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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

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Beryllium sensitivity is linked to HLA-DP genotype.

Z Wang¹, G M Farris, L S Newman

¹B-2, M888, Bioscience Division, Los Alamos National Laboratory, Los Alamos, NM 87545, USA.

|September 12, 2001

Summary

Genetic variations in the HLA-DPB1 gene, specifically the Glu69 substitution, are linked to beryllium hypersensitivity. This finding provides direct evidence of HLA-DP genotype

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Immunopeptidomics: Isolation of Mouse and Human MHC Class I- and II-Associated Peptides for Mass Spectrometry Analysis

Immunopeptidomics: Isolation of Mouse and Human MHC Class I- and II-Associated Peptides for Mass Spectrometry Analysis

Published on: October 15, 2021

Area of Science:

Immunogenetics
Occupational Medicine
Pulmonary Medicine

Background:

Chronic beryllium disease (CBD) results from beryllium exposure and genetic factors.
Beryllium hypersensitivity, a precursor to CBD, is characterized by lymphocyte proliferation upon beryllium exposure.
Specific HLA-DPB1 gene variations have been previously associated with CBD.

Purpose of the Study:

To investigate the association between HLA-DPB1 allelic variations and beryllium hypersensitivity in individuals without clinical CBD.
To determine if specific HLA-DPB1 genotypes are present in beryllium-sensitive individuals who have not developed CBD.

Main Methods:

A flow cytometry-based Lymphocyte Proliferation Test with immunophenotyping (Immuno-LPT) was employed to measure CD4+ and CD8+ T cell responses to beryllium.
HLA-DPB1 haplotypes were analyzed using automated DNA sequencing in beryllium-sensitive, non-CBD individuals.
T cell proliferation patterns were correlated with specific HLA-DPB1 genotypes.

Main Results:

Twenty-two of 25 beryllium-sensitive, non-CBD individuals carried the HLA-DPB1 gene with a glutamic acid substitution at position 69 in Exon 2 (Glu69).
A significant percentage (24%) of these individuals were Glu69 homozygotes.
CD4+ T cell responders predominantly carried rare, non-*0201 Glu69 DPB1 alleles, whereas non-CD4+ responders were common Glu69 carriers or non-Glu69 individuals.

Conclusions:

This study provides the first direct evidence linking HLA-DP genotype to the phenotypic response of beryllium sensitization.
The presence of specific HLA-DPB1 variations, particularly Glu69, is associated with beryllium hypersensitivity independent of clinical CBD development.
These findings highlight the role of immunogenetic factors in the early stages of beryllium-related diseases.