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Journal of Immunology, Infection & Inflammatory Diseases

JIIID

Aabstract

Research Article

Regulated Melanocortin Receptor 1-5 Gene Expressions in CD56+ NK Cells from Two Rheumatoid Arthritis Patients Treated with Adalimumab

Marlene Andersen, Michael Kruse Meyer, Ivan Nagaev, Olga Nagaeva, Jarl Erik Sylvester Wikberg, Lucia Mincheva-Nilsson and Grethe Neumann Andersen

Correspondence Address :

Grethe Neumann Andersen MD PhD
Department of Rheumatology
North Denmark Regional Hospital
Bispensgade 37
DK-9800 Hjorring
Denmark
Tel: 45 +/-40234094
Fax: +/-45 97640999
Email: Grethe.andersen.2@rn.dk

Received on: January 18, 2017 , Accepted on: January 31, 2017 , Published on: February 08, 2017

Citation: Marlene Andersen, Michael Kruse Meyer, Ivan Nagaev, Olga Nagaeva, Jarl Erik Sylvester Wikberg, Lucia Mincheva-Nilsson, Grethe Neumann Andersen (2017). Regulated Melanocortin Receptor 1-5 Gene Expressions in CD56+ NK Cells from Two Rheumatoid Arthritis Patients Treated with Adalimumab

Copyright: 2017 Grethe Neumann Andersen, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

  • Abstract

Abstract
Abstract
          The role of the endogenous, proresolving melanocortin system is still essentially unexplored in human auto-immune diseases. Melanocortin receptor (MCR) 1-5 genes and proteins are expressed in several leukocyte subsets and MCR1-3 and MCR5 mRNAs have been found in CD56+ natural killer (NK) cells from healthy humans. CD56+ NK cells may be decisive in the induction of auto-immunity and their cytokine profile assists in the direction of naive CD4+ T cells into specific effector or regulatory T cell subsets. We explored the possibilities of affecting CD56+ NK cell function through MCR1-5. Thus, we determined the response of MCR1-5 gene expression in active rheumatoid arthritis (RA) to TNFα inhibition (I) with adalimumab. CD56+ NK cells from RA patients treated with adalimumab were separated by immune-magnetic beads before and after three months of adalimumab treatment. Total RNA was extracted and mRNAs for MCR1-5 and a panel of cytokines were measured by qRT-PCR. All MCR genes, including MCR4, - not previously described in NK cells -, were expressed in CD56+ NK cells in active RA and reacted to adalimumab by down-regulation. In addition, the gene expression of cytokines important for CD56+ NK cell activity, i.e. especially TNFα and IFNγ were down-regulated. NK cell activity in RA may thus be modulated by MCR signalling. The response of MCR1-5 gene expressions in NK cells to adalimumab reinforces this perception. We propose that MCR signalling in NK cells may represent a new endogenous pathway to counteract autoimmune inflammation in RA.

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