HLA-DPB1 (Major Histocompatibility Complex, Class II, DP Beta 1)

P2, N=313, Active, not recruiting, Center for International Blood and Marrow Transplant Research | Recruiting --> Active, not recruiting

The frequency of the DRB1*15:01-associated haplotype (DRB1*15:01-DQB1*06:02-DPB1*02:01) was significantly higher in patients who developed both pituitary and thyroid irAEs compared to the control (14.3% vs. 3.1%, p = 0.002), and the DRB1*15:02-associated haplotype (DRB1*15:02-DQB1*06:01-DPB1*09:01) frequency was significantly higher in patients who developed pituitary irAE but not thyroid irAE compared to the control (18.1% vs. 8.9%, p = 0.006); both findings were confirmed in the validation cohort comprising 92 patients with pituitary irAE from seven hospitals. In conclusion, pituitary and thyroid irAEs are prone to co-occur and HLA-DR15-associated haplotypes are related to this co-occurrence.

Class II alleles, especially those within DQA1 and DPB1, are important genetic factors influencing AML susceptibility in the Kazakhstani population.

Finally, analysis of the additive effects of HLA allele heterozygosity in smokers identified significant associations with several 4-digit HLA alleles, including HLA-B*08:01, HLA-A*01:01, HLA-C*07:01, HLA-DQA1*05:01, HLA-DRB1*03:01, and HLA-C*03:04. Our study provides additional evidence, with added histologic subtype information, that germline HLA-II heterozygosity is inversely associated with lung cancer risk.

Autologous PBL, gene engineered to express the PIK3CAE545K-specific TCR, suppressed the in vitro growth of two cancer cell lines, which endogenously expressed the PIK3CAE545K neoantigen. This study identified three PIK3CA-specific TCRs against two shared mutations, restricted by common HLA-class II molecules, using antigen-experienced TIL and memory PBL from patients with epithelial cancers and may further allow the development of off-the-shelf T cell immunotherapy strategies targeting PIK3CA.

Tumor-derived MIF is associated with poor prognosis, likely by suppressing the immune system, but it also promotes the induction of APC-like B cells, which are associated with improved outcomes, highlighting its dual role in LUAD. These findings position MIF as a potential therapeutic target and suggest that MIFR+ B cells could serve as important prognostic markers.

This study elucidates genes in NSCLC that are highly associated with both disease progression and type II pneumocyte features as potential biomarkers of NSCLC, and predicts their potential regulatory functions as well as their impact on the immune infiltration profile of NSCLC, providing guidance for the unraveling of the immune mechanisms of NSCLC.

This study established a genetic-transcriptional regulatory framework for sintilimab-induced thyroid irAEs and identified a candidate gene set with biomarker potential. Our findings highlighted the central role of complement-driven mechanisms, providing a foundation for precision risk prediction and targeted intervention strategies that preserve antitumor efficacy while mitigating autoimmune toxicity.

Germline polymorphisms of HLA-DPB1, IL18RAP and HLA-DRB1 genes have been defined in Chinese NK/T-cell lymphoma patients, potentially affecting susceptibility to EBV-related lymphomagenesis. This review explores these epidemiological differences and how they may impact on management.

PTCy should be the preferred GVHD prophylaxis strategy for HLA-DPB1 MM URD HCT. Furthermore, within PTCy platforms, survival is comparable across HLA-DPB1 match and thus NP mismatching at HLA-DPB1 should not be a determinant in URD selection.

MR-, summary-data-based MR-, and co-localization-based approaches identified target genes associated with HCC risk, comprising 3 first-level targets (HLA-DPA1, MBTPS1, and TIMP3), 2 second-level targets (TNXB and HSD17B11), and also 4 tertiary targets (HLA-DPB1, PLD2, KLHL8, and TGFBR1). All in all, this research identifies several potential therapeutic targets relevant to the risk of HCC and provides new insights into the identification of therapeutic agents for the treatment of HCC.

Our results provide first evidence that early-onset irM with myocardial injury is linked to HLA-A*01:01-B*08:01-C*07:01, a component of the 8.1 AH, which is associated with various autoimmune diseases including idiopathic myopathies. If validated in larger cohorts, pretreatment screening for HLA-A*01:01-B*08:01-C*07:01 may help identify patients at risk of early-onset and severe irM.