IL-18 bridges innate and adaptive immunity through IFN-gamma and the CD134 pathway.
J Immunol
; 177(1): 234-45, 2006 Jul 01.
Article
en En
| MEDLINE
| ID: mdl-16785519
ABSTRACT
IL-18 induces inflammation resulting in either enhanced protection from pathogens or exacerbation of autoimmunity, and T cells are profoundly activated during these responses. How IL-18 influences T cell activation is unknown, but this study in mice shows that IL-18 boosted Ag-specific T cell clonal expansion of effector T cells and induced a subpopulation of IFN-gamma superproducing T cells. Commitment to IFN-gamma production through IL-18 was independent of NK cells and IL-12 but dependent on host-derived IFN-gamma. To determine how expansion of these effectors occurred, IL-18 was shown to induce OX40L on dendritic cells, whereas peptide stimulation induced CD134 (OX40) on specific T cells. CD134 blockade inhibited T cell effector expansion thereby reducing the number of IFN-gamma superproducers by 12-fold. Thus, independent of IL-12, IL-18 impacts T cell immunity throughout lymphoid and nonlymphoid tissue by bridging the innate and adaptive arms of the immune system through IFN-gamma and the CD134 costimulatory pathway.
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Bases de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
Adyuvantes Inmunológicos
/
Interferón gamma
/
Receptores del Factor de Necrosis Tumoral
/
Interleucina-18
Idioma:
En
Revista:
J Immunol
Año:
2006
Tipo del documento:
Article
País de afiliación:
Estados Unidos