{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T15:23:49Z","timestamp":1759332229582},"reference-count":53,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2005,11,17]],"date-time":"2005-11-17T00:00:00Z","timestamp":1132185600000},"content-version":"vor","delay-in-days":5556,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1990,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Transfer of bone marrow (BM) from autoimmunity\u2010prone mice homozygous for the lymphoproliferation (<jats:italic>lpr<\/jats:italic>) mutation to irradiated congenic +\/+ recipients has previously been shown to result in a syndrome similar to chronic graft\u2010<jats:italic>vs<\/jats:italic>.\u2010host (GVH) disease. It has been suggested that this syndrome may be due to an antigenic difference caused by the <jats:italic>lpr<\/jats:italic> mutation itself or to antigenic differences at loci closely linked to the <jats:italic>lpr<\/jats:italic> locus (Theofilopoulos, A. N. et al., <jats:italic>J. Exp. Med.<\/jats:italic> 1985. <jats:italic>162<\/jats:italic>: 1; Mosbach\u2010Ozmen, L. and Loor, F., <jats:italic>Thymus<\/jats:italic> 1987. <jats:italic>9<\/jats:italic>: 197). However, the results presented here indicate that alloantigenic differences do not play a role in this syndrome. Instead, the chronic disease observed in <jats:italic>lpr\/lpr<\/jats:italic>\u2192+\/+ BM chimeras appears to develop as a result of a functional defect associated with the <jats:italic>lpr<\/jats:italic> mutation which is expressed shortly after transfer of <jats:italic>lpr\/lpr<\/jats:italic> BM to irradiated recipients. This defect causes an increase in the levels of serum IgG<jats:sub>1<\/jats:sub> and IgG<jats:sub>2<\/jats:sub>, which peak at 4\u20135 weeks post\u2010transfer and then decline to normal levels by 9\u201310 weeks post\u2010transfer. Inflammation similar to that observed in classic GVH reactions accompanies excess IgG production in congenic +\/+ recipients but not in <jats:italic>lpr\/lpr<\/jats:italic> recipients of <jats:italic>lpr\/lpr<\/jats:italic> BM. We demonstrate that the GVH\u2010like response occurring in <jats:italic>lpr\/lpr<\/jats:italic>\u2192+\/+ chimeras is dependent on mature T cells, but that either <jats:italic>lpr\/lpr<\/jats:italic> or +\/+ T cells can support this reaction. These results suggest that transfer of <jats:italic>lpr\/lpr<\/jats:italic> BM to normal mice causes immunoregulatory disturbances which lead to nonspecific activation of T cells. We speculate that <jats:italic>lpr\/lpr<\/jats:italic> BM causes a GVH\u2010like reaction in +\/+ recipients but a systemic lupus erythematosus\u2010like syndrome in <jats:italic>lpr\/lpr<\/jats:italic> recipients because of intrinsic differences in the +\/+ and <jats:italic>lpr\/lpr<\/jats:italic> host environments. Considering these findings, the <jats:italic>lpr\/lpr<\/jats:italic>\u2192+\/+ GVH model may be useful for analysis of factors capable of inducing undesirable reactions in clinical BM transplantation between nominally histocompatible donors and recipients, in addition to being informative about the nature of the <jats:italic>lpr<\/jats:italic> mutation itself.<\/jats:p>","DOI":"10.1002\/eji.1830200926","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T03:25:28Z","timestamp":1172719528000},"page":"2057-2066","source":"Crossref","is-referenced-by-count":15,"title":["Bone marrow transplantation from mutant <i>lpr<\/i>\/<i>lpr<\/i> mice. Functional abnormalities rather than alloantigenic differences appear to determine the development of a graft\u2010<i>vs<\/i>. \u2010host\u2010like syndrome"],"prefix":"10.1002","volume":"20","author":[{"given":"Ruth D.","family":"Allen","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan D.","family":"Marshall","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John B.","family":"Roths","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charles L.","family":"Sidman","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","doi-asserted-by":"publisher","DOI":"10.1084\/jem.158.1.1"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.161.4.718"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-198808000-00021"},{"key":"e_1_2_1_5_2","first-page":"3035","volume":"15","author":"Glaziier A.","year":"1983","journal-title":"Transplant. 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