| First Author | Tse HM | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 9 | Pages | 5247-58 |
| PubMed ID | 20881184 | Mgi Jnum | J:165189 |
| Mgi Id | MGI:4836426 | Doi | 10.4049/jimmunol.1001472 |
| Citation | Tse HM, et al. (2010) NADPH oxidase deficiency regulates Th lineage commitment and modulates autoimmunity. J Immunol 185(9):5247-58 |
| abstractText | Reactive oxygen species are used by the immune system to eliminate infections; however, they may also serve as signaling intermediates to coordinate the efforts of the innate and adaptive immune systems. In this study, we show that by eliminating macrophage and T cell superoxide production through the NADPH oxidase (NOX), T cell polarization was altered. After stimulation with immobilized anti-CD3 and anti-CD28 or priming recall, T cells from NOX-deficient mice exhibited a skewed Th17 phenotype, whereas NOX-intact cells produced cytokines indicative of a Th1 response. These findings were corroborated in vivo by studying two different autoimmune diseases mediated by Th17 or Th1 pathogenic T cell responses. NOX-deficient NOD mice were Th17 prone with a concomitant susceptibility to experimental allergic encephalomyelitis and significant protection against type 1 diabetes. These data validate the role of superoxide in shaping Th responses and as a signaling intermediate to modulate Th17 and Th1 T cell responses. |
