title: Acceleration of the onset of collagen-induced arthritis by a deficiency of platelet endothelial cell adhesion molecule 1.
abstract: OBJECTIVE
  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).
  
  
  METHODS
  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-gamma (IFNgamma) 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.
  
  
  RESULTS
  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. IFNgamma 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.
  
  
  CONCLUSIONS
  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.
authors: Saga Medical School, Saga, Japan. taday@post.saga-med.ac.jp
authors: Yoshifumi
authors: Y
authors: Tada
authors: Syuichi
authors: S
authors: Koarada
authors: Fumitaka
authors: F
authors: Morito
authors: Osamu
authors: O
authors: Ushiyama
authors: Yoshio
authors: Y
authors: Haruta
authors: Futoshi
authors: F
authors: Kanegae
authors: Akihide
authors: A
authors: Ohta
authors: Alexandra
authors: A
authors: Ho
authors: Tak W
authors: TW
authors: Mak
authors: Kohei
authors: K
authors: Nagasawa
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D001323:Autoantibodies / Q000097:blood; D002465:Cell Movement; D024043:Collagen Type II / Q000276:immunology / Q000494:pharmacology; D004195:Disease Models, Animal; D006614:Hindlimb / Q000473:pathology; D007074:Immunoglobulin G / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D007596:Joints / Q000473:pathology; D008198:Lymph Nodes / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008811:Mice, Inbred DBA; D018345:Mice, Knockout; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis* / Q000235:genetics; D013154:Spleen / Q000166:cytology / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D001323:Autoantibodies; D024043:Collagen Type II; D007074:Immunoglobulin G; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D007371:Interferon-gamma