Germline BRCA1 pathogenic variants and T cell dysfunction
Journal Title
Immuno-oncology Technology
Abstract
BACKGROUND: Germline BRCA1 (gBRCA1) pathogenic variants (PVs) are the most common cause of inherited breast cancer. Preclinical studies have shown that homozygous loss of BRCA1 in T cells impairs T cell-mediated antitumour immunity. However, the consequences of heterozygous gBRCA1 on human T cell function are unknown. PATIENTS AND METHODS: We collected peripheral blood mononuclear cells (PBMCs) from healthy donors and treatment-naïve patients diagnosed with early-stage breast cancer with or without a gBRCA1 PV. T cells derived from PBMC were activated in vitro and analysed for phenotypic and functional differences. To investigate the impact of gBRCA1 PV on tumour-infiltrating lymphocytes (TILs), we carried out T cell receptor (TCR) sequencing and whole exome sequencing on triple negative breast cancer (TNBC) tumours from gBRCA1 carriers and wild-type (WT) patients. RESULTS: Patients with gBRCA1 PV had significantly reduced circulating T cell counts compared with WT individuals. BRCA1 protein was highly expressed in healthy donor activated T cells, but significantly reduced expression was observed in gBRCA1 patients compared with WT. Activated T cells from gBRCA1 carriers displayed a distinct transcriptional profile with significantly impaired proliferation and decreased effector molecule production. TCR sequencing of TILs extracted from TNBC tumours from gBRCA1 carriers revealed significantly more hyperexpanded T cell clones than in WT patients, with hyperexpansion correlating with increased tumour mutation burden (R (2) = 0.86), particularly frameshift mutations (R (2) = 0.72). CONCLUSIONS: Circulating T cells from gBRCA1 carriers exhibit intrinsic T cell dysfunction. This phenotype may be clinically relevant in the context of antitumour immunity, cancer development, progression and response to immunotherapy treatment.
Publisher
Elsevier
Keywords
Brca1; T cell dysfunction; T cell receptor; breast cancer; immunity; tumour-infiltrating lymphocyte
Research Division(s)
Cancer Biology and Stem Cells
PubMed ID
42597706
Open Access at Publisher's Site
https://doi.org/10.1016/j.iotech.2026.101601
Terms of Use/Rights Notice
Refer to copyright notice on published article.


Creation Date: 2026-08-28 10:52:06
Last Modified: 2026-08-28 10:56:27
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