{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n HLA‐DQB2 encodes the β chain of an HLA‐DQ heterodimer that participates in the presentation of antigens to CD4+ T cells. Experimental studies have demonstrated that, although this gene is relatively non‐polymorphic compared with its classical counterparts, it is functionally expressed in antigen‐presenting cells such as Langerhans cells in the epidermis. In these cells HLA‐DQB2, co‐expressed with its partner HLA‐DQA2, forms heterodimeric complexes that traffic to endosomal compartments and the cell surface, where they efficiently present antigens—including superantigens—to T cells, thus potentially influencing the local immune response in the skin (3)."}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In parallel, genetic association studies have implicated HLA‐DQB2 in several immune‐mediated conditions. For example, an intronic variant in HLA‐DQB2 has been associated with rheumatoid arthritis susceptibility independent of classical HLA‐DRB1 risk alleles (1). Moreover, genome‐wide association analyses in East Asian cohorts have identified SNPs in HLA‐DQB2 that appear to confer protective effects against chronic hepatitis B infection, although similar associations were not consistently replicated in other populations (2,4). Additionally, analysis of tuberculosis risk revealed that specific HLA‐DQB2 polymorphisms (e.g., the rs7453920 G>A substitution) are linked with an increased susceptibility to disease (5).\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these observations support a role for HLA‐DQB2 in modulating adaptive immune responses by influencing antigen presentation. Its expression in professional antigen‐presenting cells and the genetic associations with autoimmune, infectious, and inflammatory disorders suggest that even subtle variations in the gene’s regulatory regions or sequence may impact immune activation and disease pathogenesis. Thus, HLA‐DQB2 contributes to immune recognition and may serve as a potential biomarker or therapeutic target in diverse immunological conditions."}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yuta Kochi, Ryo Yamada, Kyoko Kobayashi, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Analysis of single-nucleotide polymorphisms in Japanese rheumatoid arthritis patients shows additional susceptibility markers besides the classic shared epitope susceptibility sequences."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Arthritis Rheum (2004)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/art.11366"}], "href": "https://doi.org/10.1002/art.11366"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "14730600"}], "href": "https://pubmed.ncbi.nlm.nih.gov/14730600"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "De-Ke Jiang, Xiao-Pin Ma, Hongjie Yu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Genetic variants in five novel loci including CFB and CD40 predispose to chronic hepatitis B."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hepatology (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/hep.27794"}], "href": "https://doi.org/10.1002/hep.27794"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25802187"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25802187"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Cedric Lenormand, Huguette Bausinger, Florence Gross, et al. "}, {"type": "b", "children": [{"type": "t", "text": "HLA-DQA2 and HLA-DQB2 genes are specifically expressed in human Langerhans cells and encode a new HLA class II molecule."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Immunol (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.4049/jimmunol.1103048"}], "href": "https://doi.org/10.4049/jimmunol.1103048"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22407913"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22407913"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "V R Z B Pereira, J M Wolf, G Z Stumm, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Lack of association between human leukocyte antigen polymorphisms rs9277535 and rs7453920 and chronic hepatitis B in a Brazilian population."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genet Mol Res (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.4238/gmr16029565"}], "href": "https://doi.org/10.4238/gmr16029565"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28613373"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28613373"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Xue Wang, Xudong Cao, Wanjiang Zhang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Association of human leukocyte antigens-DQB2/DPA1/DPB1 polymorphism and pulmonary tuberculosis in the Chinese Uygur population."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Genet Genomic Med (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/mgg3.544"}], "href": "https://doi.org/10.1002/mgg3.544"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30600606"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30600606"}]}]}]}