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Q: Arthritis and valvular carditis coexist in several human rheumatic diseases, including systemic lupus erythematosus, rheumatic fever, and rheumatoid arthritis. T cell receptor-transgenic K/BxN mice develop spontaneous autoantibody-associated arthritis and valvular carditis. The common Fc receptor (FcR) signaling chain is required for carditis to develop in K/BxN mice. FcR pairs with numerous receptors in a variety of cells. The aim of this study was to identify the FcR-associated receptors and Fc receptor (FcR)-expressing cells that mediate valvular carditis in this model.', 'We bred K/BxN mice lacking the genes that encode activating Fc receptors (FcRI, FcRIII, and FcRIV), and we assessed these mice for valvular carditis. We similarly evaluated complement component C3-deficient K/BxN mice. Immunohistochemistry, bone marrow transplantation, and macrophage depletion were used to define the key FcR-expressing cell type.', 'Genetic deficiency of only one of the activating Fc receptors did not prevent carditis, whereas deficiency of all 3 activating Fc receptors did. Further analysis demonstrated that FcRIII and FcRIV were the key drivers of valve inflammation; FcRI was dispensable. C3 was not required. FcR expression by radioresistant cells was critical for valvular carditis to develop, and further analysis indicated that macrophages were the key candidate FcR-expressing effectors of carditis.
A:
Do fc receptor III and Fc receptor IV on macrophages drive autoimmune valvular carditis in mice?