{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T11:07:57Z","timestamp":1760267277975,"version":"3.40.3"},"reference-count":55,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2005,7,1]],"date-time":"2005-07-01T00:00:00Z","timestamp":1120176000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Dimethyl dioctadecyl ammonium bromide (DDA) (C38H80NBr) is a nonantigenic lipoid material. DDA-induced arthritis (DIA) in the Lewis (LEW) (RT.1l) rat is a new experimental model for human rheumatoid arthritis (RA). DIA is a T cell-mediated autoimmune disease. However, the precise self\/foreign Ags associated with the disease process in DIA are not yet known. We observed that LEW rats with DIA spontaneously raised a vigorous T cell response both to 65-kDa self (rat) heat shock protein (Rhsp65) and mycobacterial hsp65 (Bhsp65), but not to another arthritis-related Ag, bovine collagen type II. The T cell response to Rhsp65 was focused predominantly on determinant regions 120\u2013134 and 213\u2013227 of the self protein. Interestingly, pretreatment of adult LEW rats using either a mixture of peptides 120\u2013134 and 213\u2013227 of Rhsp65 or a low nonarthritogenic dose of DDA induced protection against subsequent DIA. Intriguingly, the protection induced by the latter was associated with spontaneous priming of T cells specific for peptide 213\u2013227 of Rhsp65. Similarly, LEW rats neonatally tolerized against either Rhsp65 or Bhsp65 were significantly protected from subsequently induced DIA at adult stage, showing the disease-modulating attribute of the hsp65-specific T cells. Taken together, the above findings demonstrate that the hsp65-directed T cell repertoire is of significance in the pathogenesis of autoimmune arthritis induced by nonantigenic DDA. Like other animal models of RA involving hsp65, these first insights into the disease-associated Ags in the DIA model would pave the way for further understanding of the immunological aspects of induction and regulation of RA.<\/jats:p>","DOI":"10.4049\/jimmunol.175.1.219","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T01:08:21Z","timestamp":1398042501000},"page":"219-227","source":"Crossref","is-referenced-by-count":12,"title":["Heat Shock Protein 65-Reactive T Cells Are Involved in the Pathogenesis of Non-Antigenic Dimethyl Dioctadecyl Ammonium Bromide-Induced Arthritis"],"prefix":"10.1093","volume":"175","author":[{"given":"Md Younus","family":"Mia","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Malarvizhi","family":"Durai","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hong Ro","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kamal D","family":"Moudgil","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD 21201"},{"name":"Division of Rheumatology, Department of Medicine, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2005,7,1]]},"reference":[{"first-page":"95","volume-title":"Proc. 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