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
in En
| WPRIM
| ID: wpr-775416
Responsible library:
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.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Rats, Inbred Lew
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B-Lymphocytes
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Receptors, Cholinergic
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T-Lymphocytes, Helper-Inducer
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Receptor Cross-Talk
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Myasthenia Gravis, Autoimmune, Experimental
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Protein Subunits
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Disease Models, Animal
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Allergy and Immunology
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Proto-Oncogene Proteins c-bcl-6
Limits:
Animals
Language:
En
Journal:
Neuroscience Bulletin
Year:
2019
Type:
Article