T-bet Expression by Foxp3+ T Regulatory Cells is Not Essential for Their Suppressive Function in CNS Autoimmune Disease or Colitis
| Autor: | Stephen M. Anderton, Darryl G. Turner, Iris Mair, Richard A. O’Connor, Rhoanne C. McPherson |
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| Rok vydání: | 2015 |
| Předmět: |
lcsh:Immunologic diseases. Allergy
colitis Immunology Central nervous system autoimmune disease chemical and pharmacologic phenomena T-bet CXCR3 Autoimmune Diseases Immunology and Allergy Medicine Colitis Original Research Autoimmune disease EAE business.industry Effector Experimental autoimmune encephalomyelitis FOXP3 hemic and immune systems medicine.disease FOXP3 Treg In vitro 3. Good health medicine.anatomical_structure Foxp3 lcsh:RC581-607 business |
| Zdroj: | Frontiers in Immunology McPherson, R C, Turner, D G, Mair, I, O'Connor, R A & Anderton, S M 2015, ' T-bet Expression by Foxp3(+) T Regulatory Cells is Not Essential for Their Suppressive Function in CNS Autoimmune Disease or Colitis ', Frontiers in Immunology, vol. 6, pp. 69 . https://doi.org/10.3389/fimmu.2015.00069 Frontiers in Immunology, Vol 6 (2015) |
| ISSN: | 1664-3224 |
| DOI: | 10.3389/fimmu.2015.00069 |
| Popis: | Accumulation of T regulatory (Treg) cells within the central nervous system (CNS) during experimental autoimmune encephalomyelitis (EAE) is essential for the resolution of disease. CNS Treg cells have been shown to uniformly express the Th1-associated molecules, T-bet and CXCR3. Here, we report that the expression of T-bet is not required for the function of these Treg within the CNS. Using mice that lacked T-bet expression specifically within the Treg compartment, we demonstrate that there was no deficit in Treg recruitment into the CNS during EAE and no difference in the resolution of disease compared to control mice. T-bet deficiency did not impact on the in vitro suppressive capacity of Treg. Transfer of T-bet-deficient Treg was able to suppress clinical signs of either EAE or colitis. These observations demonstrate that, although Treg can acquire characteristics associated with pathogenic T effector cells, this process is not necessarily required for their suppressive capacity and the resolution of autoimmune inflammation. |
| Databáze: | OpenAIRE |
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