I n previous studies that were initiated in experimental models of different inflammatory autoimmune diseases and then extended to humans, we have shown that in the course of inflammatory autoimmune diseases, the immune system selectively generates an auto-Ab response to a few inflammatory mediators, mostly chemokines and cytokines, which are thought to participate in promoting the inflammatory process (1-6). For example, we showed that patients suffering from rheumatoid arthritis (RA) but not osteoarthritis display a significant level of neutralizing auto- Abs directed against TNF-a (tumor necrosis factor)(3). These patients did not mount any auto-Ab response either to several key inflammatory chemokines or to regulatory mediators, such as IL-10(interleukin-10) or TGF-b(tumor growth factor)(, or even the chemokine CXCL12(C-X-C motif chemokine 12), which also functions as a regulatory mediator that selects Ag-specific IL-10-producing CD4+(cluster of differentiation 4) T cells (7).