{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T03:50:51Z","timestamp":1791085851458,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2005,9,23]],"date-time":"2005-09-23T00:00:00Z","timestamp":1127433600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Autoantibodies in the form of immune complexes are known to be crucial mediators in initiating inflammation in a variety of autoimmune diseases. This has been well documented in the anti\u2010collagen\u2004II antibody\u2010induced arthritis animal model for a long time now. Recently, in the K\/B\u2004\u00d7\u2004N mouse model (the F1 of the TCR\u2010transgenic KRN and the diabetic NOD mice), anti\u2010glucose\u20106\u2010phosphate isomerase (GPI) autoantibodies have been shown to induce arthritis. Experimental work in the K\/B\u2004\u00d7\u2004N model demonstrated key roles of autoantigenic immune complexes activating the alternative pathway of complement, the subsequent association with C5aR and Fc\u03b3RIII\u2010mediated cell activation and production of the inflammatory cytokines IL\u20101 and TNF\u2010\u03b1, finally leading to joint destruction. The presence of high amounts of inflammatory cytokines and matrix\u2010degrading proteases at sites of inflammation obviously put the cytokine\u2010producing macrophages as the next target for investigation in this model. Here, we show that mice depleted of macrophages by clodronate liposome treatment are completely resistant to K\/B\u2004\u00d7\u2004N serum\u2010induced arthritis. Reconstituting clodronate liposome\u2010treated mice with macrophages from naive animals could reverse this resistance. Also, we found that deficiencies in the Wiskott\u2010Aldrich syndrome protein and CD40, which are both implicated in macrophage activation, chemotaxis and phagocytosis, are not essential in serum\u2010induced arthritis. Mast cell degranulation was seen in arthritogenic serum\u2010treated mice even in the absence of macrophages, possibly suggesting that mast cell degranulation\/activation acts hierarchically before macrophages in the inflammatory cascade of anti\u2010GPI antibody\u2010induced arthritis.<\/jats:p>","DOI":"10.1002\/eji.200526167","type":"journal-article","created":{"date-parts":[[2005,9,23]],"date-time":"2005-09-23T11:16:55Z","timestamp":1127474215000},"page":"3064-3073","source":"Crossref","is-referenced-by-count":119,"title":["A crucial role for macrophages in the pathology of K\/B\u2004\u00d7\u2004N serum\u2010induced arthritis"],"prefix":"10.1002","volume":"35","author":[{"given":"Samuel","family":"Solomon","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Narendiran","family":"Rajasekaran","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elvira","family":"Jeisy\u2010Walder","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott\u2004B.","family":"Snapper","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald","family":"Illges","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,10,6]]},"reference":[{"key":"e_1_2_7_1_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.155.1.1"},{"key":"e_1_2_7_2_2","doi-asserted-by":"crossref","first-page":"2103","DOI":"10.4049\/jimmunol.148.7.2103","article-title":"Induction of arthritis with monoclonal antibodies to collagen.","volume":"148","author":"Terato K.","year":"1992","journal-title":"J. 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