Antigen receptor-mediated B cell death is blacked by signaling via CD72 or treatment with dextran sukfate and is defective in autoimmunity-prone mice
| العنوان: | Antigen receptor-mediated B cell death is blacked by signaling via CD72 or treatment with dextran sukfate and is defective in autoimmunity-prone mice |
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| المؤلفون: | Takamasa Nomura, Hideo Yagita, Tasuku Honjo, M C Howard, Hidetaka Yakura, Hua Han, Takeshi Tsubata |
| المصدر: | International Immunology. 8:867-875 |
| بيانات النشر: | Oxford University Press (OUP), 1996. |
| سنة النشر: | 1996 |
| مصطلحات موضوعية: | Lipopolysaccharides, Immunology, B-cell receptor, Naive B cell, Receptors, Antigen, B-Cell, Apoptosis, Mice, Transgenic, CD5 Antigens, Autoimmune Diseases, Mice, Antigens, CD, medicine, Animals, Immunology and Allergy, Cytotoxic T cell, CD40 Antigens, Antigen-presenting cell, B cell, B-Lymphocytes, CD40, Mice, Inbred NZB, biology, ZAP70, Dextran Sulfate, Receptors, Interleukin, General Medicine, Molecular biology, Receptors, Interleukin-4, Antigens, Differentiation, B-Lymphocyte, Mice, Inbred C57BL, B-1 cell, medicine.anatomical_structure, Mice, Inbred DBA, biology.protein, Disease Susceptibility, Signal Transduction |
| الوصف: | Mature B cells undergo programmed cell death when surface (s) Ig is extensively multimerized. A signal that blocks death of B cells is thus required for activation of B cells in response to antigen stimulation. Here we show that only a few diverse transmembrane signals capable of inducing activation and proliferation of B cells blocked sig-mediated death of normal mature B cells, and that there is no correlation between mitogenic activity and the ability to rescue B cells from death. The results suggest that a specific signal is required for abrogating B cell death induced by sig cross-linking. Signaling via IL-4 receptor and CD40, both of which are derived from activated T cells, blocked sig-mediated death, as described previously. Signaling through a B cell antigen CD72, a counter-receptor of the pan-T antigen CD5, also blocked death of anti-Ig-treated mouse spleen B cells. CD72 signal may play a role in survival of B cells at the initial step of T-B interaction, where resting T cells recognize antigens presented by B cells. Moreover, B cell death by anti-Ig was blocked by T cell-independent antigens such as lipopolysaccharide and dextran sulfate, and spleen B cells from New Zealand mice, which are prone to autoantibody-dependent autoimmune diseases, were resistant to sig-mediated death. Mechanisms for blocking sig-mediated death may therefore be required in antibody response to foreign antigens regardless of T independence or T dependence and in autoantibody production. |
| تدمد: | 1460-2377 0953-8178 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6c3041cb58abc799aeb7ac1dcea3fa6d https://doi.org/10.1093/intimm/8.6.867 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....6c3041cb58abc799aeb7ac1dcea3fa6d |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14602377 09538178 |
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