TL1A/TNFSF15 directly induces proinflammatory cytokines, including TNF alpha, from CD3+CD161+T cells to exacerbate gut inflammation

Typeset version

 

TY  - JOUR
  - Jin, S,Chin, J,Seeber, S,Niewoehner, J,Weiser, B,Beaucamp, N,Woods, J,Murphy, C,Fanning, A,Shanahan, F,Nally, K,Kajekar, R,Salas, A,Planell, N,Lozano, J,Panes, J,Parmar, H,DeMartino, J,Narula, S,Thomas-Karyat, DA
  - 2013
  - September
  - Mucosal immunology
  - TL1A/TNFSF15 directly induces proinflammatory cytokines, including TNF alpha, from CD3+CD161+T cells to exacerbate gut inflammation
  - Validated
  - Altmetric: 9 ()
  - IFN-GAMMA PRODUCTION CROHNS-DISEASE T-CELLS INTESTINAL INFLAMMATION BOWEL-DISEASE TL1A TNFSF15 INTERLEUKIN-18 COSTIMULATOR EXPRESSION
  - 6
  - 886
  - 899
  - Tumor necrosis factor (TNF)-like cytokine 1A (TL1A)/TNF superfamily member 15 (TNFSF15) is a proinflammatory cytokine and TNF alpha superfamily member that is linked preclinically and clinically to inflammatory bowel disease (IBD). By homology and function, TNF alpha is its closest family member. In this study, we investigated the mechanism of TL1A-induced inflammation in CD4+ T cells and compared it with the TNF alpha pathway. We found that TL1A induces proinflammatory cytokines, including TNF alpha, from isolated human CD4+ CD161+ T cells, whereas these cells were resistant to TNF alpha treatment. Anti-TNF alpha failed to block TL1A-induced cytokine production, indicating that the effects of TL1A are direct. Lastly, CD161 and TL1A expression were significantly and selectively increased in gut tissue biopsies, but not in the peripheral blood, from IBD patients. Thus, TLIA not only functions upstreamof TNF alpha, driving its expression from CD161+ T cells, but is also independent of TNF alpha. These findings may have therapeutic IBD implications.
  - 10.1038/mi.2012.124
DA  - 2013/09
ER  - 
@article{V243944495,
   = {Jin,  S and Chin,  J and Seeber,  S and Niewoehner,  J and Weiser,  B and Beaucamp,  N and Woods,  J and Murphy,  C and Fanning,  A and Shanahan,  F and Nally,  K and Kajekar,  R and Salas,  A and Planell,  N and Lozano,  J and Panes,  J and Parmar,  H and DeMartino,  J and Narula,  S and Thomas-Karyat,  DA },
   = {2013},
   = {September},
   = {Mucosal immunology},
   = {TL1A/TNFSF15 directly induces proinflammatory cytokines, including TNF alpha, from CD3+CD161+T cells to exacerbate gut inflammation},
   = {Validated},
   = {Altmetric: 9 ()},
   = {IFN-GAMMA PRODUCTION CROHNS-DISEASE T-CELLS INTESTINAL INFLAMMATION BOWEL-DISEASE TL1A TNFSF15 INTERLEUKIN-18 COSTIMULATOR EXPRESSION},
   = {6},
  pages = {886--899},
   = {{Tumor necrosis factor (TNF)-like cytokine 1A (TL1A)/TNF superfamily member 15 (TNFSF15) is a proinflammatory cytokine and TNF alpha superfamily member that is linked preclinically and clinically to inflammatory bowel disease (IBD). By homology and function, TNF alpha is its closest family member. In this study, we investigated the mechanism of TL1A-induced inflammation in CD4+ T cells and compared it with the TNF alpha pathway. We found that TL1A induces proinflammatory cytokines, including TNF alpha, from isolated human CD4+ CD161+ T cells, whereas these cells were resistant to TNF alpha treatment. Anti-TNF alpha failed to block TL1A-induced cytokine production, indicating that the effects of TL1A are direct. Lastly, CD161 and TL1A expression were significantly and selectively increased in gut tissue biopsies, but not in the peripheral blood, from IBD patients. Thus, TLIA not only functions upstreamof TNF alpha, driving its expression from CD161+ T cells, but is also independent of TNF alpha. These findings may have therapeutic IBD implications.}},
   = {10.1038/mi.2012.124},
  source = {IRIS}
}
AUTHORSJin, S,Chin, J,Seeber, S,Niewoehner, J,Weiser, B,Beaucamp, N,Woods, J,Murphy, C,Fanning, A,Shanahan, F,Nally, K,Kajekar, R,Salas, A,Planell, N,Lozano, J,Panes, J,Parmar, H,DeMartino, J,Narula, S,Thomas-Karyat, DA
YEAR2013
MONTHSeptember
JOURNAL_CODEMucosal immunology
TITLETL1A/TNFSF15 directly induces proinflammatory cytokines, including TNF alpha, from CD3+CD161+T cells to exacerbate gut inflammation
STATUSValidated
TIMES_CITEDAltmetric: 9 ()
SEARCH_KEYWORDIFN-GAMMA PRODUCTION CROHNS-DISEASE T-CELLS INTESTINAL INFLAMMATION BOWEL-DISEASE TL1A TNFSF15 INTERLEUKIN-18 COSTIMULATOR EXPRESSION
VOLUME6
ISSUE
START_PAGE886
END_PAGE899
ABSTRACTTumor necrosis factor (TNF)-like cytokine 1A (TL1A)/TNF superfamily member 15 (TNFSF15) is a proinflammatory cytokine and TNF alpha superfamily member that is linked preclinically and clinically to inflammatory bowel disease (IBD). By homology and function, TNF alpha is its closest family member. In this study, we investigated the mechanism of TL1A-induced inflammation in CD4+ T cells and compared it with the TNF alpha pathway. We found that TL1A induces proinflammatory cytokines, including TNF alpha, from isolated human CD4+ CD161+ T cells, whereas these cells were resistant to TNF alpha treatment. Anti-TNF alpha failed to block TL1A-induced cytokine production, indicating that the effects of TL1A are direct. Lastly, CD161 and TL1A expression were significantly and selectively increased in gut tissue biopsies, but not in the peripheral blood, from IBD patients. Thus, TLIA not only functions upstreamof TNF alpha, driving its expression from CD161+ T cells, but is also independent of TNF alpha. These findings may have therapeutic IBD implications.
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DOI_LINK10.1038/mi.2012.124
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