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Klaus V Toyka - One of the best experts on this subject based on the ideXlab platform.
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Macrophages but not Schwann cells express Ia Antigen in experimental autoimmune neuritis.
Annals of Neurology, 1990Co-Authors: Beate Schmidt, Kurt Heininger, Bärbel Schäfer, Guido Stoll, Hans-peter Hartung, Klaus V ToykaAbstract:: This study was designed to identify which cells express major histocompatibility complex class II (Ia) Antigen in experimental autoimmune neuritis and may therefore be Antigen presenters. SerIal 1-micron-thick cryosections of ventral roots of animals with experimental autoimmune neuritis were labeled with Ox6 antibody against rat Ia, the ED1 antibody to identify monocytes/macrophages and an antiserum against S100, a marker for Schwann cells. Ia-positive cells were predominantly present before overt clinical signs and demyelination (day 12). At later stages when many axons were demyelinated, their number was markedly reduced. Few Ia-positive cells that had extending long processes, which over some distance were in immedIate contact with several myelin sheaths, were scattered in normal-appearing nerve roots at these later time points. Most of the Ia-positive cells could be identified as ED1-positive lean monocytes/macrophages, but in contrast most phagocytic macrophages in advanced stages of myelin degradation no longer expressed Ia. Ia-positive structures were invarIably negative for S100 at early and late stages of experimental autoimmune neuritis, indicating that Schwann cells did not express identifIable Ia Antigen. These findings contrast with reports of expression of major histocompatibility complex class II Antigens by Schwann cells in human neuropathies. Furthermore they do not support the notion that aberrant Ia expression by Schwann cells plays a major pathogenic role in experimental autoimmune disease of the peripheral nervous system.
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Macrophages but not Schwann cells express Ia Antigen in experimental autoimmune neuritis.
Annals of Neurology, 1990Co-Authors: Beate Schmidt, Kurt Heininger, Bärbel Schäfer, Guido Stoll, Hans-peter Hartung, Klaus V ToykaAbstract:: This study was designed to identify which cells express major histocompatibility complex class II (Ia) Antigen in experimental autoimmune neuritis and may therefore be Antigen presenters. SerIal 1-micron-thick cryosections of ventral roots of animals with experimental autoimmune neuritis were labeled with Ox6 antibody against rat Ia, the ED1 antibody to identify monocytes/macrophages and an antiserum against S100, a marker for Schwann cells. Ia-positive cells were predominantly present before overt clinical signs and demyelination (day 12). At later stages when many axons were demyelinated, their number was markedly reduced. Few Ia-positive cells that had extending long processes, which over some distance were in immedIate contact with several myelin sheaths, were scattered in normal-appearing nerve roots at these later time points. Most of the Ia-positive cells could be identified as ED1-positive lean monocytes/macrophages, but in contrast most phagocytic macrophages in advanced stages of myelin degradation no longer expressed Ia. Ia-positive structures were invarIably negative for S100 at early and late stages of experimental autoimmune neuritis, indicating that Schwann cells did not express identifIable Ia Antigen. These findings contrast with reports of expression of major histocompatibility complex class II Antigens by Schwann cells in human neuropathies. Furthermore they do not support the notion that aberrant Ia expression by Schwann cells plays a major pathogenic role in experimental autoimmune disease of the peripheral nervous system.
Edna Mozes - One of the best experts on this subject based on the ideXlab platform.
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Ia Antigen t cell interactions for a thymus independent Antigen composed of d amino acids
Proceedings of the National Academy of Sciences of the United States of America, 1993Co-Authors: Einat Zisman, Molly Dayan, Michael Sela, Edna MozesAbstract:Abstract Synthetic polypeptide Antigens of L amino acids, although bearing repeating sequences, are thymus-dependent (L-TD), whereas the same polymers composed of D amino acids are thymus-independent (D-TI), probably due to a slower rate of metabolism. Yet we found that lymph-node cells of BALB/c mice immunized with D-TI proliferate in response to it in vitro. To follow T-cell activation by D-TI, we established T-cell hybridomas to D-TI and to its analog composed of L isomers, L-TD, for comparison. The T-cell hybridomas express membrane alpha/beta T-cell receptors and secrete interleukin 2 upon stimulation with the respective Antigen. In addition, D-TI-specific hybridomas are stimulated, to a lesser extent, by the L-TD Antigen, whereas only some L-TD-specific hybridomas recognize D-TI. Moreover, biotinylated analogs of D-TI and L-TD bind to splenic Antigen-presenting cells (APCs) from BALB/c mice. Binding is inhibited by an excess of nonbiotinylated L-TD, and by an excess of a peptide comprising residues 259-271 of the human acetylcholine receptor alpha subunit, which binds to I-Ad and I-Ed molecules without prior processing. Analysis of APC lysates following incubation of the APCs with biotinylated D-TI and L-TD reveals that the biotinylated Antigen moiety is assocIated with Ia molecules. D-TI and L-TD bind to Ia molecules on intact APCs with similar KD values, 5 x 10(-8) M and 3 x 10(-8) M, respectively. However, D-TI has faster kinetics of binding than L-TD, probably due to different processing requirements. Hence, we have demonstrated a major histocompatibility complex class II-medIated T-cell response to a thymus-independent Antigen.
Beate Schmidt - One of the best experts on this subject based on the ideXlab platform.
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Macrophages but not Schwann cells express Ia Antigen in experimental autoimmune neuritis.
Annals of Neurology, 1990Co-Authors: Beate Schmidt, Kurt Heininger, Bärbel Schäfer, Guido Stoll, Hans-peter Hartung, Klaus V ToykaAbstract:: This study was designed to identify which cells express major histocompatibility complex class II (Ia) Antigen in experimental autoimmune neuritis and may therefore be Antigen presenters. SerIal 1-micron-thick cryosections of ventral roots of animals with experimental autoimmune neuritis were labeled with Ox6 antibody against rat Ia, the ED1 antibody to identify monocytes/macrophages and an antiserum against S100, a marker for Schwann cells. Ia-positive cells were predominantly present before overt clinical signs and demyelination (day 12). At later stages when many axons were demyelinated, their number was markedly reduced. Few Ia-positive cells that had extending long processes, which over some distance were in immedIate contact with several myelin sheaths, were scattered in normal-appearing nerve roots at these later time points. Most of the Ia-positive cells could be identified as ED1-positive lean monocytes/macrophages, but in contrast most phagocytic macrophages in advanced stages of myelin degradation no longer expressed Ia. Ia-positive structures were invarIably negative for S100 at early and late stages of experimental autoimmune neuritis, indicating that Schwann cells did not express identifIable Ia Antigen. These findings contrast with reports of expression of major histocompatibility complex class II Antigens by Schwann cells in human neuropathies. Furthermore they do not support the notion that aberrant Ia expression by Schwann cells plays a major pathogenic role in experimental autoimmune disease of the peripheral nervous system.
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Macrophages but not Schwann cells express Ia Antigen in experimental autoimmune neuritis.
Annals of Neurology, 1990Co-Authors: Beate Schmidt, Kurt Heininger, Bärbel Schäfer, Guido Stoll, Hans-peter Hartung, Klaus V ToykaAbstract:: This study was designed to identify which cells express major histocompatibility complex class II (Ia) Antigen in experimental autoimmune neuritis and may therefore be Antigen presenters. SerIal 1-micron-thick cryosections of ventral roots of animals with experimental autoimmune neuritis were labeled with Ox6 antibody against rat Ia, the ED1 antibody to identify monocytes/macrophages and an antiserum against S100, a marker for Schwann cells. Ia-positive cells were predominantly present before overt clinical signs and demyelination (day 12). At later stages when many axons were demyelinated, their number was markedly reduced. Few Ia-positive cells that had extending long processes, which over some distance were in immedIate contact with several myelin sheaths, were scattered in normal-appearing nerve roots at these later time points. Most of the Ia-positive cells could be identified as ED1-positive lean monocytes/macrophages, but in contrast most phagocytic macrophages in advanced stages of myelin degradation no longer expressed Ia. Ia-positive structures were invarIably negative for S100 at early and late stages of experimental autoimmune neuritis, indicating that Schwann cells did not express identifIable Ia Antigen. These findings contrast with reports of expression of major histocompatibility complex class II Antigens by Schwann cells in human neuropathies. Furthermore they do not support the notion that aberrant Ia expression by Schwann cells plays a major pathogenic role in experimental autoimmune disease of the peripheral nervous system.
Einat Zisman - One of the best experts on this subject based on the ideXlab platform.
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Ia Antigen t cell interactions for a thymus independent Antigen composed of d amino acids
Proceedings of the National Academy of Sciences of the United States of America, 1993Co-Authors: Einat Zisman, Molly Dayan, Michael Sela, Edna MozesAbstract:Abstract Synthetic polypeptide Antigens of L amino acids, although bearing repeating sequences, are thymus-dependent (L-TD), whereas the same polymers composed of D amino acids are thymus-independent (D-TI), probably due to a slower rate of metabolism. Yet we found that lymph-node cells of BALB/c mice immunized with D-TI proliferate in response to it in vitro. To follow T-cell activation by D-TI, we established T-cell hybridomas to D-TI and to its analog composed of L isomers, L-TD, for comparison. The T-cell hybridomas express membrane alpha/beta T-cell receptors and secrete interleukin 2 upon stimulation with the respective Antigen. In addition, D-TI-specific hybridomas are stimulated, to a lesser extent, by the L-TD Antigen, whereas only some L-TD-specific hybridomas recognize D-TI. Moreover, biotinylated analogs of D-TI and L-TD bind to splenic Antigen-presenting cells (APCs) from BALB/c mice. Binding is inhibited by an excess of nonbiotinylated L-TD, and by an excess of a peptide comprising residues 259-271 of the human acetylcholine receptor alpha subunit, which binds to I-Ad and I-Ed molecules without prior processing. Analysis of APC lysates following incubation of the APCs with biotinylated D-TI and L-TD reveals that the biotinylated Antigen moiety is assocIated with Ia molecules. D-TI and L-TD bind to Ia molecules on intact APCs with similar KD values, 5 x 10(-8) M and 3 x 10(-8) M, respectively. However, D-TI has faster kinetics of binding than L-TD, probably due to different processing requirements. Hence, we have demonstrated a major histocompatibility complex class II-medIated T-cell response to a thymus-independent Antigen.
Donald V Belsito - One of the best experts on this subject based on the ideXlab platform.
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immunosuppressive effects of transforming growth factor β inhibition of the induction of Ia Antigen on langerhans cells by cytokines and the contact hypersensitivity response
Journal of Investigative Dermatology, 1990Co-Authors: Seth P Epstein, Rudolf L Baer, Jeanette G Thorbecke, Donald V BelsitoAbstract:Abstract Recent reports show that transforming growth factor (TGF)-β exerts a variety of immunosuppressive activities. The present study focuses on the effects of TGF-β1 on expression of Ia Antigen by Langerhans cells. Although TGF-β1, in concentrations from 0.001 to 100 μg/ml, has no effect on constitutive expression of Ia Antigen on these cells, the in vitro up-regulation of Ia Antigen on the surface of LC by interleukin (IL)-1, tumor necrosis factor-α, interferon-γ, IL-3, and granulocyte/macrophage-colony stimulating factor is inhibited by the concommitant addition of 1 μg/ml TGF-β1. In contrast, TGF-β1 has no effect on the up-regulation induced by IL-2 or IL-6. In this report, the activity of TGF-β closely resembles that of Cyclosporine A (CsA). Similar results are seen in vivo when either TGF-β1 (5 μg, intraperitoneally [ip], daily on days 0–3) or CsA (1 mg, subcutaneously [sc], twice daily on days 0–3) are given together with IL-2 (500 U, intraperitoneally [ip], twice daily on days 1–3) or interferon-γ (4,000 U, ip, twice daily on days 1–3). Given the important role of Ia expression in cell-medIated immune reactions, the effect of TGF-β on contact sensitivity was next investigated. In doses of 5 μg, ip, daily on days 6–8, TGF-β inhibits the expression of contact reactivity in animals sensitized on day 0 and challenged on day 7. In contrast, no effect is observed on the induction of contact sensitivity in mice given TGF-β1 on days −1 to 2, sensitized on day 0, and challenged on day 7. The possible importance of antagonism between TGF-β and other cytokines, especIally IFN-γ, involved in the elicitation of contact hypersensitivity reactions is discussed.