TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease.

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  • Additional Information
    • Source:
      Publisher: Rockefeller University Press Country of Publication: United States NLM ID: 2985109R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1540-9538 (Electronic) Linking ISSN: 00221007 NLM ISO Abbreviation: J Exp Med Subsets: MEDLINE
    • Publication Information:
      Original Publication: New York, NY : Rockefeller University Press
    • Subject Terms:
      Autoimmune Diseases/*immunology ; Encephalomyelitis, Autoimmune, Experimental/*immunology ; HLA-DR3 Antigen/*immunology ; Tumor Necrosis Factor Ligand Superfamily Member 15/*deficiency; Animals ; Brain/immunology ; Brain/pathology ; Cell Differentiation ; Cell Division ; Cytokines/metabolism ; DNA Primers ; Female ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Spinal Cord/immunology ; Spinal Cord/pathology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; Tumor Necrosis Factor Ligand Superfamily Member 15/genetics ; Tumor Necrosis Factor Ligand Superfamily Member 15/physiology
    • Abstract:
      T helper type 17 (Th17) cells play an important pathogenic function in autoimmune diseases; their regulation, however, is not well understood. We show that the expression of a tumor necrosis factor receptor family member, death receptor 3 (DR3; also known as TNFRSF25), is selectively elevated in Th17 cells, and that TL1A, its cognate ligand, can promote the proliferation of effector Th17 cells. To further investigate the role of the TL1A-DR3 pathway in Th17 regulation, we generated a TL1A-deficient mouse and found that TL1A(-/-) dendritic cells exhibited a reduced capacity in supporting Th17 differentiation and proliferation. Consistent with these data, TL1A(-/-) animals displayed decreased clinical severity in experimental autoimmune encephalomyelitis (EAE). Finally, we demonstrated that during EAE disease progression, TL1A was required for the optimal differentiation as well as effector function of Th17 cells. These observations thus establish an important role of the TL1A-DR3 pathway in promoting Th17 cell function and Th17-mediated autoimmune disease.
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    • Accession Number:
      0 (Cytokines)
      0 (DNA Primers)
      0 (HLA-DR3 Antigen)
      0 (Tnfsf15 protein, mouse)
      0 (Tumor Necrosis Factor Ligand Superfamily Member 15)
    • Publication Date:
      Date Created: 20080416 Date Completed: 20080804 Latest Revision: 20211020
    • Publication Date:
      20221213
    • Accession Number:
      PMC2373838
    • Accession Number:
      10.1084/jem.20071364
    • Accession Number:
      18411337