Monocytes in rheumatoid arthritis: Circulating precursors of macrophages and osteoclasts and, their heterogeneity and plasticity role in RA pathogenesis.

  title={Monocytes in rheumatoid arthritis: Circulating precursors of macrophages and osteoclasts and, their heterogeneity and plasticity role in RA pathogenesis.},
  author={Amit Kumar Rana and Yang Li and Qiujie Dang and Fan Yang},
  journal={International immunopharmacology},
  • A. Rana, Yang Li, Fan Yang
  • Published 23 October 2018
  • Biology, Medicine
  • International immunopharmacology

Rheumatoid arthritis: Development after the emergence of a chemokine for neutrophils in the synovium

  • H. Katayama
  • Biology, Medicine
    BioEssays : news and reviews in molecular, cellular and developmental biology
  • 2021
Rheumatoid arthritis (RA) may not be a multifactorial disease; it can be hypothesized that RA is developed through a series of events following a triggering event, which is the emergence of a

CD14+CD16− monocytes are the main precursors of osteoclasts in rheumatoid arthritis via expressing Tyro3TK

Compared with HC and OA patients, the expression of Tyro3TK on CD14+CD16− monocytes in RA patients was significantly upregulated and positively correlated with the disease manifestations, such as IgM level, tender joint count, and the disease activity score.

The Role of M1/M2 Macrophage Polarization in Rheumatoid Arthritis Synovitis

The importance of the delicate M1/M2 imbalance in the different phases of the inflammatory process together with the identification of specific pathways, cytokines, and chemokines involved, and its clinical outcomes in RA is discussed.

The monocyte-to-osteoclast transition in rheumatoid arthritis: Recent findings

The factors affecting osteoclastogenesis in RA are reviewed, the anti-osteoclastogenic effects of current RA treatments are summarized, and promising therapeutic targets relating to both inflammation and osteOClastogenesis are identified.

Critical Role of Synovial Tissue–Resident Macrophage and Fibroblast Subsets in the Persistence of Joint Inflammation

It is proposed that failure of critical interactions between tissue resident cell types regulate the disease state by establishing critical cellular checkpoints within the synovium designed to suppress inflammation and restore joint homeostasis leads to the emergence of imprinted pathogenic fibroblast cell states that drive the persistence of joint inflammation.

Tumor necrosis factor alpha neutralization attenuates immune checkpoint inhibitor-induced activation of intermediate monocytes in synovial fluid mononuclear cells from patients with inflammatory arthritis

The effect of pembrolizumab on cells involved in inflammation and destruction in the synovial joint and how immunosuppressive treatments affect the pembolsumab-induced immune reactions is investigated.



Monocytes/macrophages express chemokine receptor CCR9 in rheumatoid arthritis and CCL25 stimulates their differentiation

CCR9 expression by monocytes is increased in RA and CCL25 may be involved in the differentiation of monocytes to macrophages particularly in RA.

Blood monocyte activation in rheumatoid arthritis: increased monocyte adhesiveness, integrin expression, and cytokine release

In this study, blood monocytes from RA patients exhibited features of activation related to cell adhesion, and production of extracellular IL‐1β and IL‐6 by RA monocytes was significantly enhanced compared with monocyte from normal subjects.

Recruitment of CD16+ monocytes into synovial tissues is mediated by fractalkine and CX3CR1 in rheumatoid arthritis patients.

The results suggest that FKN might preferentially mediate migration and recruitment of CD16+ monocytes, and might contribute to synovial tissue inflammation.

Functional Phenotype of Synovial Monocytes Modulating Inflammatory T-Cell Responses in Rheumatoid Arthritis (RA)

The findings suggest that the cytokine milieu of the synovial fluid shapes the unique features ofsynovial monocytes as well as their cardinal role in shaping inflammatory T-cell responses in RA.

Dendritic cells and the pathogenesis of rheumatoid arthritis

It is argued that the presentation of self‐antigen by DC and by autoantibody‐producing B cells is critical for the perpetuation of the autoimmune response.

Identification of a human peripheral blood monocyte subset that differentiates into osteoclasts

The results suggest that peripheral blood monocytes consist of two functionally heterogeneous subsets with distinct responses to RANKL, and seem to originate from CD16- monocytes, and integrin β3 is necessary for osteoclastogenesis.

Osteoclasts in arthritis and Th17 cell development.

Elevated CXCL16 expression by synovial macrophages recruits memory T cells into rheumatoid joints.

These data provide evidence that enhanced production of CXCL16 in RA synovia leads to recruitment of CxCR6+ memory T cells, thereby contributing to the inflammatory cascade associated with RA pathology.

CD56+ monocytes have a dysregulated cytokine response to lipopolysaccharide and accumulate in rheumatoid arthritis and immunosenescence

The CD14bright/CD56+ monocyte subset is expanded in aging individuals as well as in patients with RA, and the elimination of those cells in Patients with a good response towards TNF inhibiting agents indicates a possible contribution of those monocytes in the inflammatory response in RA.

SIRT1 inhibits differentiation of monocytes to macrophages: amelioration of synovial inflammation in rheumatoid arthritis

SIRT1 appears to inhibit monocyte to macrophage differentiation by suppressing PU.1 phosphorylation and inflammatory signaling, which suggests SIRT1 plays a critical role in the regulation of synovial inflammation in RA.