Studies have shown that SCID, RAG-1−/−, TCRα−/−, CD4−/−, and MHCII−/− mice display delayed or failed resolution of chlamydial primary infections, while MHCI-deficient (b2M−/−), B cell-deficient (μMT), and CD8−/− mice resolve infection with comparable kinetics to wild-type, demonstrating that CD4+ T cells are key mediators of chlamydial host defense [62,103,104,105,106]. The gene discussed is RAG1; the disease is infection.