Activated B Cells Participating in the Anti-Myelin Response Are Excluded from the Inflamed Central Nervous System in a Model of Autoimmunity that Allows for B Cell Recognition of Autoantigen

التفاصيل البيبلوغرافية
العنوان: Activated B Cells Participating in the Anti-Myelin Response Are Excluded from the Inflamed Central Nervous System in a Model of Autoimmunity that Allows for B Cell Recognition of Autoantigen
المؤلفون: Sarah L. Zhu, Rajiv W. Jain, Yodit Tesfagiorgis, Steven M. Kerfoot
المصدر: The Journal of Immunology. 199:449-457
بيانات النشر: The American Association of Immunologists, 2017.
سنة النشر: 2017
مصطلحات موضوعية: Central Nervous System, 0301 basic medicine, Encephalomyelitis, Autoimmune, Experimental, Lymphoid Tissue, T-Lymphocytes, Immunology, Central nervous system, Autoimmunity, Inflammation, Biology, Lymphocyte Activation, medicine.disease_cause, Autoantigens, Mice, 03 medical and health sciences, Myelin, 0302 clinical medicine, Cell Movement, medicine, Animals, Immunology and Allergy, Myelin Sheath, B cell, B-Lymphocytes, Effector, Mice, Inbred C57BL, B-1 cell, Disease Models, Animal, 030104 developmental biology, medicine.anatomical_structure, Spinal Cord, B7-1 Antigen, medicine.symptom, 030217 neurology & neurosurgery, CD80
الوصف: Once activated, T cells gain the ability to access both healthy and inflamed nonlymphoid tissues. They are then reactivated to remain in the tissue and exert their effector function only if they encounter their specific Ag. In this study, we set out to determine if the same is true for B cells using a mouse model of CNS autoimmunity that incorporates both T and B cell recognition of a myelin autoantigen. Both T and B cells were common infiltrates of spinal cords in diseased mice. However, unlike T cells, anti-myelin B cells were excluded from the inflamed tissue. Further, CNS B cells did not have a phenotype consistent with Ag-specific activation as it occurs in lymphatic tissue. Instead, they expressed elevated levels of CD80, indicating that B cells may contribute to local inflammation through nonantigen-specific mechanisms.
تدمد: 1550-6606
0022-1767
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ed1b57d74170a7e9670d6416b4a5806a
https://doi.org/10.4049/jimmunol.1602042
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....ed1b57d74170a7e9670d6416b4a5806a
قاعدة البيانات: OpenAIRE