MERTK and autoimmune myocarditis: In contrast, during acute injury in autoimmune myocarditis, activated fibroblasts not only inhibit the differentiation of monocytes from Ly6Clow into reparative macrophages through the upregulation of IL-17A but also promote the shedding of MER receptor tyrosine kinase (MerTK) on Ly6Chigh from macrophages, leading to an overall proinflammatory phenotype with impaired efferent cell activity [92].