sigmaplot 3.02 software Search Results


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Summary of primary antibodies
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Image Search Results


Summary of primary antibodies

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: Summary of primary antibodies

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques:

A–D, Different stages of microglial nodules in the mouse facial motor nucleus 14 d after injury in normal B6C3 mice; immunohistochemistry (brown staining) for TSP (A–C) and CD11a (D), 1 μm semithin araldite sections, methylene blue counterstain. A, Two activated microglia with slender TSP-immunoreactive processes (short arrows) adhere to an apoptotic neuron with nuclear chromatin condensation (long arrows). The arrowheads point to the TSP-negative astrocytes with clear and regular oval nuclei (also inB–D). B, Microglial phagocytosis of neuronal debris; strongly TSP-immunoreactive microglial nodule (short arrow) containing fragmented, methylene blue-counterstained cellular remnants (long arrows).C, Late stage TSP-immunoreactive microglial nodule (short arrow) consisting of three microglial cells after removal of the neuronal debris. The cellular structure of the TSP-immunoreactive nodules in this and the preceding micrograph (Fig.​(Fig.33B) is similar to that in E–H and Figure​Figure77C–F. D, Two microglial cells at the center of the nodule (m, long arrows) surrounded by CD11a-immunoreactive lymphocytes (short arrows).E–H, Colocalization of infiltrating lymphocytes and phagocytotic microglial nodules in the axotomized facial motor nucleus.E–G, Normal B6C3 mice, double immunofluorescence for thrombospondin and the T-lymphocyte markers CD3 (E), CD11a (F), and CD44 (G) 14 d after injury. Note the direct contact of T-lymphocytes (green) with the TSP-immunoreactive microglia (red). The CD44 immunoreactivity (G) is also present on the surface of axotomized motoneurons (Jones et al., 1997).H, SCID mouse facial motor nucleus, 14 d after injury. Apposition of CD11a-immunoreactive cells (green) on an IBA1-labeled microglial nodule (red). Magnification: A, 1140×;B–D, 900×; E–H, 950×.

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: A–D, Different stages of microglial nodules in the mouse facial motor nucleus 14 d after injury in normal B6C3 mice; immunohistochemistry (brown staining) for TSP (A–C) and CD11a (D), 1 μm semithin araldite sections, methylene blue counterstain. A, Two activated microglia with slender TSP-immunoreactive processes (short arrows) adhere to an apoptotic neuron with nuclear chromatin condensation (long arrows). The arrowheads point to the TSP-negative astrocytes with clear and regular oval nuclei (also inB–D). B, Microglial phagocytosis of neuronal debris; strongly TSP-immunoreactive microglial nodule (short arrow) containing fragmented, methylene blue-counterstained cellular remnants (long arrows).C, Late stage TSP-immunoreactive microglial nodule (short arrow) consisting of three microglial cells after removal of the neuronal debris. The cellular structure of the TSP-immunoreactive nodules in this and the preceding micrograph (Fig.​(Fig.33B) is similar to that in E–H and Figure​Figure77C–F. D, Two microglial cells at the center of the nodule (m, long arrows) surrounded by CD11a-immunoreactive lymphocytes (short arrows).E–H, Colocalization of infiltrating lymphocytes and phagocytotic microglial nodules in the axotomized facial motor nucleus.E–G, Normal B6C3 mice, double immunofluorescence for thrombospondin and the T-lymphocyte markers CD3 (E), CD11a (F), and CD44 (G) 14 d after injury. Note the direct contact of T-lymphocytes (green) with the TSP-immunoreactive microglia (red). The CD44 immunoreactivity (G) is also present on the surface of axotomized motoneurons (Jones et al., 1997).H, SCID mouse facial motor nucleus, 14 d after injury. Apposition of CD11a-immunoreactive cells (green) on an IBA1-labeled microglial nodule (red). Magnification: A, 1140×;B–D, 900×; E–H, 950×.

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques: Immunohistochemistry, Staining, Immunofluorescence, Labeling

Summary of primary antibodies

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: Summary of primary antibodies

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques:

CD3 immunohistochemistry in the normal and axotomized mouse facial motor nucleus. CD3-immunoreactive T-lymphocytes are absent in the normal facial nucleus (0d), but appear 1 d after axotomy (1d, arrows), reach a maximum at day 14, and disappear almost completely at 66 d (66d) after injury. The extent of the facial motor nucleus is indicated by thedotted lines in this and in the following figure (Fig.​(Fig.2).2). All magnifications 49×. Bottom right, Quantitative time course of CD3-positive cells in the axotomized and contralateral facial nuclei (mean ± SEM, n = 3 animals per time point). Note the early plateau of two to three labeled cells per section 1–4 d after axotomy, and a further 10-fold increase at day 14. No statistically significant increase on the contralateral side.

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: CD3 immunohistochemistry in the normal and axotomized mouse facial motor nucleus. CD3-immunoreactive T-lymphocytes are absent in the normal facial nucleus (0d), but appear 1 d after axotomy (1d, arrows), reach a maximum at day 14, and disappear almost completely at 66 d (66d) after injury. The extent of the facial motor nucleus is indicated by thedotted lines in this and in the following figure (Fig.​(Fig.2).2). All magnifications 49×. Bottom right, Quantitative time course of CD3-positive cells in the axotomized and contralateral facial nuclei (mean ± SEM, n = 3 animals per time point). Note the early plateau of two to three labeled cells per section 1–4 d after axotomy, and a further 10-fold increase at day 14. No statistically significant increase on the contralateral side.

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques: Immunohistochemistry, Labeling

Distribution of CD3-immunoreactive T-lymphocytes in the axotomized facial motor nucleus 14 d after injury. A, Diffuse distribution. B, A rare perivascular infiltrate (thin arrow) surrounding a large vessel (v). C, D, Focal aggregates of CD3-immunoreactive T-lymphocytes (arrows). Magnification, 49×.

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: Distribution of CD3-immunoreactive T-lymphocytes in the axotomized facial motor nucleus 14 d after injury. A, Diffuse distribution. B, A rare perivascular infiltrate (thin arrow) surrounding a large vessel (v). C, D, Focal aggregates of CD3-immunoreactive T-lymphocytes (arrows). Magnification, 49×.

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques:

Immunohistochemical distribution of MHC class I (A, B), CD3 (C, D), and CD11a (E, F) immunoreactivity in normal (A, C, E) and SCID mice (B, D, F), 14 d after facial axotomy. A, B, Strong, focal increase of MHC class I immunoreactivity in the axotomized facial motor nuclei (right side). No specific immunoreactivity on the contralateral, unoperated side. Note the similar increase in MHC class I in normal and SCID animals. Magnification, 15×. C, D, CD3 immunoreactivity. Complete absence of specific staining in the SCID animal. E, F, CD11a immunoreactivity. Note the reduction in the number of CD11a-positive cells in the immunodeficient mouse. Magnification: C–F, 110×.

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: Immunohistochemical distribution of MHC class I (A, B), CD3 (C, D), and CD11a (E, F) immunoreactivity in normal (A, C, E) and SCID mice (B, D, F), 14 d after facial axotomy. A, B, Strong, focal increase of MHC class I immunoreactivity in the axotomized facial motor nuclei (right side). No specific immunoreactivity on the contralateral, unoperated side. Note the similar increase in MHC class I in normal and SCID animals. Magnification, 15×. C, D, CD3 immunoreactivity. Complete absence of specific staining in the SCID animal. E, F, CD11a immunoreactivity. Note the reduction in the number of CD11a-positive cells in the immunodeficient mouse. Magnification: C–F, 110×.

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques: Immunohistochemical staining, Staining

A–D, Different stages of microglial nodules in the mouse facial motor nucleus 14 d after injury in normal B6C3 mice; immunohistochemistry (brown staining) for TSP (A–C) and CD11a (D), 1 μm semithin araldite sections, methylene blue counterstain. A, Two activated microglia with slender TSP-immunoreactive processes (short arrows) adhere to an apoptotic neuron with nuclear chromatin condensation (long arrows). The arrowheads point to the TSP-negative astrocytes with clear and regular oval nuclei (also inB–D). B, Microglial phagocytosis of neuronal debris; strongly TSP-immunoreactive microglial nodule (short arrow) containing fragmented, methylene blue-counterstained cellular remnants (long arrows).C, Late stage TSP-immunoreactive microglial nodule (short arrow) consisting of three microglial cells after removal of the neuronal debris. The cellular structure of the TSP-immunoreactive nodules in this and the preceding micrograph (Fig.​(Fig.33B) is similar to that in E–H and Figure​Figure77C–F. D, Two microglial cells at the center of the nodule (m, long arrows) surrounded by CD11a-immunoreactive lymphocytes (short arrows).E–H, Colocalization of infiltrating lymphocytes and phagocytotic microglial nodules in the axotomized facial motor nucleus.E–G, Normal B6C3 mice, double immunofluorescence for thrombospondin and the T-lymphocyte markers CD3 (E), CD11a (F), and CD44 (G) 14 d after injury. Note the direct contact of T-lymphocytes (green) with the TSP-immunoreactive microglia (red). The CD44 immunoreactivity (G) is also present on the surface of axotomized motoneurons (Jones et al., 1997).H, SCID mouse facial motor nucleus, 14 d after injury. Apposition of CD11a-immunoreactive cells (green) on an IBA1-labeled microglial nodule (red). Magnification: A, 1140×;B–D, 900×; E–H, 950×.

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: A–D, Different stages of microglial nodules in the mouse facial motor nucleus 14 d after injury in normal B6C3 mice; immunohistochemistry (brown staining) for TSP (A–C) and CD11a (D), 1 μm semithin araldite sections, methylene blue counterstain. A, Two activated microglia with slender TSP-immunoreactive processes (short arrows) adhere to an apoptotic neuron with nuclear chromatin condensation (long arrows). The arrowheads point to the TSP-negative astrocytes with clear and regular oval nuclei (also inB–D). B, Microglial phagocytosis of neuronal debris; strongly TSP-immunoreactive microglial nodule (short arrow) containing fragmented, methylene blue-counterstained cellular remnants (long arrows).C, Late stage TSP-immunoreactive microglial nodule (short arrow) consisting of three microglial cells after removal of the neuronal debris. The cellular structure of the TSP-immunoreactive nodules in this and the preceding micrograph (Fig.​(Fig.33B) is similar to that in E–H and Figure​Figure77C–F. D, Two microglial cells at the center of the nodule (m, long arrows) surrounded by CD11a-immunoreactive lymphocytes (short arrows).E–H, Colocalization of infiltrating lymphocytes and phagocytotic microglial nodules in the axotomized facial motor nucleus.E–G, Normal B6C3 mice, double immunofluorescence for thrombospondin and the T-lymphocyte markers CD3 (E), CD11a (F), and CD44 (G) 14 d after injury. Note the direct contact of T-lymphocytes (green) with the TSP-immunoreactive microglia (red). The CD44 immunoreactivity (G) is also present on the surface of axotomized motoneurons (Jones et al., 1997).H, SCID mouse facial motor nucleus, 14 d after injury. Apposition of CD11a-immunoreactive cells (green) on an IBA1-labeled microglial nodule (red). Magnification: A, 1140×;B–D, 900×; E–H, 950×.

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques: Immunohistochemistry, Staining, Immunofluorescence, Labeling

Ultrastructural localization of CD11a- and CD3-immunoreactivity in the 14 d axotomized facial motor nucleus.A, CD11a immunostaining of a cellular aggregate, consisting of a degenerating neuron at the center, surrounded by microglia (M), astrocytes (A), and the CD11a-positive lymphocytes (L). These CD11a-positive cells frequently showed a clear cytoplasm, deeply cleaved nuclei, and ruffled, CD11-immunoreactive cell membranes (short arrows). The curved arrow points to phagosomes in a CD11a-negative cell process adhering to a CD11a-immunoreactive cell. These phagosomes are a common, characteristic feature in the phagocytotic microglial cells. Magnification, 5400×. B, C, CD3 immunoreactivity on the cell membrane of infiltrating T-lymphocytes (T). Note the typical cleaved or deformed lymphocyte nuclei. Adjacent vessels (V) and astrocytes (A) are unlabeled. Magnification:B, 5800×; C, 6800×.

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: Ultrastructural localization of CD11a- and CD3-immunoreactivity in the 14 d axotomized facial motor nucleus.A, CD11a immunostaining of a cellular aggregate, consisting of a degenerating neuron at the center, surrounded by microglia (M), astrocytes (A), and the CD11a-positive lymphocytes (L). These CD11a-positive cells frequently showed a clear cytoplasm, deeply cleaved nuclei, and ruffled, CD11-immunoreactive cell membranes (short arrows). The curved arrow points to phagosomes in a CD11a-negative cell process adhering to a CD11a-immunoreactive cell. These phagosomes are a common, characteristic feature in the phagocytotic microglial cells. Magnification, 5400×. B, C, CD3 immunoreactivity on the cell membrane of infiltrating T-lymphocytes (T). Note the typical cleaved or deformed lymphocyte nuclei. Adjacent vessels (V) and astrocytes (A) are unlabeled. Magnification:B, 5800×; C, 6800×.

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques: Immunostaining

Effects of timing and SCID-phenotype on lymphocyte infiltration. A, Effects of consecutive, bilateral axotomy. Bilateral infiltration of CD3 lymphocytes, 14 d after transection of the right and 3 d after transection of the left facial nerve. Note the ∼10-fold higher influx of lymphocytes on the 14 d axotomized side. *p < 0.001 in a paired, two-sided Student’s t test; mean ± SD (n = 4 animals). B, C, Infiltration of CD3- (B) and CD11a-immunoreactive cells (C) in normal and SCID mice in the BALB/c genetic background, 14 d after facial nerve transection (mean ± SEM,n = 5 animals). The SCID phenotype leads to a 98% decrease in the number of CD3-positive cells (p < 0.001) and a 60% decrease in the number of CD11a-positive cells (p < 0.01). Unpaired t test.

Journal: The Journal of Neuroscience

Article Title: Immune Surveillance in the Injured Nervous System: T-Lymphocytes Invade the Axotomized Mouse Facial Motor Nucleus and Aggregate around Sites of Neuronal Degeneration

doi: 10.1523/JNEUROSCI.18-15-05804.1998

Figure Lengend Snippet: Effects of timing and SCID-phenotype on lymphocyte infiltration. A, Effects of consecutive, bilateral axotomy. Bilateral infiltration of CD3 lymphocytes, 14 d after transection of the right and 3 d after transection of the left facial nerve. Note the ∼10-fold higher influx of lymphocytes on the 14 d axotomized side. *p < 0.001 in a paired, two-sided Student’s t test; mean ± SD (n = 4 animals). B, C, Infiltration of CD3- (B) and CD11a-immunoreactive cells (C) in normal and SCID mice in the BALB/c genetic background, 14 d after facial nerve transection (mean ± SEM,n = 5 animals). The SCID phenotype leads to a 98% decrease in the number of CD3-positive cells (p < 0.001) and a 60% decrease in the number of CD11a-positive cells (p < 0.01). Unpaired t test.

Article Snippet: Statistical analysis on the number of CD3- and CD11a-immunoreactive cells per tissue was performed using Jandel Sigmaplot 3.02 software (Erkrath) using a two-tailed Student’s t test. table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Antigen Antibody Dilution Cellular IR Source CD3 α-CD3, RtM 1:500 T Chemicon (Palo Alto, CA) CD11a/αL MCA819, RtM 1:6000 T, NK Camon (Wiesbaden, Germany) CD11b/αM 5C6, RtM 1:6000 MG Camon CD44 α-CD44, RtM 1:3000 T, NK, N 1-a Chemicon MHC1 ER-HR52, RtM 1:50 pMG, MG 1-a Camon MHC2 1199293, RtM 1:1000 PVM Boehringer, Mannheim (Mannheim, Germany) NG MCA771, RtM 1:400 NG Camon TCR αβ H57-597, RtM 1:800 T 1-a Pharmingen (Hamburg, Germany) TSP α-TSP, RbP 1:6000 pMG, MG, 1-a N 1-a Alexis (Gruenberg, Germany) IBA1 α-IBA1, RbP 1:6000 MG Dr. Y. Imai, Department of Neurochemistry, National Institute of Neuroscience (Tokyo, Japan) Open in a separate window αL, αL integrin subunit; αM, αM integrin subunit; IR, immunoreactivity; MHC1, MHC class I; MHC2, MHC class II; TCRαβ, T-cell receptor αβ; TSP, thrombospondin; NG, neutrophil granulocytes; T, T-cells; NK, natural killer cells; N, neurons; MG, microglia, pMG, phagocytotic microglia (microglial nodules); PVM, perivascular macrophages; RtM, rat monoclonal; RbP, rabbit polyclonal.

Techniques: