Premium
Effector and regulatory events during natural killer–dendritic cell interactions
Author(s) -
Moretta Lorenzo,
Ferlazzo Guido,
Bottino Cristina,
Vitale Massimo,
Pende Daniela,
Mingari Maria Cristina,
Moretta Alessandro
Publication year - 2006
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/j.1600-065x.2006.00450.x
Subject(s) - biology , immunology , immune system , microbiology and biotechnology , innate immune system , dendritic cell , innate lymphoid cell , interleukin 12 , cytokine , chemokine , natural killer cell , interleukin 21 , acquired immune system , t cell , cytotoxic t cell , biochemistry , in vitro
Summary: The different cell types of the innate immune system can interact with each other and influence the quality and strength of an immune response. The cross talk between natural killer (NK) cells and myeloid dendritic cells (DCs) leads to NK cell activation and DC maturation. Activated NK cells are capable of killing DCs that fail to undergo proper maturation (‘DC editing’). Encounters between NK cells and DCs occur in both inflamed peripheral tissues and lymph nodes, where both cell types are recruited by chemokines released in the early phases of inflammatory responses. Different NK cell subsets (CD56 bright CD16 − versus CD56 + CD16 + ) differ in their homing capabilities. In particular, CD56 bright CD16 − NK cells largely predominate the lymph nodes. In addition, these two subsets display major functional differences in their cytolytic activity, cytokine production, and ability to undergo proliferation. NK cell functions are also greatly influenced by the presence of polarizing cytokines such as interleukin (IL)‐12 and IL‐4. The cytokine microenvironment reflects the presence of different cell types that secrete such cytokines in response to microbial products acting on different Toll‐like receptors (TLRs). Moreover, NK cells themselves can respond directly to microbial products by means of TLR3 and TLR9. Thus, it appears that the final outcome of a response to microbial infection may greatly vary as a result of the interactions occurring between different pathogen‐derived products and different cell types of the innate immunity system. These interactions also determine the quality and strength of the subsequent adaptive responses. Remarkably, NK cells appear to play a key role in this complex network.