Hyperconservation of the Putative Antigen Recognition Site of the MHC Class I-b Molecule TL in the Subfamily Murinae: Evidence That Thymus Leukemia Antigen Is an Ancient Mammalian Gene

Davis, Beckley K.; Cook, Richard G.; Rich, Robert R.; Rodgers, John R.

doi:10.4049/jimmunol.169.12.6890

Cited by 7 publications

(6 citation statements)

References 60 publications

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“…DNA sequence analysis revealed that the allelic differences of CD1D genes are much lower than those in MHC class Ia genes, suggesting strong conservation within CD1D genes. The divergence among CD1d alleles is comparable with that seen in MHC class Ib molecules that perform specialized immune functions, including TL, M3, and Qa-1 (29)(30)(31).…”

Section: Discussionmentioning

confidence: 60%

Polymorphisms in CD1d affect antigen presentation and the activation of CD1d-restricted T cells

Zimmer

Nguyen²,

Wang³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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CD1 proteins constitute a distinct lineage of antigen-presenting molecules specialized for the presentation of lipid antigens to T cells. In contrast to the extensive sequence polymorphism characteristic of classical MHC molecules, CD1 proteins exhibit limited sequence diversity. Here, we describe the identification and characterization of CD1d alleles in wild-derived mouse strains. We demonstrate that polymorphisms in CD1d affect the presentation of endogenous and exogenous ligands to CD1d-restricted T cells, including type I (V␣14i) and type II (non-V␣14i) natural killer T (NKT) cells. Using congenic mice, we found CD1d polymorphisms affect the thymic selection of type I NKT cells and induce allogeneic T cell responses. Collectively, results from these studies demonstrate a role for polymorphisms in influencing the development and function of CD1d-restricted T cells.T cell activation ͉ T cell development

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Section: Discussionmentioning

confidence: 60%

Polymorphisms in CD1d affect antigen presentation and the activation of CD1d-restricted T cells

Zimmer

Nguyen²,

Wang³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…The XC overlay test (9, 11) was used to test for susceptibility to virus infection in various cell lines including 2 lines derived from the Asian species Mus m. dunni, MDTF and M. dunni (13), NIH 3T3 and cell lines derived from tail fibroblasts of the wild mouse species M. n. minutoides, M. n. setulosus, and M. p. platythrix obtained from J. Rodgers (Baylor College of Medicine, Houston, TX) (25). Embryo fibroblasts were prepared from strain 129/J from The Jackson Laboratory.…”

Section: Methodsmentioning

confidence: 99%

Origin, antiviral function and evidence for positive selection of the gammaretrovirus restriction gene Fv1 in the genus Mus

Yan

Buckler-White

Wollenberg

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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The Fv1 virus resistance gene is a coopted endogenous retrovirus (ERV) sequence related to the gag gene of the MuERV-L ERV family. Three major Fv1 resistance alleles have been identified in laboratory mice, and they target virus capsid genes to produce characteristic patterns of resistance to mouse leukemia viruses (MLVs). We identified Fv1 in 3 of the 4 Mus subgenera; its absence from Coelomys and 1 of 3 species of Pyromys indicate Fv1 was acquired shortly after the origin of the Mus genus. We sequenced Fv1 genes from 21 mice representative of the major taxonomic groups of Mus . Two lines of evidence indicate that Fv1 has had antiviral function for 7 million years of evolution. First, 2 species of African pygmy mice (subgenus Nannomys ) show an Fv1 -like MLV resistance, and transduced cells expressing the Nannomys Fv1 gene reproduce this resistance pattern. Second, sequence comparisons suggest that Fv1 has been involved in genetic conflicts throughout Mus evolution. We found evidence for strong positive selection of Fv1 and identified 6 codons that show evidence of positive selection: 3 codons in the C-terminal region including 2 previously shown to contribute to Fv1 restriction in laboratory mice, and 3 codons in a 10-codon segment overlapping the major homology region of Fv1 ; this segment is known to be involved in capsid multimerization. This analysis suggests that Fv1 has had an antiviral role throughout Mus evolution predating exposure of mice to the MLVs restricted by laboratory mouse Fv1 , and suggests a mechanism for Fv1 restriction.

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“…This process led to variable numbers of T23/T11, T22/T10, T25, and T18/T3-like paralogous genes, pseudogenes and gene fragments (42). For example, the TL antigen (43), which is expressed on intestinal epithelium and thymocytes, can be encoded by one (H2-T3), two (H2-T3 and -T18) or three genes (in A/J), depending on the strain. Qa-1 b is encoded in BALB/c by the H2-T23 d gene (originally Gene D37), whereas H2-T11 d (originally named T10c) from BALB/c is a pseudogene due to a one base deletion leading to a frame-shift and early stop in exon 2 (44).…”

Section: Introductionmentioning

confidence: 99%

Expression of the Mouse MHC Class Ib H2-T11 Gene Product, a Paralog of H2-T23 (Qa-1) with Shared Peptide-Binding Specificity

Chen

Reyes-Vargas

Dai

et al. 2014

The Journal of Immunology

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The mouse MHC class Ib gene H2-T11 is 95% identical at the DNA level to H2-T23, which encodes Qa-1, one of the most studied MHC class Ib molecules. H2-T11 mRNA was observed to be expressed widely in tissues of C57BL/6 mice, with highest levels in thymus. To circumvent the availability of a specific mAb, cells were transduced with cDNA encoding T11 with a substituted α3 domain. Hybrid T11D3 protein was expressed at high levels similar to control T23D3 molecules on the surface of both TAP+ and TAP− cells. Soluble T11D3 was generated by folding in vitro with Qdm, the dominant peptide presented by Qa-1. The circular dichroism spectrum of this protein was similar to that of other MHC class I molecules, and it was observed to bind labeled Qdm peptide with rapid kinetics. By contrast to the Qa-1 control, T11 tetramers did not react with cells expressing CD94/NKG2A, supporting the conclusion that T11 cannot replace Qa-1 as a ligand for NK cell inhibitory receptors. T11 also failed to substitute for Qa-1 in the presentation of insulin to a Qa-1-restricted T cell hybridoma. Despite divergent function, T11 was observed to share peptide-loading specificity with Qa-1. Direct analysis by tandem mass spectrometry of peptides eluted from T11D3 and T23D3 isolated from Hela cells demonstrated a diversity of peptides with a clear motif that was shared between the two molecules. Thus T11 is a paralog of T23 encoding an MHC class Ib molecule that shares peptide-binding specificity with Qa-1 but differs in function.

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Hyperconservation of the Putative Antigen Recognition Site of the MHC Class I-b Molecule TL in the Subfamily Murinae: Evidence That Thymus Leukemia Antigen Is an Ancient Mammalian Gene

Cited by 7 publications

References 60 publications

Polymorphisms in CD1d affect antigen presentation and the activation of CD1d-restricted T cells

Polymorphisms in CD1d affect antigen presentation and the activation of CD1d-restricted T cells

Origin, antiviral function and evidence for positive selection of the gammaretrovirus restriction gene Fv1 in the genus Mus

Expression of the Mouse MHC Class Ib H2-T11 Gene Product, a Paralog of H2-T23 (Qa-1) with Shared Peptide-Binding Specificity

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