Resumen
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.
Idioma original | English (US) |
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Páginas (desde-hasta) | 5247-5258 |
Número de páginas | 12 |
Publicación | Journal of Immunology |
Volumen | 185 |
N.º | 9 |
DOI | |
Estado | Published - nov 1 2010 |
Publicado de forma externa | Sí |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology