Enhancement of T Follicular Helper Cell-Mediated Humoral Immunity Reponses During Development of Experimental Autoimmune Myasthenia Gravis / 神经科学通报·英文版
Neuroscience Bulletin
; (6): 507-518, 2019.
Article
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| WPRIM
| ID: wpr-775416
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WPRO
ABSTRACT
Myasthenia gravis (MG) is a prototypical antibody-mediated neurological autoimmune disease with the involvement of humoral immune responses in its pathogenesis. T follicular helper (Tfh) cells have been implicated in many autoimmune diseases. However, whether and how Tfh cells are involved in MG remain unclear. Here, we established and studied a widely-used and approved animal model of human MG, the rat model with acetylcholine receptor alpha (AChRα) subunit (R-AChR)-induced experimental autoimmune myasthenia gravis (EAMG). This model presented mild body-weight loss 10 days after the first immunization (representing the early stage of disease) and more obvious clinical manifestations and body-weight loss 7 days after the second immunization (representing the late stage of disease). AChR-specific pre-Tfh cells and mature Tfh cells were detected in these two stages, respectively. In co-cultures of Tfh cells and B cells, the number of IgG2b-secreting B cells and the level of anti-AChR antibodies in the supernatant were higher in the cultures containing EAMG-derived Tfh cells. In immunohistochemistry and immunofluorescence assays, a substantial number of CD4/Bcl-6 T cells and a greater number of larger germinal centers were observed in lymph node tissues resected from EAMG rats. Based on these results, we hypothesize that an AChR-specific Tfh cell-mediated humoral immune response contributes to the development of EAMG.
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Base de datos:
WPRIM
Asunto principal:
Ratas Endogámicas Lew
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Linfocitos B
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Receptores Colinérgicos
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Linfocitos T Colaboradores-Inductores
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Receptor Cross-Talk
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Miastenia Gravis Autoinmune Experimental
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Subunidades de Proteína
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Modelos Animales de Enfermedad
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Alergia e Inmunología
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Proteínas Proto-Oncogénicas c-bcl-6
Límite:
Animals
Idioma:
En
Revista:
Neuroscience Bulletin
Año:
2019
Tipo del documento:
Article