{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:02:38Z","timestamp":1791223358394,"version":"4.1.0"},"reference-count":37,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2007,7,30]],"date-time":"2007-07-30T00:00:00Z","timestamp":1185753600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2007,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Treatment of rheumatoid arthritis and other autoimmune disorders with anti\u2013tumor necrosis factor (anti\u2010TNF) agents is associated with an increased risk of reactivation of latent <jats:italic>Mycobacterium tuberculosis<\/jats:italic>. While the mechanism of action of abatacept is fundamentally different from that of anti\u2010TNF therapies, its effect on the protective response to latent tuberculosis is not known. We undertook this study to determine the effect of abatacept treatment in a murine model of chronic <jats:italic>M tuberculosis<\/jats:italic> infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Chronic <jats:italic>M tuberculosis<\/jats:italic> infection was established in C57BL\/6 mice. Four months after infection, mice were treated for up to 16 weeks with abatacept, anti\u2013murine TNF antibody, or vehicle. The primary end point was survival; body weight, bacterial load, histologic features, interferon\u2010\u03b3 (IFN\u03b3) production by T cells, and cellular infiltration were also assessed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Abatacept\u2010 and vehicle\u2010treated groups both maintained control of <jats:italic>M tuberculosis<\/jats:italic> infection, with 100% survival after 16 weeks of treatment. These 2 groups had no significant differences in body weight, no clinically relevant differences in bacterial load in the lungs, lymph nodes, or spleen, and no differences in the mean percentage of total or activated T cells, macrophages, neutrophils, or B cells, or in IFN\u03b3 production in the lung or lymph nodes. In contrast, 100% mortality was seen in the anti\u2010TNF antibody\u2013treated group by week 9, with significant body weight loss and increased bacterial load in the lungs, lymph nodes, and spleen. Furthermore, the anti\u2010TNF antibody\u2013treated group had increased pathology consistent with the exacerbation of <jats:italic>M tuberculosis<\/jats:italic> infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Abatacept did not impair the ability of mice to control a chronic <jats:italic>M tuberculosis<\/jats:italic> infection. In contrast, mice treated with anti\u2010TNF therapy showed increased pathology and bacterial load, with 100% mortality by week 9. The clinical significance of these findings has not yet been determined.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.22750","type":"journal-article","created":{"date-parts":[[2007,7,30]],"date-time":"2007-07-30T16:21:03Z","timestamp":1185812463000},"page":"2557-2565","source":"Crossref","is-referenced-by-count":65,"title":["Abatacept treatment does not exacerbate chronic <i>Mycobacterium tuberculosis<\/i> infection in mice"],"prefix":"10.1002","volume":"56","author":[{"given":"Carolyn L.","family":"Bigbee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daryl G.","family":"Gonchoroff","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Vratsanos","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven G.","family":"Nadler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen G.","family":"Haggerty","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JoAnne L.","family":"Flynn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2007,7,30]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.11137"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011110"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1086\/383317"},{"key":"e_1_2_7_5_2","first-page":"33","article-title":"What are the risks of biologic therapy in rheumatoid arthritis? 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