Frontiers in Immunology (Oct 2024)
Activating STAT3 mutations in CD8+ T-cells correlate to serological positivity in rheumatoid arthritis
- Katharine B. Moosic,
- Katharine B. Moosic,
- Katharine B. Moosic,
- Thomas L. Olson,
- Thomas L. Olson,
- Mark Freijat,
- Samara Khalique,
- Cait E. Hamele,
- Cait E. Hamele,
- Bryna Shemo,
- Bryna Shemo,
- Jesse Boodoo,
- William Baker,
- Gitanjali Khurana,
- Matthew Schmachtenberg,
- Matthew Schmachtenberg,
- Tristin Duffy,
- Tristin Duffy,
- Aakrosh Ratan,
- Aakrosh Ratan,
- Aakrosh Ratan,
- Erika Darrah,
- Felipe Andrade,
- Marieke Jones,
- Kristine C. Olson,
- Kristine C. Olson,
- David J. Feith,
- David J. Feith,
- Donald L. Kimpel,
- Thomas P. Loughran,
- Thomas P. Loughran
Affiliations
- Katharine B. Moosic
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Katharine B. Moosic
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Katharine B. Moosic
- Department of Pathology, School of Medicine, University of Virginia, Charlottesville, VA, United States
- Thomas L. Olson
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Thomas L. Olson
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Mark Freijat
- Division of Rheumatology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Samara Khalique
- Division of Rheumatology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Cait E. Hamele
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Cait E. Hamele
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Bryna Shemo
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Bryna Shemo
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Jesse Boodoo
- Division of Rheumatology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- William Baker
- Division of Rheumatology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Gitanjali Khurana
- Division of Rheumatology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Matthew Schmachtenberg
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Matthew Schmachtenberg
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Tristin Duffy
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Tristin Duffy
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Aakrosh Ratan
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Aakrosh Ratan
- Center for Public Health Genomics, School of Medicine, University of Virginia, Charlottesville, VA, United States
- Aakrosh Ratan
- Department of Public Health Sciences, School of Medicine, University of Virginia, Charlottesville, VA, United States
- Erika Darrah
- Division of Rheumatology, The Johns Hopkins School of Medicine, Baltimore, MD, United States
- Felipe Andrade
- Division of Rheumatology, The Johns Hopkins School of Medicine, Baltimore, MD, United States
- Marieke Jones
- Department of Public Health Sciences, School of Medicine, University of Virginia, Charlottesville, VA, United States
- Kristine C. Olson
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Kristine C. Olson
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- David J. Feith
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- David J. Feith
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Donald L. Kimpel
- Division of Rheumatology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- Thomas P. Loughran
- University of Virginia Cancer Center, University of Virginia School of Medicine, Charlottesville, VA, United States
- Thomas P. Loughran
- Division of Hematology/Oncology, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States
- DOI
- https://doi.org/10.3389/fimmu.2024.1466276
- Journal volume & issue
-
Vol. 15
Abstract
ObjectivesLarge granular lymphocyte (LGL) leukemia is a rare hematologic malignancy characterized by clonal expansion of cytotoxic T-cells frequent somatic activating STAT3 mutations. Based on the disease overlap between LGL leukemia rheumatoid arthritis (RA)a putative role for CD8+ T-cells in RA we hypothesized that STAT3 mutations may be detected in RA patient CD8+ T-cells correlate with clinical characteristics.MethodsBlood samples, clinical parameters, and demographics were collected from 98 RA patients and 9 healthy controls (HCs). CD8+ cell DNA was isolated and analyzed via droplet digital (dd)PCR to detect STAT3 mutations common in LGL leukemia: Y640F, D661Y, and the S614 to G618 region. STAT3 data from 99 HCs from a public dataset supplemented our 9 HCs.ResultsRA patients had significantly increased presence of STAT3 mutations compared to controls (Y640F p=0.0005, D661Y p=0.0005). The majority of these were low variant allele frequency (VAF) (0.008-0.05%) mutations detected in a higher proportion of the RA population (31/98 Y640F, 17/98 D661Y) vs. HCs (0/108 Y640F, 0/108 D661Y). In addition, 3/98 RA patients had a STAT3 mutation at a VAF >5% compared to 0/108 controls. Serological markers, RF and anti-CCP positivity, were more frequently positive in RA patients with STAT3 mutation relative to those without (88% vs 59% RF, p=0.047; 92% vs 58% anti-CCP, p=0.031, respectively).ConclusionsSTAT3 activating mutations were detected in RA patient CD8+ cells and associated with seropositivity. Thus, STAT3 activating mutations may play a role in disease pathogenesis in a subset of RA patients.
Keywords
- rheumatoid arthritis
- large granular lymphocytic leukemia
- anti-citrullinated protein antibodies
- CD8-positive T-lymphocytes
- rheumatoid factor
- stat3