1 (620-CM-025), rhIL8 (208-IL-050), rhFck (365-FR-025), or rhChemerin (2324-CM-025; obtained from R&D Systems), as indicated in each figure.

Techniques: Migration, Isolation, Incubation, Control

Journal: Cell reports

Article Title: HCMV vCXCL1 Binds Several Chemokine Receptors and Preferentially Attracts Neutrophils over NK Cells by Interacting with CXCR2.

doi: 10.1016/j.celrep.2016.04.042

Figure Lengend Snippet: Figure 4. RvCXCL1 Induces Naive NK Cell Migration via CX3CR1 and CXCR1 (A) Freshly isolated NK cells were incubated with and without 0.1 mg and 1 mg (indicated on the left side of the ﬁgure) of rhIL8 (red histograms, left), rhFck (blue histograms, middle), or rvCXCL1 (green histograms, right), at 37C for 1 hr. Next, cells were stained with anti-CX3CR1 (two upper rows) or with anti-CXCR1 (two lower rows). Open gray histograms show the staining of the chemokine receptors on untreated cells. Filled gray histograms show staining of the untreated NK cells with an isotype control. The backgrounds of the treated cells were similar to the untreated cells and are not shown in the ﬁgure. See also Table S2. (B) Binding of vCXCL1-Ig to 293T-CX3CR1 transfectant (black open histogram) or to the 293T parental cells (gray open histogram). Filled gray histogram is the staining of the control fusion protein (control-Ig) on the 293T-CX3CR1-transfected cells. Staining of the parental 293T cells with control-Ig was similar to the 293T- CX3CR1-transfected cells and is not shown in the ﬁgure. (C) Freshly isolated NK cells were incubated for 1 hr with and without the proteins indicated on the x axis. RvCXCL1 was placed in the bottom chamber, and migration was performed for 3 hr at 37C. Migrating cells were counted by FACS. NK cell migration toward rvCXCL1 without pre-blocking was set as 100%, and the results are presented as % of migration. *p < 0.05. NS, not signiﬁcant. Figure shows one representative experiment out of three performed.

Techniques: Migration, Isolation, Incubation, Staining, Control, Binding Assay, Transfection, Blocking Assay

Journal: Cell reports

Article Title: HCMV vCXCL1 Binds Several Chemokine Receptors and Preferentially Attracts Neutrophils over NK Cells by Interacting with CXCR2.

doi: 10.1016/j.celrep.2016.04.042

Figure Lengend Snippet: Figure 5. RvCXCL1 Induces Neutrophil Migration via CXCR1 and CXCR2 (A) Freshly isolated neutrophils were stained with mAb against CD16 and CEACAM1 (left dot plot). The double positive fraction (red square) was stained with speciﬁc antibodies against the chemokine receptors CXCR1, CXCR2, and CX3CR1. (B) Transwell migration assays were performed using freshly isolated neutrophils toward the recombinant proteins indicated on the x axis (rhFck, rhIL8, or rvCXCL1). The number of migrating cells was quantiﬁed by FACS, following a 30-min incubation period, at 37C. Percent of migrating cells out of total input cells was calculated. Data are presented as mean ± SEM (n = 6). (C) Freshly isolated neutrophils were incubated with and without 0.1 mg and 1 mg (indicated in the left of the ﬁgure) of rhIL8 (red histograms, left) or rvCXCL1 (green histograms, right) for 10 min at 37C, followed by staining with anti-CXCR1 (two upper rows) or anti-CXCR2 (two lower rows). Open gray histograms show chemokine receptors staining of the untreated cells. Filled gray histograms represent staining of the untreated cells with an isotype control. The backgrounds of the treated cells were similar to the untreated cells and are not shown in the ﬁgure. (D) Freshly isolated neutrophils were incubated at 37C for 10 min with or without the proteins indicated on the x axis. RvCXCL1 was placed in the bottom chamber, and the migrating neutrophils were counted using FACS following 30 min incubation at 37C. Neutrophil migration toward rvCXCL1 after pre-blocking with rhFck was set as 100%, and the results are presented as % of migration. *p < 0.05. **p < 0.005. Figure shows one representative experiment out of three performed. See also Table S3.

Techniques: Migration, Isolation, Staining, Recombinant, Incubation, Control, Blocking Assay

Journal: Cell reports

Article Title: HCMV vCXCL1 Binds Several Chemokine Receptors and Preferentially Attracts Neutrophils over NK Cells by Interacting with CXCR2.

doi: 10.1016/j.celrep.2016.04.042

Figure Lengend Snippet: Figure 6. Neutrophils Migrate Faster and More Efﬁciently Than NK Cells in Response to rvCXCL1 (A) A transwell migration assay was performed using rvCXCL1, rhIL8, or rhFck as the chemoattractant with either freshly isolated neutrophils (gray triangles) or NK cells (black squares) placed in the upper chamber for 10, 20, and 30 min at 37C. Migration of untreated neutrophils and NK cells at the beginning of the experiment was set as 1, and the results are presented as FI. Figure shows one representative experiment out of two performed. (B) Diagram that describes competitive transwell migration assay in which NK cells and neutrophils were incubated together at the upper chamber and their ability to migrate toward rvCXCL1 (lower chamber) is determined. (C) Competitive transwell migration assays described in (B) was performed for 30 min (left panel) and 3 hr (right panel). Percent of migrating cells out of total input cells was calculated separately for neutrophils (gray) and NK cells (black). Data are presented as mean ± SEM (n = 3). *p < 0.05. **p < 0.005. ***p < 0.0005.

Techniques: Transwell Migration Assay, Isolation, Migration, Incubation

Journal: Cell reports

Article Title: HCMV vCXCL1 Binds Several Chemokine Receptors and Preferentially Attracts Neutrophils over NK Cells by Interacting with CXCR2.

doi: 10.1016/j.celrep.2016.04.042

Figure Lengend Snippet: Figure 7. Reduced Neutrophil and NK Cell Migration in the Absence of UL146 during HCMV Infection (A) Freshly isolated neutrophils were incubated with increasing concentrations (indicated in the x axis) of rvCXCL1 (gray circles) for 30 min at 37C, followed by staining with anti-CXCR2. MFI of CXCR2 expression without blocking was set on 100%, and the residual CXCR2 expression was calculated. Estimated levels of vCXCL1 following infection of HFF cells with WT HCMV are shown as blue square on the graph. (B) HFFs were infected (MOI of 0.5) with WT HCMV (blue circles) or DUL146 (red circles), and supernatants containing progeny viruses were harvested at the indicated hours postinfection (x axis). The plaque-forming units (PFU) were determined using a standard plaque assay on HFF monolayers. (C and D) HFF cells were infected with WT HCMV or with HCMV DUL146 at a MOI of 1. Three days postinfection, cell supernatants were collected and used for transwell migration assays with either neutrophils (C) or NK cells (D). Neutrophils and NK cell migration toward supernatants from mock-infected HFF was set as 1, and the results are presented as FI. (E and F) Freshly isolated neutrophils were incubated at 37C for 30 min with or without the proteins indicated on the x axis. Transwell migration assays were performed with neutrophils (E) or NK cells (F) toward supernatant from mock-infected or WT-HCMV-infected HFFs. Neutrophils and NK cell migration toward supernatants from mock-infected cells was set as 1, and the results are presented as FI. *p < 0.05. **p < 0.005. ***p < 0.0005. (G) HCMV-infected endothelial cells secrete vCXCL1 (1) and recruit both neutrophils and NK cells to the infection site (2). Migration of NK cells is dependent on CXCR1 and CX3CR1 receptors, whereas neutrophil migration is dependent on CXCR2 and CXCR1. Neutrophils migrate faster and more efﬁciently in comparison to NK cells due to their CXCR2 receptor (3). Therefore, neutrophils reach the infection site early and can disseminate the virus while proceeding to travel throughout the body (4). This enables the virus to maintain a pool of HCMV-infected cells. NK cells that migrate toward vCXCL1 will get to the infection site at a later time point (5) and will be subverted by HCMV-immune evasion tactics.

Techniques: Migration, Infection, Isolation, Incubation, Staining, Expressing, Blocking Assay, Plaque Assay, Comparison, Virus

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