Evaluation of Atypical Chemokine Receptor Expression in T Cell Subsets

Cells. 2022 Dec 16;11(24):4099. doi: 10.3390/cells11244099.

Abstract

Chemokines are molecules that pertain to a family of small cytokines and can generate cell chemotaxis through the interaction with their receptors. Chemokines can trigger signaling via conventional G-protein-coupled receptors or through atypical chemokine receptors. Currently, four atypical chemokine receptors have been are described (ACKR1, ACKR2, ACKR3 and ACKR4). ACKRs are expressed in various cells and tissues, including T lymphocytes. These receptors' main function is related to the internalization and degradation of chemokines, as well as to the inflammation control. However, the expression of these receptors in human T lymphocytes is unclear in the literature. The objective of this study was to evaluate the expression of ACKRs in different subpopulations of T lymphocytes. For this, peripheral blood from healthy donors was used to analyze the expression of ACKR2, ACKR3 and ACKR4 by immunophenotyping CD4, CD8 T lymphocytes and, in their subsets, naive, transition and memory. Results obtained in this study demonstrated that ACKR2, ACKR3 and ACKR4 receptors were expressed by T lymphocytes subsets in different proportions. These receptors are highly expressed in the cytoplasmic milieu of all subsets of T lymphocytes, therefore suggesting that their expression in plasma membrane is regulated after transcription, and it must be dependent on a stimulus, which was not identified in our study. Thus, regarding ACKRs function as scavenger receptors, at least for the ACKR3, this function does not impair the chemotaxis exert for their ligand compared to the typical counterpart receptor.

Keywords: ACKR; T cell; atypical chemokine receptors; chemokines; memory; naïve.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chemokines* / metabolism
  • Chemotaxis
  • Cytokines* / metabolism
  • Humans
  • Receptors, Chemokine* / metabolism
  • Signal Transduction
  • T-Lymphocyte Subsets* / metabolism

Substances

  • Chemokines
  • Cytokines
  • Receptors, Chemokine

Grants and funding

This research was funded by FAPESP, funding number: 2018/00094-9.