NK Cells

An integral link between innate and adaptive immunity has been largely demonstrated.96-98 The early participation of NK cells in response to pathogen/cancer invasion might influence the subsequent development of an adaptive immune response, perhaps providing cues to indicate a "nonself"/"dangerous" encounter. Furthermore, an aberrant innate reaction to self tissue might promote an autoimmune disease, as demonstrated by the fact that NK cells are required for the development of experimental autoimmune myasthenia gravis in mice.99 Therefore, adaptive immunity cannot longer be studied without taking into consideration the influence exerted by innate immunity mediators on antigen-specific T cell activity.

Figure 2. IL-10 effects on relationship with innate and adaptive immune response cell mediators. ROS: reactive oxygen species; NO: nitric oxide; NK cell: natural killer cell; M0: macrophage; DC: dendritic cell; Tr cell: T regulatory cell; Th1/Th2 cell: T helper 1/T helper 2 cell; CTL: cytotoxic T lymphocytes.

Figure 2. IL-10 effects on relationship with innate and adaptive immune response cell mediators. ROS: reactive oxygen species; NO: nitric oxide; NK cell: natural killer cell; M0: macrophage; DC: dendritic cell; Tr cell: T regulatory cell; Th1/Th2 cell: T helper 1/T helper 2 cell; CTL: cytotoxic T lymphocytes.

Although IL-10 negatively affects IFNy and TNFa production by NK cells in vitro [34] we and others have reported on the stimulating effects of this cytokine on NK cell cytotoxicity both in vitro and in preclinical models.100'101

These observations support the hypothesis that, at an early stage of the immune response, IL-10 might induce destruction of "abnormal" cells by stimulating the innate arm of the immune system, which in turn would lead to secondary beneficial effects on the incoming adaptive immune response97 In fact, NK cell-mediated cytolysis of target cells would provide DC with adequate amounts of relevant antigens,102 chemotaxis-related molecules (e.g., chemotac-tic peptides)103 and danger signal molecules (e.g., heat shock proteins, double stranded DNA),104 which ultimately initialize the process of DC maturation (Fig. 2). Of note, IL-10, by augmenting the expression of toll-like receptors on the monocyte lineage,105 can enhance their sensibility to danger signal molecular mediators.106 Upon addition of a secondary stimulus (e.g., IL-2, IL-12) in secondary lymphatic organs,107 the balance is then shifted towards full maturation of DC, with consequent production of costimulatory molecules and cytokines with proliferative/ activating effects on naive T cells.108

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