Th1 and Th17 cells are resistant towards T cell activation-induced downregulation of CD6.

Clin Immunol

Laboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine, University Hospital Cologne, University of Cologne, Cologne, Germany; Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, Cologne, Germany. Electronic address:

Published: May 2022

Background: The cell surface molecule CD6 is a modulator of T cell receptor (TCR) signaling. Recently, it has been reported that CD6 is downregulated on CD4+ T cells following T cell activation. This mechanism could limit the efficacy of anti-CD6 therapeutical antibodies.

Methods: We analyzed CD6 expression on activated and non-activated Th1 cells and Th17 cells by flow cytometry.

Results: Our experiments confirmed a significant downregulation of CD6 on IFNγ- and IL17-negative CD4+ T cells from healthy individuals and from patients with rheumatoid arthritis following T cell activation with anti-CD3 and anti-CD28 antibodies. In contrast, CD6 expression remained stable on activated Th17 cells and Th1 cells.

Conclusions: Th1 and Th17 cells are resistant towards T cell activation-induced downregulation of CD6. These findings are relevant for the future development of CD6 targeting therapies and show that CD6 expression is differentially regulated in CD4+ T cell subsets.

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http://dx.doi.org/10.1016/j.clim.2022.109025DOI Listing

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