RGD Reference Report - Acceleration of the onset of collagen-induced arthritis by a deficiency of platelet endothelial cell adhesion molecule 1. - Rat Genome Database

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Acceleration of the onset of collagen-induced arthritis by a deficiency of platelet endothelial cell adhesion molecule 1.

Authors: Tada, Y  Koarada, S  Morito, F  Ushiyama, O  Haruta, Y  Kanegae, F  Ohta, A  Ho, A  Mak, TW  Nagasawa, K 
Citation: Tada Y, etal., Arthritis Rheum. 2003 Nov;48(11):3280-90.
RGD ID: 6771222
Pubmed: PMID:14613294   (View Abstract at PubMed)
DOI: DOI:10.1002/art.11268   (Journal Full-text)

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. CONCLUSION: 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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Arthritis severityISOPecam1 (Mus musculus)6771222; 6771222 RGD 
Experimental Arthritis severityIMP 6771222 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Pecam1  (platelet and endothelial cell adhesion molecule 1)

Genes (Mus musculus)
Pecam1  (platelet/endothelial cell adhesion molecule 1)

Genes (Homo sapiens)
PECAM1  (platelet and endothelial cell adhesion molecule 1)


Additional Information