Neutrophils orchestrate their own recruitment in murine arthritis through C5aR and FcγR signaling.

ABSTRACT: Neutrophil recruitment into the joint is a hallmark of inflammatory arthritides, including rheumatoid arthritis (RA). In a mouse model of autoantibody-induced inflammatory arthritis, neutrophils infiltrate the joint via multiple chemoattractant receptors, including the leukotriene B(4) (LTB(4)) receptor BLT1 and the chemokine receptors CCR1 and CXCR2. Once in the joint, neutrophils perpetuate their own recruitment by releasing LTB(4) and IL-1β, presumably after activation by immune complexes deposited on joint structures. Two pathways by which immune complexes may activate neutrophils include complement fixation, resulting in the generation of C5a, and direct engagement of Fcγ receptors (FcγRs). Previous investigations showed that this model of autoantibody-induced arthritis requires the C

SUBMITTER: Sadik CD 

PROVIDER: S-EPMC3503206 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature