scholarly journals Differential Transcript Profiles of MHC Class Ib(Qa-1, Qa-2, and Qa-10) andAireGenes during the Ontogeny of Thymus and Other Tissues

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Breno Luiz Melo-Lima ◽  
Adriane Feijó Evangelista ◽  
Danielle Aparecida Rosa de Magalhães ◽  
Geraldo Aleixo Passos ◽  
Philippe Moreau ◽  
...  
Keyword(s):  
Immune Responses ◽  
Mhc Class I ◽  
Nk Cell ◽  
Expression Patterns ◽  
Class I ◽  
Temporal Association ◽  
Mhc Class Ib ◽  
Thymic Medulla ◽  
Nonclassical Mhc ◽  
Transcript Profiles

Qa-2 and Qa-1 are murine nonclassical MHC class I molecules involved in the modulation of immune responses by interacting with T CD8+and NK cell inhibitory receptors. During thymic education, theAiregene imposes the expression of thousands of tissue-related antigens in the thymic medulla, permitting the negative selection events. Aiming to characterize the transcriptional profiles of nonclassical MHC class I genes in spatial-temporal association with theAireexpression, we evaluated the gene expression ofH2-Q7(Qa-2),H2-T23(Qa-1),H2-Q10(Qa-10), andAireduring fetal and postnatal development of thymus and other tissues. In the thymus,H2-Q7(Qa-2) transcripts were detected at high levels throughout development and were positively correlated withAireexpression during fetal ages.H2-Q7(Qa-2) andH2-T23(Qa-1) showed distinct expression patterns with gradual increasing levels according to age in most tissues analyzed.H2-Q10(Qa-10) was preferentially expressed by the liver. TheAiretranscriptional profile showed increased levels during the fetal period and was detectable in postnatal ages in the thymus. Overall, nonclassical MHC class I genes started to be expressed early during the ontogeny. Their levels varied according to age, tissue, and mouse strain analyzed. This differential expression may contribute to the distinct patterns of mouse susceptibility/resistance to infectious and noninfectious disorders.

scholarly journals Ly-49s3 Is a Promiscuous Activating Rat NK Cell Receptor for Nonclassical MHC Class I-Encoded Target Ligands

2002 ◽  
Vol 169 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Christian Naper ◽  
Shigenari Hayashi ◽  
Lise Kveberg ◽  
Eréne C. Niemi ◽  
Lewis L. Lanier ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Nk Cell ◽  
Cell Receptor ◽  
Class I ◽  
Nonclassical Mhc ◽  
Nk Cell Receptor

scholarly journals Murine CD160, Ig-Like Receptor on NK Cells and NKT Cells, Recognizes Classical and Nonclassical MHC Class I and Regulates NK Cell Activation

2005 ◽  
Vol 175 (7) ◽  
pp. 4426-4432 ◽  
Author(s):  
Motoi Maeda ◽  
Carmine Carpenito ◽  
Ryan C. Russell ◽  
Jyoti Dasanjh ◽  
Linnea L. Veinotte ◽  
...  
Keyword(s):  
Nk Cells ◽  
Mhc Class I ◽  
Cell Activation ◽  
Nk Cell ◽  
Nkt Cells ◽  
Class I ◽  
Nonclassical Mhc

II. One size fits all: nonclassical MHC molecules fulfill multiple roles in epithelial cell function

1998 ◽  
Vol 274 (2) ◽  
pp. G227-G231 ◽  
Author(s):  
Richard S. Blumberg
Keyword(s):  
Epithelial Cell ◽  
Mhc Class I ◽  
Cell Biology ◽  
Cell Function ◽  
Surface Glycoprotein ◽  
Class I ◽  
Human Major Histocompatibility Complex ◽  
Cell Surface Glycoprotein ◽  
Mhc Molecules ◽  
Nonclassical Mhc

The human major histocompatibility complex (MHC) on chromosome 6 encodes three classical class I genes: human leukocyte antigen-A (HLA-A), HLA-B, and HLA-C. These polymorphic genes encode a 43- to 45-kDa cell surface glycoprotein that, in association with the 12-kDa β2-microglobulin molecule, functions in the presentation of nine amino acid peptides to the T cell receptor of CD8-bearing T lymphocytes and killer inhibitory receptors on natural killer cells. In addition to these ubiquitously expressed polymorphic proteins, the human genome also encodes a number of nonclassical MHC class I-like, or class Ib, genes that in general encode nonpolymorphic molecules involved in a variety of specific immunologic functions. Many of these genes, including CD1, the neonatal Fc receptor for immunoglobulin G, HLA-G, the MHC class I chain-related gene A, and Hfe, are prominently displayed on epithelial cells, suggesting an important role in epithelial cell biology.

scholarly journals ERAP1 Controls the Interaction of the Inhibitory Receptor KIR3DL1 With HLA-B51:01 by Affecting Natural Killer Cell Function

2021 ◽  
Vol 12 ◽  
Author(s):  
Silvia D’Amico ◽  
Valerio D’Alicandro ◽  
Mirco Compagnone ◽  
Patrizia Tempora ◽  
Giusy Guida ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Cell Function ◽  
Nk Cell ◽  
Killer Cell ◽  
Cell Subset ◽  
Human Tumor ◽  
Hla Class I ◽  
Class I ◽  
Pharmacological Inhibition ◽  
Mhc Class I Molecules

The endoplasmic reticulum aminopeptidase ERAP1 regulates innate and adaptive immune responses by trimming peptides for presentation by major histocompatibility complex (MHC) class I molecules. Previously, we have shown that genetic or pharmacological inhibition of ERAP1 on murine and human tumor cell lines perturbs the engagement of NK cell inhibitory receptors Ly49C/I and Killer-cell Immunoglobulin-like receptors (KIRs), respectively, by their specific ligands (MHC class I molecules), thus leading to NK cell killing. However, the effect of ERAP1 inhibition in tumor cells was highly variable, suggesting that its efficacy may depend on several factors, including MHC class I typing. To identify MHC class I alleles and KIRs that are more sensitive to ERAP1 depletion, we stably silenced ERAP1 expression in human HLA class I-negative B lymphoblastoid cell line 721.221 (referred to as 221) transfected with a panel of KIR ligands (i.e. HLA-B*51:01, -Cw3, -Cw4 and -Cw7), or HLA-A2 which does not bind any KIR, and tested their ability to induce NK cell degranulation and cytotoxicity. No change in HLA class I surface expression was detected in all 221 transfectant cells after ERAP1 depletion. In contrast, CD107a expression levels were significantly increased on NK cells stimulated with 221-B*51:01 cells lacking ERAP1, particularly in the KIR3DL1-positive NK cell subset. Consistently, genetic or pharmacological inhibition of ERAP1 impaired the recognition of HLA-B*51:01 by the YTS NK cell overexpressing KIR3DL1*001, suggesting that ERAP1 inhibition renders HLA-B*51:01 molecules less eligible for binding to KIR3DL1. Overall, these results identify HLA-B*51:01/KIR3DL1 as one of the most susceptible combinations for ERAP1 inhibition, suggesting that individuals carrying HLA-B*51:01-like antigens may be candidates for immunotherapy based on pharmacological inhibition of ERAP1.

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