HMSD report

I. Expression across cell types

Insufficient scRNA-seq data for expression of HMSD at single-cell level.

II. Expression across tissues

sc-RNAseq data

Insufficient scRNA-seq data for expression of HMSD at tissue level.

III. Associated gene sets

GO_0002253Biological processactivation of immune response
GO_0032729Biological processpositive regulation of type II interferon production
GO_0019835Biological processcytolysis
GO_0005575Cellular componentcellular_component
GO_0005615Cellular componentextracellular space
GO_0004867Molecular functionserine-type endopeptidase inhibitor activity
GO_0003674Molecular functionmolecular_function

IV. Literature review

[source]
Gene nameHMSD
Protein nameMinor histocompatibility protein HMSD variant form (HSMD-v) [Cleaved into: Minor histocompatibility antigen ACC-6 (mHA ACC-6)]
Serpin-like protein HMSD (Minor histocompatibility protein HMSD) (Minor histocompatibility serpin domain-containing protein)
SynonymsC18orf53
DescriptionFUNCTION: Putative serine protease inhibitor. .

FUNCTION: This splice variant of HMSD is the precursor of the histocompatibility antigen ACC-6. More generally, minor histocompatibility antigens (mHags) refer to immunogenic peptide which, when complexed with MHC, can generate an immune response after recognition by specific T-cells. The peptides are derived from polymorphic intracellular proteins, which are cleaved by normal pathways of antigen processing. The binding of these peptides to MHC class I or class II molecules and its expression on the cell surface can stimulate T-cell responses and thereby trigger graft rejection or graft-versus-host disease (GVHD) after hematopoietic stem cell transplantation from HLA-identical sibling donor. GVHD is a frequent complication after bone marrow transplantation (BMT), due to mismatch of minor histocompatibility antigen in HLA-matched sibling marrow transplants. However, associated with GVHD, a favorable graft-versus-leukemia (GVL) can be induced by donor-recipient disparities in mHags. ACC-6 is presented to the cell surface by MHC HLA-B*4403. This complex specifically elicits donor-cytotoxic T-lymphocyte (CTL) reactivity against hematologic malignancies after treatment by HLA-identical allogenic BMT. It induces cell recognition and lysis by CTL. Immunogenicity of most autosomal mHags results from single-nucleotide polymorphisms that cause amino-acid substitutions within epitopes, leading to the differential recognition of peptides between donor and recipient. .

AccessionsA8MTL9
ENST00000526932.1 [P0C7T4-1]
ENST00000408945.5 [A8MTL9-1]
P0C7T4