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Article: Acceleration of the Onset of Collagen-Induced Arthritis by a Deficiency of Platelet Endothelial Cell Adhesion Molecule 1

TitleAcceleration of the Onset of Collagen-Induced Arthritis by a Deficiency of Platelet Endothelial Cell Adhesion Molecule 1
Authors
Issue Date2003
Citation
Arthritis and Rheumatism, 2003, v. 48, n. 11, p. 3280-3290 How to Cite?
AbstractObjective. 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-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. 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. 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. 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.
Persistent Identifierhttp://hdl.handle.net/10722/291663
ISSN
2015 Impact Factor: 8.955
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTada, Yoshifumi-
dc.contributor.authorKoarada, Syuichi-
dc.contributor.authorMorito, Fumitaka-
dc.contributor.authorUshiyama, Osamu-
dc.contributor.authorHaruta, Yoshio-
dc.contributor.authorKanegae, Futoshi-
dc.contributor.authorOhta, Akihide-
dc.contributor.authorHo, Alexandra-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorNagasawa, Kohei-
dc.date.accessioned2020-11-17T14:54:51Z-
dc.date.available2020-11-17T14:54:51Z-
dc.date.issued2003-
dc.identifier.citationArthritis and Rheumatism, 2003, v. 48, n. 11, p. 3280-3290-
dc.identifier.issn0004-3591-
dc.identifier.urihttp://hdl.handle.net/10722/291663-
dc.description.abstractObjective. 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-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. 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. 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. 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.-
dc.languageeng-
dc.relation.ispartofArthritis and Rheumatism-
dc.titleAcceleration of the Onset of Collagen-Induced Arthritis by a Deficiency of Platelet Endothelial Cell Adhesion Molecule 1-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/art.11268-
dc.identifier.pmid14613294-
dc.identifier.scopuseid_2-s2.0-0242579458-
dc.identifier.volume48-
dc.identifier.issue11-
dc.identifier.spage3280-
dc.identifier.epage3290-
dc.identifier.isiWOS:000186451100037-
dc.identifier.issnl0004-3591-

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