Daiya Ohara

Abstract Autoimmune T cells orchestrate joint inflammation and pain in concert with synovial macrophages; however, the mechanisms governing the development and functional diversification of these macrophages remain unclear. Using a model of T helper 17 cell (TH17 cell)–mediated autoimmune arthritis, we show that joint-infiltrating Ly6Chi monocytes in response to autoimmune TH17 cells, rather than resident synovial macrophages, are the primary mediators of disease pathogenesis.

Abstract Excessive activation of interleukin-17-producing helper T (TH17) cells can cause autoimmune tissue inflammation. However, how TH17 cells enhance their pathogenicity within target tissues and whether destabilized regulatory T cells contribute to pathogenic TH17 cell populations remain unclear.

Abstract In mammals, fertilization takes place followed by fetus development in the maternal body, so the number of fetuses that exceeds the mother's capacity increases the frequency of stunted growth and stillbirths, while an excessive number of pups increases postnatal stunting and maternal child-rearing stress, which is detrimental to offspring procreation and species maintenance.