TL Genes in Asian Wild Mice: The Evolutionary Conserved Nonclassical Class I Genes of the Major Histocompatibility Complex

2015 ◽  
pp. 159-177
Author(s):  
Yuichi Obata ◽  
Kazuo Moriwaki ◽  
Toshihiko Shiroishi ◽  
Yoko Satta ◽  
Naoyuki Takahata ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Class I ◽  
Major Histocompatibility ◽  
Wild Mice ◽  
Histocompatibility Complex ◽  
Nonclassical Class

scholarly journals The Murine Nonclassical Class I Major Histocompatibility Complex–like CD1.1 Molecule Protects Target Cells from Lymphokine-activated Killer Cell Cytolysis

1999 ◽  
Vol 189 (3) ◽  
pp. 483-491 ◽  
Author(s):  
Chew Shun Chang ◽  
Laurent Brossay ◽  
Mitchell Kronenberg ◽  
Kevin P. Kane
Keyword(s):  
Major Histocompatibility Complex ◽  
Nk Cell ◽  
Killer Cell ◽  
Class I ◽  
Target Cells ◽  
Inhibitory Receptor ◽  
Major Histocompatibility ◽  
Lymphokine Activated Killer Cell ◽  
Histocompatibility Complex ◽  
Nonclassical Class

Classical class I major histocompatibility complex (MHC) molecules, as well as the nonclassical class I histocompatibility leukocyte antigen (HLA)-E molecule, can negatively regulate natural killer (NK) cell cytotoxicity through engagement of NK inhibitory receptors. We show that expression of murine (m)CD1.1, a nonpolymorphic nonclassical MHC class I–like molecule encoded outside the MHC, protects NK-sensitive RMA/S target cells from adherent lymphokine-activated killer cell (A-LAK) cytotoxicity. Passage of effector cells in recombinant interleukin (rIL)-2 enhanced protection by mCD1.1, suggesting an expansion of relevant A-LAK population(s) or modulation of A-LAK receptor expression. Murine CD1.1 conferred protection from lysis by rIL-2–activated spleen cells of recombination activating gene (Rag)-1−/− mice, which lack B and T cells, demonstrating that mCD1.1 can protect RMA/S cells from lysis by NK cells. An antibody specific for mCD1.1 partially restored A-LAK lysis of RMA/S.CD1.1 transfectants, indicating that cell surface mCD1.1 can confer protection from lysis; therefore, mCD1.1 possibly acts through interaction with an NK inhibitory receptor. CD1.1 is by far the most divergent class I molecule capable of regulating NK cell activity. Finally, mCD1.1 expression rendered RMA/S cells resistant to lysis by A-LAK of multiple mouse strains. The conserved structure of mCD1.1 and pattern of mCD1.1 resistance from A-LAK lysis suggest that mCD1.1 may be a ligand for a conserved NK inhibitory receptor.

scholarly journals Classical and Nonclassical Class I Major Histocompatibility Complex Molecules Exhibit Subtle Conformational Differences That Affect Binding to CD8αα

2000 ◽  
Vol 275 (20) ◽  
pp. 15232-15238 ◽  
Author(s):  
George F. Gao ◽  
Benjamin E. Willcox ◽  
Jessica R. Wyer ◽  
Jonathan M. Boulter ◽  
Christopher A. O'Callaghan ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Class I ◽  
Major Histocompatibility ◽  
Complex Molecules ◽  
Histocompatibility Complex ◽  
Nonclassical Class

Role of nonclassical class I genes of the chicken major histocompatibility complex Rfp-Y locus in transplantation immunity

2003 ◽  
Vol 55 (9) ◽  
pp. 647-651 ◽  
Author(s):  
Pierrick Thoraval ◽  
Marielle Afanassieff ◽  
Dani�le Bouret ◽  
Gillette Luneau ◽  
Evelyne Esnault ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Class I ◽  
Major Histocompatibility ◽  
Transplantation Immunity ◽  
Histocompatibility Complex ◽  
Chicken Major Histocompatibility Complex ◽  
Nonclassical Class

scholarly journals Human Cytomegalovirus Protein US2 Interferes with the Expression of Human HFE, a Nonclassical Class I Major Histocompatibility Complex Molecule That Regulates Iron Homeostasis

2001 ◽  
Vol 75 (21) ◽  
pp. 10557-10562 ◽  
Author(s):  
Sayeh Vahdati Ben-Arieh ◽  
Baruch Zimerman ◽  
Nechama I. Smorodinsky ◽  
Margalit Yaacubovicz ◽  
Chana Schechter ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Human Cytomegalovirus ◽  
Viral Protein ◽  
Complex Molecule ◽  
Class I ◽  
Major Histocompatibility ◽  
Class I Mhc ◽  
Classical Class ◽  
Histocompatibility Complex ◽  
Nonclassical Class

ABSTRACT HFE is a nonclassical class I major histocompatibility complex (MHC) molecule that is mutated in the autosomal recessive iron overload disease hereditary hemochromatosis. There is evidence linking HFE with reduced iron uptake by the transferrin receptor (TfR). Using a panel of HFE and TfR monoclonal antibodies to examine human HFE (hHFE)-expressing cell lines, we demonstrate the expression of stable and fully glycosylated TfR-free and TfR-associated hHFE/β2m complexes. We show that both the stability and assembly of hHFE complexes can be modified by the human cytomegalovirus (HCMV) viral protein US2, known to interfere with the expression of classical class I MHC molecules. HCMV US2, but not US11, targets HFE molecules for degradation by the proteasome. Whether this interference with the regulation of iron metabolism by a viral protein is a means of potentiating viral replication remains to be determined. The reduced expression of classical class I MHC and HFE complexes provides the virus with an efficient tool for altering cellular metabolism and escaping certain immune responses.

scholarly journals Control of rat natural killer cell-mediated allorecognition by a major histocompatibility complex region encoding nonclassical class I antigens.

1994 ◽  
Vol 180 (2) ◽  
pp. 641-651 ◽  
Author(s):  
J T Vaage ◽  
C Naper ◽  
G Løvik ◽  
D Lambracht ◽  
A Rehm ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Nk Cells ◽  
Natural Killer ◽  
Class I ◽  
F1 Hybrids ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Nonclassical Class

The ability of natural killer (NK) cells to eliminate normal allogeneic hemic cells is well established in several species including mice, rats, and humans. The controlling elements for NK susceptibility in these species map to the major histocompatibility complex (MHC), but in contrast to findings in mice and humans, the mode of inheritance is not always recessive in rats. This finding is not easily explained by the missing self and hemopoietic histocompatibility (Hh) models for NK recognition, and has led to the idea that certain alloantigens may trigger NK cell reactivity. In our in vitro system for assessing rat NK alloreactivity, we have employed target and inhibitor cells from a large panel of MHC congenic, intra-MHC recombinant and MHC mutant rat strains, as well as appropriate F1 hybrids between them, and we show the following: (a) The nonclassical class I (RT1.C) region was most important in determining the susceptibility of target cells to alloreactive NK cells in vitro. Lymphocyte susceptibility to lysis in vivo also mapped to the C region, which supports the concept that the in vivo and in vitro alloreactivity assays reflect the same recognition process. (b) Four different RT1-controlled NK allospecificities (represented by the u, l, a, and n haplotypes) could be discerned when we used polyclonal NK cells from the PVG (RT1c) strain as effector cells. Three of the target specificities recognized were controlled mainly by the RT1.C region. (c) The expression of RT1.C region-controlled parental strain NK allodeterminants could be demonstrated in F1 hybrids heterozygous for the C region alone and were therefore inherited nonrecessively. (d) Loss of an RT1.C region-controlled NK allospecificity could be shown with the MHC mutant LEW.1LM1 rat strain characterized by a genomic deletion of about 100 kb of the C region. Taken together, these observations have demonstrated a major importance of the nonclassical class I region, i.e., RT1.C, in controlling rat NK allorecognition, and have thereby assigned a hitherto undescribed immunological property to this region. Furthermore, some of the present data are consistent with the existence of polymorphic NK-triggering alloantigens that are coded for by the RT1.C region.

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