Inborn errors of immunity underlie clonal T cell expansions in large granular lymphocyte leukemia

BACKGROUNDT cell large granular lymphocyte leukemia (T-LGLL) is a lymphoproliferative disorder of cytotoxic T lymphocytes (CTLs), often with gain-of-function STAT3 mutations. T-LGLL represents a unique model for the study of persistent CTL expansions. Albeit autoimmunity is implied, various paradoxical observations led us to investigate whether immunodeficiency traits underpin T-LGLL.METHODSThis is a comprehensive immunogenomic study of 92 consecutive patients from a large T-LGLL cohort with full laboratory-clinical characterization (n = 271). Whole-exome profiling of variants associated with inborn errors of immunity (IEI) and somatic mutations in T cell lymphoid drivers was analyzed. Single-cell RNA-Seq and TCR-Seq in T-LGLL samples and RNA-Seq in T cell cancer cell lines were utilized to establish biological correlations.RESULTSLymphocytopenia and/or hypogammaglobulinemia were identified in 186 of 241 (77%) T-LGLL patients. Genetic screening for IEI revealed 43 rare heterozygous variants in 38 different immune genes in 34 of 92 (36%) patients (vs. 167/63,026 [0.26%] in controls). High-confidence deleterious variants associated with dominant, adult-onset IEIs were detected in 15 of 92 (16%) patients. Carriers showed atypical features otherwise tied to the cryptic IEI, such as earlier onset, lower lymphocyte counts, lower STAT3 mutational rate, and higher proportions of hypogammaglobulinemia and immune cytopenia/bone marrow failure than noncarriers. Somatic mutational landscape, RNA-Seq, and TCR-Seq analyses supported immune imbalance caused by the IEI variants and interactions with somatic mutations in T cell lymphoid drivers.CONCLUSIONSOur findings in T-LGLL reveal that maladaptive CTL expansions may stem from cryptic immunodeficiency traits and open the horizon of IEIs to clonal hematopoiesis and bone marrow failure.FUNDINGNIH; Aplastic Anemia and MDS International Foundation; VeloSano; Edward P. Evans Foundation; Instituto de Salud Carlos III; European Research Council; European Research Area Network on Personalised Medicine; Academy Finland; Cancer Foundation Finland.

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Journal
Journal of Clinical Investigation
Published
2025-05-01
DOI
https://doi.org/10.1172/jci184431
Primary Topic
Immunodeficiency and Autoimmune Disorders
Type
article
Field-Weighted Citation Impact
0.00

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article

Inborn errors of immunity underlie clonal T cell expansions in large granular lymphocyte leukemia

Luca Guarnera, Carlos Bravo‐Pérez, Satu M. Mustjoki, Christopher Haddad et al.
Journal of Clinical Investigation
Immunodeficiency and Autoimmune Disorders
article

Inborn errors of immunity underlie clonal T cell expansions in large granular lymphocyte leukemia

Luca Guarnera, Carlos Bravo‐Pérez, Satu M. Mustjoki, Christopher Haddad, Valeria Visconte, Arooj Ahmed, Nakisha D Williams, Olisaemeka Ogbue, Naomi Kawashima, Jani Huuhtanen, Carmelo Gurnari, Arda Durmaz, Simona Pagliuca, Serhan Ünlü, Mark Orland, Jaroslaw Pawel Maciejewski, Aashray Mandala, Yasuo Kubota, Michaela Witt, Zachary Brady
article en

Abstract

BACKGROUNDT cell large granular lymphocyte leukemia (T-LGLL) is a lymphoproliferative disorder of cytotoxic T lymphocytes (CTLs), often with gain-of-function STAT3 mutations. T-LGLL represents a unique model for the study of persistent CTL expansions. Albeit autoimmunity is implied, various paradoxical observations led us to investigate whether immunodeficiency traits underpin T-LGLL.METHODSThis is a comprehensive immunogenomic study of 92 consecutive patients from a large T-LGLL cohort with full laboratory-clinical characterization (n = 271). Whole-exome profiling of variants associated with inborn errors of immunity (IEI) and somatic mutations in T cell lymphoid drivers was analyzed. Single-cell RNA-Seq and TCR-Seq in T-LGLL samples and RNA-Seq in T cell cancer cell lines were utilized to establish biological correlations.RESULTSLymphocytopenia and/or hypogammaglobulinemia were identified in 186 of 241 (77%) T-LGLL patients. Genetic screening for IEI revealed 43 rare heterozygous variants in 38 different immune genes in 34 of 92 (36%) patients (vs. 167/63,026 [0.26%] in controls). High-confidence deleterious variants associated with dominant, adult-onset IEIs were detected in 15 of 92 (16%) patients. Carriers showed atypical features otherwise tied to the cryptic IEI, such as earlier onset, lower lymphocyte counts, lower STAT3 mutational rate, and higher proportions of hypogammaglobulinemia and immune cytopenia/bone marrow failure than noncarriers. Somatic mutational landscape, RNA-Seq, and TCR-Seq analyses supported immune imbalance caused by the IEI variants and interactions with somatic mutations in T cell lymphoid drivers.CONCLUSIONSOur findings in T-LGLL reveal that maladaptive CTL expansions may stem from cryptic immunodeficiency traits and open the horizon of IEIs to clonal hematopoiesis and bone marrow failure.FUNDINGNIH; Aplastic Anemia and MDS International Foundation; VeloSano; Edward P. Evans Foundation; Instituto de Salud Carlos III; European Research Council; European Research Area Network on Personalised Medicine; Academy Finland; Cancer Foundation Finland.

Journal of Clinical InvestigationVol. 135(9)
University of Rome Tor Vergata (IT), Centre National de la Recherche Scientifique (FR), Cleveland Clinic (US), University of Helsinki (FI), Helsinki University Hospital (FI), Hospital General Universitario Morales Meseguer (ES), Université de Lorraine (FR), Aalto University (FI)
Aplastic Anemia and MDS International Foundation, Edward P. Evans Foundation, Vera and Joseph Dresner Foundation, Syöpäsäätiö, National Institutes of Health, Instituto de Salud Carlos III, National Heart, Lung, and Blood Institute
Zero hunger
Openalex Percentile: Top 90%
Immunodeficiency and Autoimmune Disorders
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