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We showed that mPGES-1 null mice had a significantly reduced incidence and severity of collagen-induced arthritis compared with wild-type (WT) mice associated with a marked reduction in Abs to type II collagen. In this study, we further elucidated the role of mPGES-1 in the humoral immune response. Basal levels of serum IgM and IgG were significantly reduced in mPGES-1 null mice. Compared with WT mice, mPGES-1 null mice exhibited a significant reduction of hapten-specific serum Abs in response to immunization with the T cell\u2013dependent (TD) Ag DNP-keyhole limpet hemocyanin. Immunization with the T cell\u2013independent type 1 Ag trinitrophenyl-LPS or the T cell\u2013independent type 2 Ag DNP-Ficoll revealed minimal differences between strains. Germinal center formation in the spleen of mPGES-1 null and WT mice were similar after immunization with DNP-keyhole limpet hemocyanin. To determine whether the effect of mPGES-1 and PGE2 was localized to hematopoietic or nonhematopoietic cells, we generated bone marrow chimeras. We demonstrated that mPGES-1 deficiency in nonhematopoietic cells was the critical factor for reduced TD Ab production. We conclude that mPGES-1 and PGE2-dependent phenotypic changes of nonhematopoietic\/mesenchymal stromal cells play a key role in TD humoral immune responses in vivo. These findings may have relevance to the pathogenesis of rheumatoid arthritis and other autoimmune inflammatory diseases associated with autoantibody formation.<\/jats:p>","DOI":"10.4049\/jimmunol.1301942","type":"journal-article","created":{"date-parts":[[2013,10,15]],"date-time":"2013-10-15T02:37:29Z","timestamp":1381804649000},"page":"4979-4988","source":"Crossref","is-referenced-by-count":11,"title":["Reduced T Cell\u2013Dependent Humoral Immune Response in Microsomal Prostaglandin E Synthase-1 Null Mice Is Mediated by Nonhematopoietic Cells"],"prefix":"10.1093","volume":"191","author":[{"given":"Fumiaki","family":"Kojima","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, University of Kentucky , Lexington, KY 40536"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrey","family":"Frolov","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, University of Kentucky , Lexington, KY 40536"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rahul","family":"Matnani","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, University of Kentucky , Lexington, KY 40536"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jerold G","family":"Woodward","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky , Lexington, KY 40536"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leslie J","family":"Crofford","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, University of Kentucky , Lexington, KY 40536"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2013,11,15]]},"reference":[{"key":"2025032405581787800_r1","doi-asserted-by":"crossref","first-page":"198","DOI":"10.1016\/j.biocel.2009.09.015","article-title":"Prostaglandin E2 at new glance: novel insights in functional diversity offer therapeutic chances","volume":"42","author":"Legler","year":"2010","journal-title":"Int. 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