Full Papers
A link between CD8+CD27-CD28- T cells expressing chemerin chemokine-like receptor 1 and rheumatoid arthritis
E. Jeong1, J.-Y. Jung2, M.J. Lee3, H.-A. Kim4, H.Y. Yang5, K. Kim6, S. Park7
- Department of Microbiology, Ajou University School of Medicine, Suwon; and Department of Biomedical Sciences, The Graduate School, Ajou University, Suwon, Republic of Korea.
- Department of Rheumatology, Ajou University School of Medicine, Suwon, Republic of Korea.
- Department of Microbiology, Ajou University School of Medicine, Suwon, Republic of Korea.
- Department of Rheumatology, Ajou University School of Medicine, Suwon, Republic of Korea.
- Department of Microbiology, Ajou University School of Medicine, Suwon; and Department of Biomedical Sciences, The Graduate School, Ajou University, Suwon, Republic of Korea.
- Department of Microbiology, Ajou University School of Medicine, Suwon; and Department of Biomedical Sciences, The Graduate School, Ajou University, Suwon, Republic of Korea.
- Department of Microbiology, Ajou University School of Medicine, Suwon; and Department of Biomedical Sciences, The Graduate School, Ajou University, Suwon, Republic of Korea. sinsun@ajou.ac.kr
CER15869
2023 Vol.41, N°5
PI 1105, PF 1113
Full Papers
PMID: 36200942 [PubMed]
Received: 22/05/2022
Accepted : 01/09/2022
In Press: 04/10/2022
Published: 03/05/2023
Abstract
OBJECTIVES:
Transcription of the chemerin chemokine-like receptor 1 (CMKLR1) has been observed in T cell subsets, but its role in T cells has not been well studied. As previously reported, the levels of its ligand, chemerin, are increased in the plasma and synovial fluid of patients with rheumatoid arthritis (RA); hence, we aimed to explore the expression and role of CMKLR1 in the T cells of these patients.
METHODS:
Peripheral blood and synovial fluid from patients with RA or osteoarthritis and healthy individuals were collected to analyse the frequency of CD27-CD28- T cells and the expression of CMKLR1 and TNF-α by flow cytometry. Chemotaxis of T cells was assessed using a Transwell migration assay. Chemerin levels were measured using an enzyme-linked immunosorbent assay.
RESULTS:
CMKLR1 was preferentially expressed in CD27-CD28- T cell subsets. Its surface levels were reduced by stimulation with anti-CD3 antibody or chemerin. We found a correlation between CMKLR1+CD8+CD27-CD28- T cell frequency and disease activity score 28 of RA. Chemerin treatment up-regulated but CMKLR1 inhibitor treatment down-regulated TNF-α expression in CD8+CD27-CD28- T cells, half of which express CMKLR1 on average. Moreover, chemerin induced migration of these cells. Analysis of blood and synovial fluid samples of RA showed a reduction of CMKLR1+CD27-CD28- T cell levels in the synovial fluid, with a few exceptions.
CONCLUSIONS:
Our results suggest that CMKLR1 expression in T cells may be involved in RA pathogenesis through modulation of TNF-α expression and cell migration.
