ReviewNK cell regulation of T cell-mediated responses
Section snippets
NK cell regulation of T cell-mediated responses through the production of cytokines, chemokines, and interactions with DC
NK cells promote adaptive immune responses through their production of type 1 and type 2 cytokines or chemokines. Following viral infections, the NK cell production of IFN-γ plays a key role in the initial antiviral response, for example by activating macrophages to secrete IL-12 that is crucial for the differentiation of T cell into Th1 effectors and for the development of CD8+ cytotoxic cells (Biron et al., 1999, French and Yokoyama, 2003). After murine cytomegalovirus (MCMV) infection, IFN-γ
Expression of costimulatory ligands on activated NK cells allow direct interactions with T cells
Previously, NK cells have been assumed to participate in adaptive immune responses by an indirect mechanism that involves their secretion of cytokines or chemokines in response to stimulation by pro-inflammatory cytokines or interferons produced by myeloid cells or non-hematopoietic cells due to infection with pathogens. However, there is emerging data suggesting the possibility that activated NK cells might also communicate directly with T cells by a process involving cognate cell–cell
Acknowledgments
L.L.L. is an American Cancer Society Research Professor and A.Z. was a recipient of an American–Italian Cancer Foundation Fellowship and of a research contract with the University of Rome “La Sapienza”. These studies were supported by NIH grant CA89294 and a grant from A.I.R.C. to A.S.
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Cited by (86)
Hepatitis C virus-induced NK cell activation causes metzincin-mediated CD16 cleavage and impaired antibody-dependent cytotoxicity
2017, Journal of HepatologyCitation Excerpt :NK cells can recognize tumor or virus-infected cells without prior sensitization [2] and directly kill them by release of cytoplasmic granules containing cytolytic molecules, such as granzyme and perforin [3]. Moreover, NK cells are able to secrete a set of cytokines (TNF-α, IFN-γ, IL-10) and chemokines (CCL2-CCL5 and CXCL8), which can sustain/suppress adaptive immune responses and influence trafficking of dendritic [4,5] and T cells [6] in the inflammation sites. Despite the traditional view that NK cell activity is concentrated during the acute phase of infections [reviewed in 7], over the past several years, the dual function of the NK cell activity, e.g. recognition and killing of target cells and the coordination of the adaptive immune response, has been addressed in chronic viral infections, including hepatitis C virus (HCV) infection, which is characterized by a high propensity to evolve to chronic liver disease [8].
Evaluation of endometrial natural killer cell expression of CD4, CD103, and CD16 cells in women with unexplained infertility
2016, Journal of Reproductive ImmunologyKiller immunoglobulin-like receptor and their HLA ligands in Guillain-Barré Syndrome
2014, Journal of NeuroimmunologySuppression of NK cells and regulatory T lymphocytes in cats naturally infected with feline infectious peritonitis virus
2013, Veterinary MicrobiologyCitation Excerpt :Since both NK cells and Tregs represent important players in CMI and given their crucial role in the development of adaptive immune responses (Kos and Engleman, 1996; Robbins et al., 2007), it is worth to dissect their roles during a FIPV infection. A strong innate NK cell-mediated immune response is often responsible for an acute viral control, exemplified during FIV and cytomegalovirus infections (Zingoni et al., 2005; Howard et al., 2010), while Treg enhancement suppresses anti-viral responses (Li et al., 2008). NK cell deficiencies regularly lead to severe recurrent viral diseases (Wood et al., 2011) and Treg deficiencies lead to damaging pathology (Luhn et al., 2007).