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Christian Münz^a,b,c, Ralph M. Steinman^a,b,c, and Shin-ichiro Fujii^a,b,c

^a C.M. is at the Laboratory of Viral Immunobiology and the Christopher H. Browne Center for Immunology and Immune Diseases, The Rockefeller University, New York, NY 10021.
^b R.M.S. is at the Laboratory of Cellular Physiology and Immunology and the Christopher H. Browne Center for Immunology and Immune Diseases, The Rockefeller University, New York, NY 10021.
^c S.-i.F. is at the Research Unit for Cellular Immunotherapy, Research Center for Allergy and Immunology (RCAI), RIKEN YOKOHAMA, Yokohama City, Kanagawa, 230-0045, Japan.

CORRESPONDENCE C.M.: munzc{at}rockefeller.edu

Abstract
Pathogen recognition by Toll-like receptors (TLRs) on dendritic cells (DCs) leads to DC maturation and the initiation of adaptive immunity. Recent studies have shown that innate lymphocytes—natural killer (NK), natural killer T (NKT), and T cells—also trigger DC maturation. This interaction in turn expands and activates innate lymphocytes and initiates adaptive T cell immunity. Here, we comment on the evidence that these pathways are TLR independent and have the potential to respond to infection, malignancy, and immunotherapy.

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