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Furthermore, signal transducer and activator of transcription 3 (\n                    <jats:italic>STAT3<\/jats:italic>\n                    ) mutations are frequently detected in PRCA patients, but their association with cellular immune abnormalities is not well understood. In order to elucidate the immunogenetic backgrounds of PRCA, we conducted human leucocyte antigen (HLA) typing in 39 PRCA patients. The results showed a significantly higher allele frequency of HLA\u2010B*44:03:01, \u2010C*14:03, \u2010DRB1*13:02, compared to HLA database. Additionally, analysis of inferred HLA haplotypes revealed significantly increased frequencies of two haplotypes: HLA\u2010A*24:02\u2010C*07:02\u2010B*07:02\u2010DRB1*01:01 and \u2010A*33:03\u2010C*14:03\u2010B*44:03:01\u2010DRB1*13:02. Clonotypic analyses of T\u2010cell receptor beta (TCR\u03b2) chain revealed that 80% of the PRCA cases possessed mono\u2010 or oligoclonally expanded T cells. Particularly among those with\n                    <jats:italic>STAT3<\/jats:italic>\n                    mutations, the \u2018QGXG\u2019 motif in 15 AA sequences of TCR\u03b2 complementarity\u2010determining regions 3 (CDR3) regions was specifically recognized. These findings suggest that a specific immunogenetic background defined by particular HLA alleles, the expansion of somewhat limited T\u2010cell clones and\n                    <jats:italic>STAT3<\/jats:italic>\n                    \u2010mutated T cells are involved in the pathogenesis of chronic acquired PRCA.\n                  <\/jats:p>","DOI":"10.1111\/bjh.70475","type":"journal-article","created":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T08:20:26Z","timestamp":1775550026000},"page":"1797-1805","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Immunological features of acquired pure red cell aplasia: Specific human leucocyte antigen alleles, signal transducer and activator of transcription 3 mutations and a unique T\u2010cell receptor beta motif"],"prefix":"10.1111","volume":"208","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-1585-6704","authenticated-orcid":false,"given":"Naruaki","family":"Yamashita","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory Investigation, Graduate School of Medicine Shinshu University  Matsumoto Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0178-5332","authenticated-orcid":false,"given":"Toru","family":"Kawakami","sequence":"additional","affiliation":[{"name":"Department of Haematology and Medical Oncology Shinshu University School of Medicine  Matsumoto Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuji","family":"Matsuzawa","sequence":"additional","affiliation":[{"name":"Department of Haematology and Medical Oncology Shinshu University School of Medicine  Matsumoto 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