Abstract
Natural killer (NK) cells and epithelial cells can interact closely at sites of inflammation, contributting to the pathogenesis of inflammatory diseases such as contact hypersensitivity. However, NK cells can be found to infiltrate lesions of several skin diseases and may play an important role in the innate immune response. The interaction between NK cells and the skin are particularly interesting. Epithelial tissues, including skin and airway, are continuously exposed to pathogens, allergens and environmental contaminants, requiring profound regulation of the innate and adaptive immune systems. Skin, the largest immune tissue in the body, is composed of epidermis, dermis and appendices, including hair follicles, sebaceous glands and sweat glands. To accumulate and infiltrate within epithelial lesions, chemokine and adhesion molecules are induced by NK cells releasing several cytokines and cytotoxic granules such as interferon (IFN)-γ, tumor necrosis factor (TNF)-α, granulocyte macrophage-colony stimulating factor (GM-CSF), IL-5 and IL-8.Under physiological conditions, intra- and peri-epithelial NK cells are very scarce, while their number often sharply increases when epithelia undergo inflammatory changes: Apparently, NK cells and epithelial cells start their interactions after inflammation is induced. NK cells and epithelial cells start interactions after inflammation is induced. The interaction is initiated by adhesion molecules, chemokine and its receptors and cytolytic proteins. NK cells accumulate into inflamed lesions without T cell help using chemokine, chemokine receptors, adhesion molecules and cytokines. Then, NK cells release cytolytic proteins that induce apoptosis of epithelium. Thus, the conventional strategy of treating inflammatory diseases of the epithelium by inhibiting T cell responses should be complemented by modulating NK cell-epithelial cell interactions.
