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Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation
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| Zeitschriftentitel: | Arthritis & Rheumatism |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Arthritis & Rheumatism, 35, 1992, 4, S. 434-442 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Baccala, Roberto Smith, Lawrence R. Vestberg, Mikael Peterson, Per A. Cole, Barry C. Theofilopoulos, Argyrios N. Baccala, Roberto Smith, Lawrence R. Vestberg, Mikael Peterson, Per A. Cole, Barry C. Theofilopoulos, Argyrios N. |
|---|---|
| author |
Baccala, Roberto Smith, Lawrence R. Vestberg, Mikael Peterson, Per A. Cole, Barry C. Theofilopoulos, Argyrios N. |
| spellingShingle |
Baccala, Roberto Smith, Lawrence R. Vestberg, Mikael Peterson, Per A. Cole, Barry C. Theofilopoulos, Argyrios N. Arthritis & Rheumatism Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation Pharmacology (medical) Immunology Rheumatology Immunology and Allergy |
| author_sort |
baccala, roberto |
| spelling |
Baccala, Roberto Smith, Lawrence R. Vestberg, Mikael Peterson, Per A. Cole, Barry C. Theofilopoulos, Argyrios N. 0004-3591 1529-0131 Wiley Pharmacology (medical) Immunology Rheumatology Immunology and Allergy http://dx.doi.org/10.1002/art.1780350413 <jats:title>Abstract</jats:title><jats:p><jats:italic>Objective.</jats:italic> <jats:italic>Mycoplasma arthritidis</jats:italic> mitogen (MAM) is mitogenic for mouse, rat, and human T cells, and behaves as a superantigen in mice through its capacity to bind to the α chain of I‐E molecules and engage entire sets of T cells expressing specific V<jats:sub>β</jats:sub>. Here, we have attempted to fully characterize the V<jats:sub>β</jats:sub>‐engaging activities of MAM in mice, and define similar activities in rats and humans.</jats:p><jats:p><jats:italic>Methods.</jats:italic> Multiprobe RNase‐protection assays and mice transgenic for human DRα, DRβ, and DRαβ were utilized for this purpose.</jats:p><jats:p><jats:italic>Results.</jats:italic> MAM‐reactive V<jats:sub>β</jats:sub> in the mouse included not only the previously reported V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, V<jats:sub>β</jats:sub>8.2, and V<jats:sub>β</jats:sub>8.3, but also V<jats:sub>β</jats:sub>5.1. In the rat, engagement of V<jats:sub>β</jats:sub>5.1, V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, and V<jats:sub>β</jats:sub>8.2, but not V<jats:sub>β</jats:sub>8.3, was documented, whereas in humans, the engaged V<jats:sub>β</jats:sub> included primarily V<jats:sub>β</jats:sub>19.1 (alternatively termed V<jats:sub>β</jats:sub>17.1) and, to a lesser extent, V<jats:sub>β</jats:sub>3.1, V<jats:sub>β</jats:sub>11.1, V<jats:sub>β</jats:sub>12.1, and V<jats:sub>β</jats:sub>13.1. In DR transgenic Eα<jats:sup>‐</jats:sup>Eβ<jats:sup>‐</jats:sup> mice, presentation of MAM and engagement of specific V<jats:sub>β</jats:sub> was effected by DRα.</jats:p><jats:p><jats:italic>Conclusions.</jats:italic> Homologous V<jats:sub>β</jats:sub> are engaged by MAM in mice, rats, and humans, presumably through a binding site similar to that proposed previously for other superantigens. MAM presentation primarily via the nonpolymorphic DRα makes it unlikely that there is involvement of such a superantigen in the pathogenesis of autoimmune diseases known to be associated with certain DR haplotypes. The possibility cannot be excluded, however, that superantigen‐activated T cells may lead to disease by cross‐reactions with self‐antigens presented by particular DR haplotypes.</jats:p> <i>Mycoplasma arthritidis</i> mitogen. V<sub>β</sub> engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation Arthritis & Rheumatism |
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Wiley, 1992 |
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Wiley, 1992 |
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1992 |
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Arthritis & Rheumatism |
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49 |
| title |
Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_unstemmed |
Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_full |
Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_fullStr |
Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_full_unstemmed |
Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_short |
Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_sort |
<i>mycoplasma arthritidis</i> mitogen. v<sub>β</sub> engaged in mice, rats, and humans, and requirement of hla‐drα for presentation |
| topic |
Pharmacology (medical) Immunology Rheumatology Immunology and Allergy |
| url |
http://dx.doi.org/10.1002/art.1780350413 |
| publishDate |
1992 |
| physical |
434-442 |
| description |
<jats:title>Abstract</jats:title><jats:p><jats:italic>Objective.</jats:italic> <jats:italic>Mycoplasma arthritidis</jats:italic> mitogen (MAM) is mitogenic for mouse, rat, and human T cells, and behaves as a superantigen in mice through its capacity to bind to the α chain of I‐E molecules and engage entire sets of T cells expressing specific V<jats:sub>β</jats:sub>. Here, we have attempted to fully characterize the V<jats:sub>β</jats:sub>‐engaging activities of MAM in mice, and define similar activities in rats and humans.</jats:p><jats:p><jats:italic>Methods.</jats:italic> Multiprobe RNase‐protection assays and mice transgenic for human DRα, DRβ, and DRαβ were utilized for this purpose.</jats:p><jats:p><jats:italic>Results.</jats:italic> MAM‐reactive V<jats:sub>β</jats:sub> in the mouse included not only the previously reported V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, V<jats:sub>β</jats:sub>8.2, and V<jats:sub>β</jats:sub>8.3, but also V<jats:sub>β</jats:sub>5.1. In the rat, engagement of V<jats:sub>β</jats:sub>5.1, V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, and V<jats:sub>β</jats:sub>8.2, but not V<jats:sub>β</jats:sub>8.3, was documented, whereas in humans, the engaged V<jats:sub>β</jats:sub> included primarily V<jats:sub>β</jats:sub>19.1 (alternatively termed V<jats:sub>β</jats:sub>17.1) and, to a lesser extent, V<jats:sub>β</jats:sub>3.1, V<jats:sub>β</jats:sub>11.1, V<jats:sub>β</jats:sub>12.1, and V<jats:sub>β</jats:sub>13.1. In DR transgenic Eα<jats:sup>‐</jats:sup>Eβ<jats:sup>‐</jats:sup> mice, presentation of MAM and engagement of specific V<jats:sub>β</jats:sub> was effected by DRα.</jats:p><jats:p><jats:italic>Conclusions.</jats:italic> Homologous V<jats:sub>β</jats:sub> are engaged by MAM in mice, rats, and humans, presumably through a binding site similar to that proposed previously for other superantigens. MAM presentation primarily via the nonpolymorphic DRα makes it unlikely that there is involvement of such a superantigen in the pathogenesis of autoimmune diseases known to be associated with certain DR haplotypes. The possibility cannot be excluded, however, that superantigen‐activated T cells may lead to disease by cross‐reactions with self‐antigens presented by particular DR haplotypes.</jats:p> |
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| author | Baccala, Roberto, Smith, Lawrence R., Vestberg, Mikael, Peterson, Per A., Cole, Barry C., Theofilopoulos, Argyrios N. |
| author_facet | Baccala, Roberto, Smith, Lawrence R., Vestberg, Mikael, Peterson, Per A., Cole, Barry C., Theofilopoulos, Argyrios N., Baccala, Roberto, Smith, Lawrence R., Vestberg, Mikael, Peterson, Per A., Cole, Barry C., Theofilopoulos, Argyrios N. |
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| description | <jats:title>Abstract</jats:title><jats:p><jats:italic>Objective.</jats:italic> <jats:italic>Mycoplasma arthritidis</jats:italic> mitogen (MAM) is mitogenic for mouse, rat, and human T cells, and behaves as a superantigen in mice through its capacity to bind to the α chain of I‐E molecules and engage entire sets of T cells expressing specific V<jats:sub>β</jats:sub>. Here, we have attempted to fully characterize the V<jats:sub>β</jats:sub>‐engaging activities of MAM in mice, and define similar activities in rats and humans.</jats:p><jats:p><jats:italic>Methods.</jats:italic> Multiprobe RNase‐protection assays and mice transgenic for human DRα, DRβ, and DRαβ were utilized for this purpose.</jats:p><jats:p><jats:italic>Results.</jats:italic> MAM‐reactive V<jats:sub>β</jats:sub> in the mouse included not only the previously reported V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, V<jats:sub>β</jats:sub>8.2, and V<jats:sub>β</jats:sub>8.3, but also V<jats:sub>β</jats:sub>5.1. In the rat, engagement of V<jats:sub>β</jats:sub>5.1, V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, and V<jats:sub>β</jats:sub>8.2, but not V<jats:sub>β</jats:sub>8.3, was documented, whereas in humans, the engaged V<jats:sub>β</jats:sub> included primarily V<jats:sub>β</jats:sub>19.1 (alternatively termed V<jats:sub>β</jats:sub>17.1) and, to a lesser extent, V<jats:sub>β</jats:sub>3.1, V<jats:sub>β</jats:sub>11.1, V<jats:sub>β</jats:sub>12.1, and V<jats:sub>β</jats:sub>13.1. In DR transgenic Eα<jats:sup>‐</jats:sup>Eβ<jats:sup>‐</jats:sup> mice, presentation of MAM and engagement of specific V<jats:sub>β</jats:sub> was effected by DRα.</jats:p><jats:p><jats:italic>Conclusions.</jats:italic> Homologous V<jats:sub>β</jats:sub> are engaged by MAM in mice, rats, and humans, presumably through a binding site similar to that proposed previously for other superantigens. MAM presentation primarily via the nonpolymorphic DRα makes it unlikely that there is involvement of such a superantigen in the pathogenesis of autoimmune diseases known to be associated with certain DR haplotypes. The possibility cannot be excluded, however, that superantigen‐activated T cells may lead to disease by cross‐reactions with self‐antigens presented by particular DR haplotypes.</jats:p> |
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| spelling | Baccala, Roberto Smith, Lawrence R. Vestberg, Mikael Peterson, Per A. Cole, Barry C. Theofilopoulos, Argyrios N. 0004-3591 1529-0131 Wiley Pharmacology (medical) Immunology Rheumatology Immunology and Allergy http://dx.doi.org/10.1002/art.1780350413 <jats:title>Abstract</jats:title><jats:p><jats:italic>Objective.</jats:italic> <jats:italic>Mycoplasma arthritidis</jats:italic> mitogen (MAM) is mitogenic for mouse, rat, and human T cells, and behaves as a superantigen in mice through its capacity to bind to the α chain of I‐E molecules and engage entire sets of T cells expressing specific V<jats:sub>β</jats:sub>. Here, we have attempted to fully characterize the V<jats:sub>β</jats:sub>‐engaging activities of MAM in mice, and define similar activities in rats and humans.</jats:p><jats:p><jats:italic>Methods.</jats:italic> Multiprobe RNase‐protection assays and mice transgenic for human DRα, DRβ, and DRαβ were utilized for this purpose.</jats:p><jats:p><jats:italic>Results.</jats:italic> MAM‐reactive V<jats:sub>β</jats:sub> in the mouse included not only the previously reported V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, V<jats:sub>β</jats:sub>8.2, and V<jats:sub>β</jats:sub>8.3, but also V<jats:sub>β</jats:sub>5.1. In the rat, engagement of V<jats:sub>β</jats:sub>5.1, V<jats:sub>β</jats:sub>6, V<jats:sub>β</jats:sub>8.1, and V<jats:sub>β</jats:sub>8.2, but not V<jats:sub>β</jats:sub>8.3, was documented, whereas in humans, the engaged V<jats:sub>β</jats:sub> included primarily V<jats:sub>β</jats:sub>19.1 (alternatively termed V<jats:sub>β</jats:sub>17.1) and, to a lesser extent, V<jats:sub>β</jats:sub>3.1, V<jats:sub>β</jats:sub>11.1, V<jats:sub>β</jats:sub>12.1, and V<jats:sub>β</jats:sub>13.1. In DR transgenic Eα<jats:sup>‐</jats:sup>Eβ<jats:sup>‐</jats:sup> mice, presentation of MAM and engagement of specific V<jats:sub>β</jats:sub> was effected by DRα.</jats:p><jats:p><jats:italic>Conclusions.</jats:italic> Homologous V<jats:sub>β</jats:sub> are engaged by MAM in mice, rats, and humans, presumably through a binding site similar to that proposed previously for other superantigens. MAM presentation primarily via the nonpolymorphic DRα makes it unlikely that there is involvement of such a superantigen in the pathogenesis of autoimmune diseases known to be associated with certain DR haplotypes. The possibility cannot be excluded, however, that superantigen‐activated T cells may lead to disease by cross‐reactions with self‐antigens presented by particular DR haplotypes.</jats:p> <i>Mycoplasma arthritidis</i> mitogen. V<sub>β</sub> engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation Arthritis & Rheumatism |
| spellingShingle | Baccala, Roberto, Smith, Lawrence R., Vestberg, Mikael, Peterson, Per A., Cole, Barry C., Theofilopoulos, Argyrios N., Arthritis & Rheumatism, Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation, Pharmacology (medical), Immunology, Rheumatology, Immunology and Allergy |
| title | Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_full | Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_fullStr | Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_full_unstemmed | Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_short | Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| title_sort | <i>mycoplasma arthritidis</i> mitogen. v<sub>β</sub> engaged in mice, rats, and humans, and requirement of hla‐drα for presentation |
| title_unstemmed | Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation |
| topic | Pharmacology (medical), Immunology, Rheumatology, Immunology and Allergy |
| url | http://dx.doi.org/10.1002/art.1780350413 |