RESUMO
FcγR is a significant opsonin receptor located on the surface of immune cells, playing a crucial role in Ab-dependent cell-mediated immunity. Our previous work revealed opposite expression trends of FcγRII and FcγRIII in flounder mIgM+ B lymphocytes after phagocytosis of antiserum-opsonized Edwardsiella tarda. This observation suggests that FcγRII and FcγRIII might serve distinct functions in Ig-opsonized immune responses. In this study, we prepared rFcγRIII as well as its corresponding Abs to investigate the potential roles of FcγRII and FcγRIII in the Ab-dependent immune response of IgM+ B cells. Our findings indicate that, unlike FcγRII, FcγRIII does not participate in Ab-dependent cellular phagocytosis. Instead, it is involved in cytokine production and bacterial killing in mIgM+ B lymphocytes. Additionally, we identified platelet-derived ADAM17 as a key factor in regulating FcγRIII shedding and cytokine release in mIgM+ B lymphocytes. These results elucidate the functions of FcγRII and FcγRIII in the innate immunology of mIgM+ B lymphocytes and contribute to an improved understanding of the regulatory roles of FcγRs in the phagocytosis of teleost B lymphocytes.
