Intracellular cytokine staining of splenocytes showed that, in addition to Th17 cells, lack of SR-A also dramatically reduced the frequency of Th1 cells, i.e., TNF-α-producing CD4+ T cells (Fig. 7g), underscoring an important role of SR-A in arthritis-associated inflammation. The gene discussed is CD4; the disease is arthritic joint disease.