Platelet endothelial cell adhesion molecule 1 (PECAM‐1; CD31) is a member of the immunoglobulin superfamily that is expressed in platelets, leukocytes, and endothelial cells. PECAM‐1 has been shown to play a role in transendothelial migration of leukocytes and contains immunoreceptor tyrosine‐based inhibitory motifs in its cytoplasmic tail and inhibits cellular responses. We examined the role of PECAM‐1 in the development of collagen‐induced arthritis (CIA).

CIA was induced in PECAM‐1–deficient DBA/1 mice. The incidence of arthritis and the arthritis index were examined. Anti–type II collagen (anti‐CII) antibody levels and interferon‐γ (IFNγ) production by lymph node cells and spleen cells were determined. Lymphocytes from arthritic PECAM‐1–deficient and wild‐type mice were labeled with dye, transferred to arthritic PECAM‐1^+/− mice, and cell migration to inflamed joints was examined.

PECAM‐1–deficient mice showed accelerated onset of arthritis and increased severity only during the early phase. Anti‐CII antibody levels were also increased during the early phase. IFNγ production by lymph node cells and spleen cells from PECAM‐1–deficient mice in response to CII was higher than that in wild‐type mice. Lymphocytes from arthritic PECAM‐1–deficient mice showed accelerated migration to inflamed joints, but not lymph nodes or spleen. The development of anti‐CII antibody–induced arthritis was similar in PECAM‐1–deficient and wild‐type mice.

These results indicate that PECAM‐1 negatively regulates humoral and cell‐mediated immune responses and lymphocyte migration into joints and, consequently, the development of CIA. In addition, the role of PECAM‐1 in the transendothelial migration of leukocytes appears to be redundant in this model.