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      Sustained TL1A (TNFSF15) expression on both lymphoid and myeloid cells leads to mild spontaneous intestinal inflammation and fibrosis

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          Abstract

          TL1A is a member of the TNF superfamily, and its expression is increased in the mucosa of inflammatory bowel disease patients. Moreover, patients with certain TNFSF15 variants over-express TL1A and have a higher risk of developing strictures in the small intestine. Consistently, mice with sustained Tl1a expression in either lymphoid or myeloid cells develop spontaneous ileitis and increased intestinal collagen deposition. Transgenic (Tg) mice with constitutive Tl1a expression in both lymphoid and myeloid cells were generated to assess their in vivo consequence. Constitutive expression of Tl1a in both lymphoid and myeloid cells showed increased spontaneous ileitis and collagen deposition than WT mice. T cells with constitutive expression of Tl1a in both lymphoid and myeloid cells were found to have a more activated phenotype, increased gut homing marker CCR9 expression, and enhanced Th1 and Th17 cytokine activity than WT mice. Although no differences in T cell activation marker, Th1 or Th17 cytokine activity, ileitis, or collagen deposition were found between constitutive Tl1a expression in lymphoid only, myeloid only, or combined lymphoid and myeloid cells. Double hemizygous Tl1a-Tg mice appeared to have worsened ileitis and intestinal fibrosis. Our findings confirm that TL1A-DR3 interaction is involved in T cell-dependent ileitis and fibrosis.

          Author and article information

          Journal
          1886
          122234
          European Journal of Microbiology and Immunology
          EuJMI
          Akadémiai Kiadó, co-published with Springer Science+Business Media B.V., Formerly Kluwer Academic Publishers B.V.
          2062-509X
          2062-8633
          1 March 2013
          : 3
          : 1
          : 11-20
          Affiliations
          [ 1 ] F. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA
          [ 2 ] Department of Gastroenterology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China
          [ 3 ] Center for Inflammatory Bowel Diseases, David Geffen School of Medicine, UCLA, Los Angeles, CA, 90095, USA
          [ 4 ] F. Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, 8700 Beverly Blvd., Suite 4065, Los Angeles, CA, 90048, USA
          Author notes
          [* ] (310) 423-7724, targans@ 123456cshs.org
          [** ] (310) 423-7724, david.shih@ 123456csmc.edu
          Article
          2
          10.1556/EuJMI.3.2013.1.2
          3638202
          23638306
          8dafac58-250a-4f00-9557-32ef34b2dd03
          History
          : 4 January 2013
          : 13 January 2013

          Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
          fibrosis,ileitis,mucosal inflammation,transgenic

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