{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:39:01Z","timestamp":1791275941740,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2004,5,6]],"date-time":"2004-05-06T00:00:00Z","timestamp":1083801600000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2004,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>A disease resembling the human spondylarthropathies develops in HLA\u2013B27\u2013transgenic rats. This disease in rats is mediated by CD4+ T cells, but antigen\u2010presenting cells (APCs) may also play a role. Dendritic cells (DCs) have been reported to be defective in allogeneic mixed lymphocyte culture in this model. Here, we further investigated the functional defect of APCs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>DCs and B cells from nontransgenic, HLA\u2013B27 (33\u20133)\u2013transgenic, and HLA\u2013B7 (120\u20134)\u2013transgenic rats were used to stimulate T cells. Surface expression of HLA\u2013B transgene and rat molecules on APCs and the formation of conjugates between DCs and T cells were monitored by flow cytometry.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We observed a strikingly defective stimulation of allogeneic and syngeneic T lymphocytes by APCs from HLA\u2013B27 but not HLA\u2013B7 rats, even if stimulation was driven in the presence of anti\u2013T cell receptor (TCR) antibody. We found no evidence that HLA\u2013B27 DCs were immature, lacked production of some diffusible factor, or produced an inhibitory factor for T cells. When comparing the levels of expression of class II major histocompatibility complex, CD2, intercellular adhesion molecule 1, lymphocyte function\u2013associated antigen 1, B7, and CD40 molecules at the surface of DCs from 33\u20103, 120\u20104, and nontransgenic rats, we found little difference. However, HLA\u2013B27\u2013transgenic DCs formed fewer conjugates with T cells than did nontransgenic DCs. Furthermore, the proportion of conjugates formed between DCs and T cells, as well as the difference between nontransgenic and HLA\u2013B27\u2013transgenic DCs, were in large part reduced by blocking CD86 on DCs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>We confirmed defective stimulation of T cells by APCs in HLA\u2013B27 rats, the mechanism of which appears to implicate APC\/T cell contact, independent of TCR engagement. In addition, decreased use of the CD86 costimulatory molecule by B27 DCs was observed. Impaired costimulatory function could result in a loss of tolerance toward microbial flora in this model.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.20211","type":"journal-article","created":{"date-parts":[[2004,5,6]],"date-time":"2004-05-06T20:03:54Z","timestamp":1083873834000},"page":"1624-1635","source":"Crossref","is-referenced-by-count":68,"title":["Defective costimulatory function is a striking feature of antigen\u2010presenting cells in an HLA\u2013B27\u2013transgenic rat model of 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