{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,10]],"date-time":"2024-07-10T16:31:38Z","timestamp":1720629098880},"reference-count":24,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2005,12,5]],"date-time":"2005-12-05T00:00:00Z","timestamp":1133740800000},"content-version":"vor","delay-in-days":5939,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1989,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>BALB\/c mice rendered tolerant to alloantigens by neonatal injection of semiallogeneic (C57BL\/6 x BALB\/c)F<jats:sub>1<\/jats:sub> spleen cells develop a thrombocytopenia in association with an autoimmune lupus\u2010like syndrome. The possible mechanisms involved in the thrombocytopenia were investigated. The development of thrombocytopenia was first detected at 3 weeks of age coinciding with the start of the other autoimmune manifestations and was always related to a state of tolerance and B cell chimerism. There was a significant increase of megakaryocytes in bone marrow and spleens from thrombocytopenic tolerant mice and radiolabeled platelets from these mice were more rapidly eliminated from the bloodstream than normal platelets when injected into normal recipients. A significant correlation between the spleen weight and the decrease of the circulating platelets was observed, although some mice with severe thrombocytopenia had only a moderate spleen enlargement.<\/jats:p><jats:p>Thrombocytopenia significantly correlates with the levels of platelet\u2010associated IgG (PAIgG) but not with anti\u2010single\u2010stranded DNA antibodies or circulating immune complexes. Platelets from mice with high levels of PAIgG had a shorter life\u2010span when injected into normal mice than those from mice with low or normal PAIgG. The possibility that PAIgG are partially due to antibodies reacting specifically with platelet membrane components was analyzed. First, F(ab')<jats:sub>2<\/jats:sub> Ig fragments from tolerant mice were shown to bind to normal platelets, in contrast to F(ab')<jats:sub>2<\/jats:sub> Ig fragments from normal mice. Second, some monoclonal antibodies produced by hybridomas derived from tolerant mice reacted <jats:italic>in vitro<\/jats:italic> with platelets and induced a transient thrombocytopenia after i.v. injection into normal mice.<\/jats:p><jats:p>These data suggest that the thrombocytopenia observed in tolerant mice is the result of a peripheral hyperdestruction of platelets associated with (a) hypersplenism, (b) nonspecific fixation of immunoglobulins, probably as immune complexes and (c) with autoantibodies reacting specifically with platelets. It may represent an interesting model for human chronic idiopathic thrombocytopenia.<\/jats:p>","DOI":"10.1002\/eji.1830190925","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T11:09:23Z","timestamp":1172747363000},"page":"1693-1699","source":"Crossref","is-referenced-by-count":4,"title":["Thrombocytopenia associated with the induction of neonatal tolerance to alloantigens: Immunopathogenic mechanisms"],"prefix":"10.1002","volume":"19","author":[{"given":"Jes\u00faS","family":"Merino","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui\u2010Yu","family":"Qin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephane","family":"Schurmans","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Denise","family":"Gretener","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Georges E.","family":"Grau","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul H.","family":"Lambert","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,12,5]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1098\/rstb.1959.0008"},{"key":"e_1_2_1_3_2","first-page":"203","volume":"59","author":"Hard R. 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