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- Publisher Website: 10.1002/art.11268
- Scopus: eid_2-s2.0-0242579458
- PMID: 14613294
- WOS: WOS:000186451100037
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Article: Acceleration of the Onset of Collagen-Induced Arthritis by a Deficiency of Platelet Endothelial Cell Adhesion Molecule 1
Title | Acceleration of the Onset of Collagen-Induced Arthritis by a Deficiency of Platelet Endothelial Cell Adhesion Molecule 1 |
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Authors | |
Issue Date | 2003 |
Citation | Arthritis and Rheumatism, 2003, v. 48, n. 11, p. 3280-3290 How to Cite? |
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-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 Identifier | http://hdl.handle.net/10722/291663 |
ISSN | 2015 Impact Factor: 8.955 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Tada, Yoshifumi | - |
dc.contributor.author | Koarada, Syuichi | - |
dc.contributor.author | Morito, Fumitaka | - |
dc.contributor.author | Ushiyama, Osamu | - |
dc.contributor.author | Haruta, Yoshio | - |
dc.contributor.author | Kanegae, Futoshi | - |
dc.contributor.author | Ohta, Akihide | - |
dc.contributor.author | Ho, Alexandra | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Nagasawa, Kohei | - |
dc.date.accessioned | 2020-11-17T14:54:51Z | - |
dc.date.available | 2020-11-17T14:54:51Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Arthritis and Rheumatism, 2003, v. 48, n. 11, p. 3280-3290 | - |
dc.identifier.issn | 0004-3591 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291663 | - |
dc.description.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-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.language | eng | - |
dc.relation.ispartof | Arthritis and Rheumatism | - |
dc.title | Acceleration of the Onset of Collagen-Induced Arthritis by a Deficiency of Platelet Endothelial Cell Adhesion Molecule 1 | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1002/art.11268 | - |
dc.identifier.pmid | 14613294 | - |
dc.identifier.scopus | eid_2-s2.0-0242579458 | - |
dc.identifier.volume | 48 | - |
dc.identifier.issue | 11 | - |
dc.identifier.spage | 3280 | - |
dc.identifier.epage | 3290 | - |
dc.identifier.isi | WOS:000186451100037 | - |
dc.identifier.issnl | 0004-3591 | - |