Measurement of colony-stimulating factors in synovial fluid: potential clinical value

Bell, A. L.; Magill, M.K.; McKane, W R; Kirk, F.; Irvine, A.

doi:10.1007/bf00262295

Cited by 48 publications

(27 citation statements)

References 18 publications

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“…In this study, we demonstrated that the GM-CSF is essential for CD1b+ iDC differentiation from FcγR-activated monocytes by showing that FcγR activated monocytes up-regulated GM-CSF and addition of anti-GM-CSF monoclonal Ab suppressed CD1b + DC differentiation. GM-CSF is thought to participate in autoimmune disease, with mRNA and protein detected in inflamed tissues of autoimmune disease patients (20). However, the relative potencies of FcγR activation vs. GM-CSF in inducing CD1b expression were different.…”

Section: Discussionmentioning

confidence: 99%

Activation of FcγRI on Monocytes Triggers Differentiation into Immature Dendritic Cells That Induce Autoreactive T Cell Responses

Tanaka

Krutzik²,

Sieling³

et al. 2009

The Journal of Immunology

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The formation of immune complexes results in activation of the innate immune system and subsequent induction of host inflammatory responses. In particular, the binding of IgG immune complexes to FcγR on monocytes triggers potent inflammatory responses leading to tissue injury in disease. We investigated whether activation of monocytes via FcγR induced cell differentiation, imparting specific inflammatory functions of the innate immune response. Human IgG alone induced monocytes to differentiate into cells with an immature dendritic cell (iDC) phenotype, including up-regulation of CD1b, CD80, CD86, and CD206. Differentiation into CD1b+ iDC was dependent on activation via CD64 (FcγRI) and induction of GM-CSF. The human IgG-differentiated iDC were phenotypically different from GM-CSF-derived iDC at the same level of CD1b expression, with higher cell surface CD86, but lower MHC class II, CD32, CD206, and CD14. Finally, in comparison to GM-CSF-derived iDC, IgG-differentiated iDC were more efficient in activating T cells in both autologous and allogeneic mixed lymphocyte reactions but less efficient at presenting microbial Ag to T cells. Therefore, activation of FcγRI on monocytes triggers differentiation into specialized iDC with the capacity to expand autoreactive T cells that may contribute to the pathogenesis of immune complex-mediated tissue injury.

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Section: Discussionmentioning

confidence: 99%

Activation of FcγRI on Monocytes Triggers Differentiation into Immature Dendritic Cells That Induce Autoreactive T Cell Responses

Tanaka

Krutzik²,

Sieling³

et al. 2009

The Journal of Immunology

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“…In patients with RA, GM-CSF is expressed in the synovial membrane and the level of GM-CSF is increased in the synovial fluid [39]. Increased expression of GM-CSF receptors is found on circulating monocytes [40], which promotes the subsequent maturation and activation of macrophages in the synovium.…”

Section: Extracellular Target In Ramentioning

confidence: 99%

Future therapeutic targets in rheumatoid arthritis?

Cheung

McInnes

2017

Semin Immunopathol

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Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by persistent joint inflammation. Without adequate treatment, patients with RA will develop joint deformity and progressive functional impairment. With the implementation of treat-to-target strategies and availability of biologic therapies, the outcomes for patients with RA have significantly improved. However, the unmet need in the treatment of RA remains high as some patients do not respond sufficiently to the currently available agents, remission is not always achieved and refractory disease is not uncommon. With better understanding of the pathophysiology of RA, new therapeutic approaches are emerging. Apart from more selective Janus kinase inhibition, there is a great interest in the granulocyte macrophage-colony stimulating factor pathway, Bruton’s tyrosine kinase pathway, phosphoinositide-3-kinase pathway, neural stimulation and dendritic cell-based therapeutics. In this review, we will discuss the therapeutic potential of these novel approaches.

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“…85 Serum levels of GM-CSF are raised prior to the clinical onset of disease 86 and it is found at high levels in RA synovial fluid (up to 250 pg/mL). 87 Anti-GM-CSF antibodies have been shown to ameliorate CIA 88 and have separate and additive effect over IL-17 inhibition alone in suppressing Streptococcal cell wallinduced arthritis. 89 This has led to the development of biological agents to neutralize both soluble GM-CSF and block its receptor (GM-CSFR).…”

Section: Anti-gm-csf Therapiesmentioning

confidence: 99%