Rheumatoid arthritis (RA) is best known as a chronic inflammatory disease caused by the immune system inappropriately attacking the joints. However, the autoimmune response also leads to the recruitment and/or differentiation of cells known as osteoclasts -- which are cells that degrade and resorb bone. Current treatments for patients with RA target either the joint-specific immune response or the osteoclast-mediated bone erosion.
Now, in a study appearing online on October 19 in advance of publication in the November print issue of the Journal of Clinical Investigation, researchers from Washington University have shown that the protein PLC-gamma-2, which was already known to regulate the differentiation of B cells (one of the immune cells crucial to the autoimmune response seen in RA), is required for normal osteoclast development and function in mice. Roberta Faccio and colleagues therefore suggest that targeting PLC-gamma-2 might lead to control of both the immune-mediated joint destruction and osteoclast-mediated bone erosion seen in RA.