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Front Immunol. 2015 Nov 19;6:571. doi: 10.3389/fimmu.2015.00571. eCollection 2015.

The Interplay Between Monocytes/Macrophages and CD4(+) T Cell Subsets in Rheumatoid Arthritis.

Frontiers in immunology

Ceri A Roberts, Abigail K Dickinson, Leonie S Taams

Affiliations

  1. Centre for Molecular and Cellular Biology of Inflammation (CMCBI), Division of Immunology, Infection and Inflammatory Disease, King's College London , London , UK.

PMID: 26635790 PMCID: PMC4652039 DOI: 10.3389/fimmu.2015.00571

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by inflammation of the synovial lining (synovitis). The inflammation in the RA joint is associated with and driven by immune cell infiltration, synovial hyperproliferation, and excessive production of proinflammatory mediators, such as tumor necrosis factor α (TNFα), interferon γ (IFNγ), interleukin (IL)-1β, IL-6, and IL-17, eventually resulting in damage to the cartilage and underlying bone. The RA joint harbors a wide range of immune cell types, including monocytes, macrophages, and CD4(+) T cells (both proinflammatory and regulatory). The interplay between CD14(+) myeloid cells and CD4(+) T cells can significantly influence CD4(+) T cell function, and conversely, effector vs. regulatory CD4(+) T cell subsets can exert profound effects on monocyte/macrophage function. In this review, we will discuss how the interplay between CD4(+) T cells and monocytes/macrophages may contribute to the immunopathology of RA.

Keywords: T helper cell; Treg; cell polarization; immune regulation; inflammation; myeloid cell; rheumatoid arthritis

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