{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T10:58:02Z","timestamp":1790506682125,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2006,4,3]],"date-time":"2006-04-03T00:00:00Z","timestamp":1144022400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:title>SUMMARY<\/jats:title>\n                  <jats:p>\n                    <jats:italic>One of the most important immunopathological consequence of intraperitoneal alveolar echinococcosis (AE) in the mouse is suppression of T cell\u2010mediated immune responses. We investigated whether and how intraperitoneal macrophages (M\u00d8s) are, respectively, implicated as antigen\u2010presenting cells (APCs). In a first step we showed that peritoneal M\u00d8s from infected mice (AE\u2010M\u00d8s) exhibited a reduced ability to present a conventional antigen (chicken ovalbumin, C\u2010Ova) to specific responder lymph node T cells. In a subsequent step, AE\u2010M\u00d8s as well as na\u00efve M\u00d8s (positive control) proved their ability to uptake and process C\u2010Ova fluorescein isthiocyanate (FITC). Furthermore, in comparison with na\u00efve M\u00d8s, the surface expression of Ia molecules was up\u2010regulated on AE\u2010M\u00d8s at the early stage of infection, suggesting that AE\u2010M\u00d8s provide the first signal via the antigen\u2013Ia complex. To study the accessory activity of M\u00d8s, AE\u2010M\u00d8s obtained at the early and late stages of infection were found to decrease Con A\u2010induced proliferation of peritoneal na\u00efve T cells as well as of AE\u2010sensitized peritoneal T cells, in contrast to stimulation with na\u00efve M\u00d8s. The status of accessory molecules was assessed by analysing the expression level of costimulatory molecules on AE\u2010M\u00d8s, with na\u00efve M\u00d8s as controls. It was found that B7\u20101 (CD80) and B7\u20102 (CD86) expression remained unchanged, whereas CD40 was down\u2010regulated and CD54 (= ICAM\u20101) was slightly up\u2010regulated. In a leucocyte reaction of AE\u2010M\u00d8s with na\u00efve or AE\u2010T cells, both types of T cells increased their proliferative response when CD28 \u2013 the ligand of B7 receptors \u2013 was exposed to anti\u2010CD28 in cultures. Conversely to na\u00efve M\u00d8s, pulsing of AE\u2010M\u00d8s with agonistic anti\u2010CD40 did not even partially restore their costimulatory activity and failed to increase na\u00efve or AE\u2010T cell proliferation. Neutralizing anti\u2010B7\u20101, in combination with anti\u2010B7\u20102, reduced na\u00efve and AE\u2010T cell proliferation, whereas anti\u2010CD40 treatment of na\u00efve M\u00d8s increased their proliferative response to Con A. These results point at the key role of B7 receptors as accessory molecules and the necessity of the integrity of CD40\u2010expression by na\u00efve M\u00d8s to improve their accessory activity. Taken together, the obstructed presenting\u2010activity of AE\u2010M\u00d8s appeared to trigger an unresponsiveness of T cells, contributing to the suppression of their clonal expansion during the chronic phase of AE\u2010infection.<\/jats:italic>\n                  <\/jats:p>","DOI":"10.1111\/j.1365-3024.2006.00836.x","type":"journal-article","created":{"date-parts":[[2006,4,3]],"date-time":"2006-04-03T10:48:42Z","timestamp":1144061322000},"page":"373-385","source":"Crossref","is-referenced-by-count":33,"title":["Intraperitoneal\n                    <i>Echinococcus multilocularis<\/i>\n                    infection in C57BL\/6 mice affects CD40 and B7 costimulator expression on peritoneal macrophages and impairs peritoneal T cell activation"],"prefix":"10.1111","volume":"28","author":[{"given":"N.","family":"MEJRI","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B.","family":"GOTTSTEIN","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,4,25]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00436-002-0659-7"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.69.10.6074-6083.2001"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2567.2004.01885.x"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0001-706X(02)00220-6"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2567.1999.00723.x"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.niox.2004.03.002"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0001-706X(02)00230-9"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-3024.2001.00374.x"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0147-9571(96)00019-7"},{"key":"e_1_2_6_11_2","first-page":"652","article-title":"Echinococcus multilocularis antigens modify accessory cell function of macrophages","volume":"74","author":"Rakha NK","year":"1991","journal-title":"Immunology"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00926566"},{"key":"e_1_2_6_13_2","first-page":"67","article-title":"Cellular immune response in Echinococcus multilocularis infection in humans. 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Evidence for the presence of CD8dull suppressor cells in spleens of mice intraperitoneally infected with E. multilocularis","volume":"147","author":"Kizaki T","year":"1991","journal-title":"J Immunol"},{"key":"e_1_2_6_29_2","doi-asserted-by":"crossref","first-page":"525","DOI":"10.1128\/iai.61.2.525-533.1993","article-title":"Suppression of T\u2010cell proliferation by CD8+ T cells induced in the presence of protoscolices of Echinococcus multilocularis in vitro","volume":"61","author":"Kizaki T","year":"1993","journal-title":"Infect Immun"},{"key":"e_1_2_6_30_2","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/10.6.775"},{"key":"e_1_2_6_31_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.9.4210"},{"key":"e_1_2_6_32_2","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5699(96)10030-X"},{"key":"e_1_2_6_33_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.273.5283.1862"},{"key":"e_1_2_6_34_2","unstructured":"ChessL.Blockade of the CD40L\/CD40 pathway. 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