HLA class I sequence-based typing

Santamaría, Pere; Lindstrom, Alan L.; Boyce-Jacino, Michael T.; Myster, Steve H.; Barbosa, José; Faras, Anthony J.; Rich, Stephen S.

doi:10.1016/0198-8859(93)90141-m

Cited by 129 publications

(65 citation statements)

References 24 publications

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“…These authors suggest that allogeneic T cells may have a higher affinity for class II antigens when these molecules are complexed to epithelial-specific antigens. The arguments in favor of this possibility are that T cells directed at nonphysiologically presented autologous peptides are not deleted (37), that MHC molecules on different cell types may not be recognized in the same way by T cells ( 17,38,39), and that MHC class-II peptides involved in allorecognition may originate from exogenous proteins (40). However, this hypothesis does not fit very well with the data presented in this article because specificity studies were performed using BLCL cultured in the presence of 10% FCS.…”

Section: Resultsmentioning

confidence: 99%

Specificity of T cells invading the skin during acute graft-vs.-host disease after semiallogeneic bone marrow transplantation.

Gaschet

Mahé²,

Milpied³

et al. 1993

J. Clin. Invest.

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The mechanisms responsible for skin lesions during acute graft-vs.-host disease (aGVHD) after allogeneic bone marrow transplantation (BMT) are poorly understood. The exact role of various effector cell populations and "major" (particularly HLA-DP) or "minor" antigens as target molecules is not known. To investigate the nature of cells responsible for tissue injury, we cultured T cells from skin biopsy first with interleukin 2 (IL-2) alone and then in polyclonal activation conditions to avoid in vitro antigenic sensitization before specificity testing. We applied this method to two biopsies performed during aGVHD after semiallogeneic BMT and obtained cytotoxic T cells against four graft mismatches: CD8+ T cells against HLA-A2.2 and HLA-B27 and CD4+ T cells against HLADPlO and HLA-DP401. This demonstrates that T cells with documented specificity can be obtained from an aGVHD lesion without antigenic selection. Moreover, these data directly implicate DP as a potential target antigen for aGVHD. (J. Clin. Invest. 1993. 91:12-20.)

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Section: Resultsmentioning

confidence: 99%

Specificity of T cells invading the skin during acute graft-vs.-host disease after semiallogeneic bone marrow transplantation.

Gaschet

Mahé²,

Milpied³

et al. 1993

J. Clin. Invest.

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“…b Cell lines defective in ␤ 2 m expression (27, 30 -32). c Cell lines defective in HLA-A, B, C H chain expression (28,29).…”

Section: Expression Of Erap1 and Erap2 In Ebv-b Cell Linesmentioning

confidence: 99%

Expression of Endoplasmic Reticulum Aminopeptidases in EBV-B Cell Lines from Healthy Donors and in Leukemia/Lymphoma, Carcinoma, and Melanoma Cell Lines

Fruci

Ferracuti

Limongi

et al. 2006

The Journal of Immunology

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Peptide trimming in the endoplasmic reticulum (ER), the final step required for the generation of most HLA class I-binding peptides, implicates the concerted action of two aminopeptidases, ERAP1 and ERAP2. Because defects in the expression of these peptidases could lead to aberrant surface HLA class I expression in tumor cells, we quantitatively assayed 14 EBV-B cell lines and 35 human tumor cell lines of various lineages for: 1) expression and enzymatic activities of ERAP1 and ERAP2; 2) ER peptide-trimming activity in microsomes; 3) expression of HLA class I H chains and TAP1; and 4) surface HLA class I expression. ERAP1 and ERAP2 expression was detectable in all of the EBV-B and tumor cell lines, but in the latter it was extremely variable, sometimes barely detectable, and not coordinated. The expression of the two aminopeptidases corresponded well to the respective enzymatic activities in most cell lines. A peptide-trimming assay in microsomes revealed additional enzymatic activities, presumably contributed by other unidentified aminopeptidases sharing substrate specificity with ERAP2. Interestingly, surface HLA class I expression showed significant correlation with ERAP1 activity, but not with the activity of either ERAP2 or other unidentified aminopeptidases. Transfection with ERAP1 or ERAP2 of two tumor cell lines selected for simultaneous low expression of the two aminopeptidases resulted in the expected, moderate increases of class I surface expression. Thus, low and/or imbalanced expression of ERAP1 and probably ERAP2 may cause improper Ag processing and favor tumor escape from the immune surveillance.

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“…As shown in Table I, the induction was greater than 5-fold in two of the cell lines tested. Untransfected K562 cells were included as a negative control for the probe because they do not express any endogenous HLA-A mRNA (37).…”

Section: A Transfected Full-length Hla-a2 Gene Is Inducible With Ifn-␥mentioning

confidence: 99%

A 3′-Transcribed Region of the HLA-A2 Gene Mediates Posttranscriptional Stimulation by IFN-γ

Snyder

Waring

Sheng

et al. 2001

The Journal of Immunology

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The expression of several MHC class I genes is up-regulated at the transcriptional level by IFN-γ. Posttranscriptional mechanisms also have been implicated, but not well characterized. To investigate the mechanism of IFN-γ stimulation of the human MHC class I gene HLA-A2, several human tumor cell lines were transfected with reporter gene constructs driven by the HLA-A2 promoter. We have previously shown that the extended 525-bp HLA-A2 promoter alone, which includes a 5′ IFN-stimulated response element consensus sequence, is not sufficient for IFN-γ response in either K562 or Jurkat cells. In the current study, stable transfection of a genomic HLA-A2 gene construct, containing both 5′- and 3′-flanking sequences, resulted in stimulation of the gene by IFN-γ. Nuclear run-on assays revealed that, unlike other class I genes, IFN-γ stimulation of HLA-A mRNA accumulation occurs almost entirely through posttranscriptional mechanisms. RNA stability assays showed that the effect is not mediated by alteration of the half-life of the HLA-A2 mRNA. Formation of the 3′ end was unaffected by IFN-γ treatment. Sequences that mediate the majority of IFN-γ induction of HLA-A2 mRNA reside in a 127-bp 3′-transcribed region of the gene. This region contains the terminal splice site, the usage of which is not affected by IFN-γ treatment. These results demonstrate a novel posttranscriptional mechanism of regulation of MHC class I genes by IFN-γ.

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HLA class I sequence-based typing

Cited by 129 publications

References 24 publications

Specificity of T cells invading the skin during acute graft-vs.-host disease after semiallogeneic bone marrow transplantation.

Specificity of T cells invading the skin during acute graft-vs.-host disease after semiallogeneic bone marrow transplantation.

Expression of Endoplasmic Reticulum Aminopeptidases in EBV-B Cell Lines from Healthy Donors and in Leukemia/Lymphoma, Carcinoma, and Melanoma Cell Lines

A 3′-Transcribed Region of the HLA-A2 Gene Mediates Posttranscriptional Stimulation by IFN-γ

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