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Significance Genetic linkage to major histocompatibility complex class II proteins has been observed in many immunological disorders; yet, little is known about the underlying mechanisms of these associations. For chronic beryllium disease (CBD), the linkage toHLA-DPB1 alleles encoding a glutamic acid at position 69 of the β-chain is well established. We tested whether the presence of HLA-DP2 is sufficient for the development of a disease-specific model of CBD. HLA-DP2 transgenic mice developed a beryllium-specific adaptive immune response composed of CD4+ T cells that secrete Th1-type cytokines and are HLA-DP2-restricted, thus replicating the major features of the human disease. In addition, regulatory T cells modulate granuloma formation in the lungs of beryllium oxide-exposed HLA-DP2 transgenic mice.

Regulatory T cells modulate granulomatous inflammation in an HLA-DP2 transgenic murine model of beryllium-induced disease