Rheumatoid arthritis

Correlation of Professional Antigen‐Presenting Tbet + CD11c + B Cells With Bone Destruction in Untreated Rheumatoid Arthritis

Arthritis RheumatolPublished Mechanistic study

Authors' conclusion

This study suggests that Tbet+CD11c+ MBCs contribute to the pathogenesis of RA by promoting bone destruction through antigen presentation, T cell activation, and Th17 polarization.

Study context

Population
Patients with untreated rheumatoid arthritis (RA) (untreated RA (uRA)); peripheral blood memory B cells (MBCs)Single-cell RNA sequencing (scRNA-seq) n = 4
Participants
36 patients
Outcome
Association between CD21-/lowTbet+CD11c+ MBCs and joint destruction and other clinical parameters; functional properties of these cells
Methodological detailsflow cytometry, single-cell RNA sequencing, V(D)J sequencing, in vitro coculture
  • Flow cytometry
  • Single-cell RNA sequencing
  • V(D)J sequencing
  • In vitro coculture

Main finding

As reported in the abstract

Unique signature of up-regulated genes associated with antigen presentation functions, mirrored in synovial counterparts
>150

Original publication

Correlation of Professional Antigen‐Presenting Tbet + CD11c + B Cells With Bone Destruction in Untreated Rheumatoid Arthritis. Arthritis Rheumatol. Published 21 May 2024. doi:10.1002/art.42857

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