Natural killer cells in atopic and autoimmune diseases of the skin

Natural killer (NK) cells are best known for their ability to recognize and kill tumor cells and virally infected cells and for their ability to produce large amounts of some cytokines, such as IFN-γ. Recent research has substantially expanded our view on the function of NK cells in the immune system in health and disease. In addition to the better-studied functions in cancer and autoimmunity, contributions from NK cells to allergies and various skin diseases have emerged. We briefly recount the traditional NK cell functions before focusing on their roles in atopic dermatitis, psoriasis, alopecia areata, and pemphigus vulgaris. Although this field is still developing, strong data are available that indicate NK cell involvement. In patients with allergic diseases, the production of T_H2 cytokines by NK cells contributes to the known immune deviation. In patients with psoriasis, their pathophysiologic role seems to be especially the production of IFN-γ. NK cell overactivation can be found in patients with alopecia areata and pemphigus vulgaris. Many details are still unclear; however, we believe that there is solid evidence that NK cells actively participate in a number of diseases that have not been traditionally linked to this type of lymphocyte.

Key words: Natural killer cells, skin, allergy, autoimmunity

Abbreviations used: AA, Alopecia areata, AD, Atopic dermatitis, AR, Activating receptor, CHS, Contact hypersensitivity, CMV, Cytomegalovirus, DC, Dendritic cell, IDEC, Inflammatory dendritic epidermal cell, ILT2, Immunoglobulin-like transcript 2, IP, Immune privilege, IR, Inhibitory receptor, KIR, Killer immunoglobulin receptor, LC, Langerhans cell, LTi, Lymphoid tissue inducer, MICA, MHC class I chain-related protein, MIF, Macrophage migration inhibitory factor, NK, Natural killer, NKT, Natural killer T, PNM, Proximal nail matrix, PV, Pemphigus vulgaris, Tip-DC, Dendritic cell (CD11c⁺CD1c^–) that secretes TNF-α and produces inducible nitric oxide synthase