PMID- 33453247
OWN - NLM
STAT- MEDLINE
DCOM- 20210226
LR  - 20210226
IS  - 1879-0631 (Electronic)
IS  - 0024-3205 (Linking)
VI  - 269
DP  - 2021 Mar 15
TI  - Role of CCL2/CCR2 axis in the immunopathogenesis of rheumatoid arthritis: Latest 
      evidence and therapeutic approaches.
PG  - 119034
LID - S0024-3205(21)00019-9 [pii]
LID - 10.1016/j.lfs.2021.119034 [doi]
AB  - Evidence suggests that uncontrolled immune system responses and their components 
      play a significant role in developing rheumatoid arthritis (RA), which is 
      considered an autoimmune disease (AD). Among immune system mediators, cytokines 
      and chemokines are involved in numerous physiological and pathological processes. 
      CCL2 or monocyte chemoattractant protein-1 (MCP-1) is known as a CC chemokine 
      that can induce the locomotion and recruitment of monocytes and macrophages to 
      the site of injury. When CCL2 binds to its receptors, the most important of which 
      is CCR2, various signaling pathways are triggered, eventually leading to various 
      immunological events such as inflammation. This chemokine also participates in 
      several events involved in RA pathogenesis, such as osteoclastogenesis, migration 
      of effector T cells to the RA synovium tissue, and angiogenesis. In this review 
      article, the role of the CCL2/CCR2 axis in RA pathogenesis and the immunotherapy 
      opportunities based on CCL2/CCR2 axis targeting has been discussed based on 
      existing investigations.
CI  - Copyright (c) 2021 Elsevier Inc. All rights reserved.
FAU - Moadab, Fatemeh
AU  - Moadab F
AD  - Student Research Committee, Rafsanjan University of Medical Sciences, Rafsanjan, 
      Iran; Department of Immunology, School of Medicine; Molecular Medicine Research 
      Center, Institute of Basic Medical Sciences Research, Rafsanjan University of 
      Medical Sciences, Rafsanjan, Iran.
FAU - Khorramdelazad, Hossein
AU  - Khorramdelazad H
AD  - Department of Immunology, School of Medicine; Molecular Medicine Research Center, 
      Institute of Basic Medical Sciences Research, Rafsanjan University of Medical 
      Sciences, Rafsanjan, Iran.
FAU - Abbasifard, Mitra
AU  - Abbasifard M
AD  - Department of Internal Medicine, Ali-Ibn Abi-Talib Hospital, School of Medicine; 
      Molecular Medicine Research Center, Institute of Basic Medical Sciences Research, 
      Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Electronic address: 
      dr.mabbasifard@gmail.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210113
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Chemokine CCL2)
RN  - 0 (Receptors, CCR2)
SB  - IM
MH  - Animals
MH  - Arthritis, Rheumatoid/*immunology/metabolism/*pathology/therapy
MH  - Chemokine CCL2/*metabolism
MH  - Humans
MH  - Immunotherapy/methods
MH  - Receptors, CCR2/*metabolism
OTO - NOTNLM
OT  - CCL2
OT  - CCR2
OT  - Cartilage destruction
OT  - MCP-1
OT  - Rheumatoid arthritis
EDAT- 2021/01/17 06:00
MHDA- 2021/02/27 06:00
CRDT- 2021/01/16 20:08
PHST- 2020/11/17 00:00 [received]
PHST- 2021/01/02 00:00 [revised]
PHST- 2021/01/07 00:00 [accepted]
PHST- 2021/01/17 06:00 [pubmed]
PHST- 2021/02/27 06:00 [medline]
PHST- 2021/01/16 20:08 [entrez]
AID - S0024-3205(21)00019-9 [pii]
AID - 10.1016/j.lfs.2021.119034 [doi]
PST - ppublish
SO  - Life Sci. 2021 Mar 15;269:119034. doi: 10.1016/j.lfs.2021.119034. Epub 2021 Jan 
      13.