CD4 and myasthenia gravis: In the case of early-onset anti-AChR MG, the thymic germinal centers overexpress pro-inflammatory cytokines and thymic epithelial cells in response to AChR stimulation, presenting AChR subunits to autoreactive CD4+ T cells (Th1), thereby upregulating IL-4 and IL-6 and stimulating B cell proliferation to promote the production of anti-AChR antibodies [87].