Both CD1d antigen presentation and interleukin-12 are required to activate natural killer T cells during Trypanosoma cruzi infection.
Mechanisms of natural killer T (NKT)-cell activation remain unclear. Here, we report that during Trypanosoma cruzi infection, interleukin-12 (IL-12) deficiency or anti-CD1d antibody treatment prevents normal activation. The required IL-12 arises independently of MyD88. The data support a model of normal NKT-cell activation that requires IL-12 and TCR stimulation.
Duthie
Malcolm S
MS
Infectious Disease Research Institute, 1124 Columbia St., Suite 600, Seattle, WA 98104, USA.
Kahn
Maria
M
White
Maria
M
Kapur
Raj P
RP
Kahn
Stuart J
SJ
D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D018949:Antigens, CD1 / Q000378:metabolism*; D055610:Antigens, CD1d; D014355:Chagas Disease / Q000276:immunology* / Q000469:parasitology; D018664:Interleukin-12 / Q000378:metabolism*; D007694:Killer Cells, Natural / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D014349:Trypanosoma cruzi / Q000472:pathogenicity*
D018949:Antigens, CD1; D055610:Antigens, CD1d; D018664:Interleukin-12
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