CD4 and arthritic joint disease: In another model (transfer of self-reactive CD4+ cells from KRN-TCR transgenic mice into recipient animals), Chevalier et al. observed that deficiency in CD4+ cells of signaling of lymphocytic activation molecule-associated protein (SAP) (a protein known to promote Tfh cell differentiation during GC formation) protects mice from the induction of arthritis, indicating that long-lasting interactions between T and B cells and GC formation are required for the development of the disease (115).