{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,29]],"date-time":"2026-03-29T21:28:03Z","timestamp":1774819683028,"version":"3.50.1"},"reference-count":15,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,11,17]],"date-time":"2005-11-17T00:00:00Z","timestamp":1132185600000},"content-version":"vor","delay-in-days":7260,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1986,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The mutant <jats:italic>lpr<\/jats:italic> gene causes a generalized massive T cell proliferation and an associated autoimmune disease in mice. The <jats:italic>lpr<\/jats:italic> T cells bear unusual membrane phenotypes and play a causative role in the pathogenesis of autoimmune disease through excess production of some lymphokines. Therefore, the \u201caberrant\u201d T cells in <jats:italic>lpr<\/jats:italic> mice may be normal regulatory T cells in non\u2010<jats:italic>lpr<\/jats:italic>\u2010bearing mice, if nonproliferative. We thus attempted to produce a xenogeneic monoclonal antibody (ALP\u20101) directed against the <jats:italic>lpr<\/jats:italic> T cells. The ALP\u20101 monoclonal antibody reacted with the antigen Lp\u20101 distributing on about one half of the proliferating lymph node cells from MRL\/Mp\u2010<jats:italic>lpr\/lpr<\/jats:italic> mice but not on the cells from non\u2010<jats:italic>lpr<\/jats:italic>\u2010bearing mice. Nevertheless, a significant number of Lp\u20101<jats:sup>+<\/jats:sup> cells appeared in the lymph node and spleen cells from these normal mice after <jats:italic>in vitro<\/jats:italic> stimulation with mitogens. Functional studies revealed that either the treatment with ALP\u20101 plus complement of the antigen\u2010primed splenic T cells from non\u2010<jats:italic>lpr<\/jats:italic>\u2010bearing mice or the addition of ALP\u20101 alone all but completely abolished the development of plaque\u2010forming cells against sheep red blood cells in T\u2010B cell co\u2010culture. Pretreatment of spleen cells with ALP\u20101 plus complement, however, did not affect other <jats:italic>in vitro<\/jats:italic> T cell functions such as mitogen\u2010induced proliferative responses, interleukin 2 production, response in mixed lymphocyte culture (MLC) and the MLC\u2010induced cytotoxic T cell activities. Thus, Lp\u20101<jats:sup>+<\/jats:sup> T cells in normal mice are unique T cells that may play an important regulatory role in humoral immune response.<\/jats:p>","DOI":"10.1002\/eji.1830160121","type":"journal-article","created":{"date-parts":[[2007,2,28]],"date-time":"2007-02-28T21:58:41Z","timestamp":1172699921000},"page":"109-112","source":"Crossref","is-referenced-by-count":5,"title":["T cells bearing unique membrane antigen and their regulatory role in humoral immune response in mice"],"prefix":"10.1002","volume":"16","author":[{"given":"Yasuo","family":"Ishida","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Iwao","family":"Sekigawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaru","family":"Hamaoki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshinao","family":"Takenouchi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wako","family":"Yumura","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hidetoshi","family":"Sato","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshikazu","family":"Shirai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,11,17]]},"reference":[{"key":"e_1_2_1_2_2","first-page":"1246","volume":"36","author":"Murphy E. 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