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Evolution of NK-mediated target recognition under the pressure of physiologic or pathologic stimuli

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194520 Year: Pages: 190 DOI: 10.3389/978-2-88919-452-0 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-02-05 17:24:33
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Abstract

Since their discovery NK cells have come out as potential tools to fight cancer and viruses. This finding early urged different groups to study the mechanisms governing NK cell function. The identification of the MHC-I-specific inhibitory receptors (i.e. KIRs, NKG2A and certain Ly49 molecules) allowed defining rather rapidly how NK cells could avoid self-aggression and how they could be directed towards targets that were forced, by viral infection or tumor transformation, to down-regulate MHC-I expression. In a second time, also the repertoire of surface activating receptors addressing NK cytotoxicity towards tumors and pathogens was mostly defined. In spite of the first findings, however, most recent studies may suggest that NK cells and their receptors might not have been evolved to kill tumor targets and, perhaps, they might have been only partially influenced, in their evolution, by the need of recognizing viruses. Indeed certain NK receptors known to activate NK cell cytotoxicity (NKp30, DNAM-1, NKp80) can also participate at regulatory interactions occurring between NK and myeloid cells. In addition, a peculiar NK cell subset which intensively populate decidua during the first trimester of pregnancy, through the engagement of specific receptors and the interaction with decidual DC, produce chemokines and pro-angiogenic cytokines, and induce Tregs. Thus, in this context, NK cells favor decidua vascularization and development of the (semiallogeneic) foetus in a tolerant environment. Viruses have nevertheless played an important role in shaping the NK cell receptor repertoire. Several studies have unveiled clues of the evolutionary struggle between these pathogens and NK cells. Different NK receptors, including NKp46, NKp30, NKp44, NKG2D, NKG2C, Ly49, and certain KIRs have been demonstrated to recognize virus-encoded or virus-induced ligands. The expression of TLR specifically recognizing microbial products, together with the unexpected role of KIR3DL2 in shuttling these products to TLR-containing endosomes have also been documented in NK cells. On the other side, different viral immune evasion molecules have been shown to interfere with the expression of ligands for T or NK cell activating receptors. In addition, viral infections can occur in the reproductive stage of life cycle, and may represent a serious threat for the species propagation. Thus the control of viruses, together with the maintenance of foetus during pregnancy, should represent major evolutionary forces in shaping NK-receptors. Along this line, the NK-mediated control of tumors should not be under the same evolutionary pressure, as tumors mostly appear later in the life cycle, and the recognition of tumor-encoded ligands may be less efficient (as the NK cell receptors might have not been selected for such aim). This may be the reason why, although displaying strong antitumor activity in vitro, NK cells could hardly contain tumor burden in vivo. In addition the pathogen-driven evolution of NK cell function may also favor the role of NK cells in the insurgence of immune-mediated diseases. This research topic will collect contributions that may clarify the relationships between the evolution of the NK receptors and their role in an efficient recognition of viruses and tumor cells or in immune-mediated diseases.

Major Histocompatibility Complex (MHC) in Health and Disease

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ISBN: 9783039280728 9783039280735 Year: Pages: 375 DOI: 10.3390/books978-3-03928-073-5 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2020-04-07 23:07:08
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Abstract

The major histocompatibility complex (MHC) is a highly polymorphic and diverse multigene locus in all jawed vertebrate species that has an integral role in adaptive/innate immune systems, transplantation, and infectious and autoimmune diseases. The MHC supra-locus in mammalian vertebrates is usually partitioned into three distinct regions, known as classes I, II, and III, which, to varying extents, can be found conserved in nonmammalian jawed vertebrates, such as bony fish, amphibians, and bird lineages. The MHC gene region is characterized particularly by the expression of class I and class II glycoproteins that bind peptides derived from intracellular or extracellular antigens to circulating T-cells. While this expressed antigenic specificity remains the predominant interest with respect to MHC function and polymorphism in a population, a broader concept has emerged that examines the MHC as a multifunctional polymorphic controller that facilitates and regulates genome diversity with a much greater array of functions and effects than just MHC-restricted antigen recognition. This volume of 19 reprints presented by various experts and collected from the Special Issue of Cells on “MHC in Health and Disease” covers a broad range of topics on the genomic diversity of the MHC regulatory system in various vertebrate species, including MHC class I, II, and III genes; innate and adaptive immunity; neurology; transplantation; haplotypes; infectious and autoimmune diseases; fecundity; conservation; allelic lineages; and evolution. Taken together, these articles demonstrate the immense complexity and diversity of the MHC structure and function within and between different vertebrate species.

Keywords

MHC-I- and MHC-II-dependent inter-individual recognition --- MHC-II-associated sperm-egg recognition --- MHC-I-based mother-fetus recognition --- giant panda --- long-fragment super haplotype --- MHC --- genetic drift --- haplotype --- crested ibis --- founder effect --- bottleneck --- conservation genetics --- selection --- fish --- MHC --- polymorphism --- disease resistance --- quantitative trait loci (QTL) studies --- evolution --- HCP5 --- lncRNA --- MHC --- HLA --- human endogenous retrovirus (HERV) --- cancer --- autoimmune diseases --- competing endogenous RNA (ceRNA) --- human immunodeficiency virus (HIV) --- human papillomavirus (HPV) --- astrogliosis --- PNS/CNS interface --- microglial reaction --- synaptic covering --- ?2m knockout mice --- HLA-B27 --- viral peptides --- computational analysis --- ankylosing spondylitis --- KIR --- KIR–HLA pairs --- ethnic populations in China --- molecular dynamics simulation --- major histocompatibility complex --- antigen --- T-cell receptor --- domain movements --- autoimmunity --- risk genes --- expression --- regulation --- swine leukocyte antigen --- reproductive performance --- production trait --- haplotype --- micro-mini-pigs --- disease association --- haplotype --- HLA polymorphism --- major histocompatibility complex (MHC) --- pedigree --- phase --- protocol --- single nucleotide polymorphism (SNP) --- T1DGC --- type 1 diabetes (T1D) --- BK virus --- polyomavirus --- nephropathy --- human leukocyte antigen-E --- kidney transplantation --- MHC --- ancestral haplotype --- autoimmune disease --- cynomolgus macaque --- Macaca fascicularis --- MHC polymorphism --- experimental medicine --- nonhuman primate models --- DXO --- DOM3Z --- NELF-E --- RD --- SKIV2L --- SKI2W --- STK19 --- RP1 --- NSDK --- RLR --- miR1236 --- SVA --- RNA quality control --- 5??3? RNA decay --- 3??5? mRNA turnover --- antiviral immunity --- interferon ? --- promoter-proximal transcriptional pause --- exosomes --- nuclear kinase --- hepatocellular carcinoma --- Ski complex --- trichohepatoenteric syndrome --- melanoma --- major histocompatibility complex --- MHC --- evolution --- nonclassical --- fish --- MHC genes --- birds --- disease resistance --- orthology --- life history --- gene duplication --- long-read sequencing --- high-throughput sequencing --- concerted evolution --- ecology --- MHC --- major histocompatibility complex --- Old World camels --- camels --- dromedary --- Bactrian camel --- SNP --- n/a

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