Details

Autor(en) / Beteiligte

• Olumuyiwa-Akeredolu, Oore-ofe
• Page, Martin J.
• Soma, Prashilla
• Pretorius, Etheresia

Titel

Platelets: emerging facilitators of cellular crosstalk in rheumatoid arthritis

Ist Teil von

• Nature reviews. Rheumatology, 2019-04, Vol.15 (4), p.237-248

Ort / Verlag

London: Nature Publishing Group UK

Erscheinungsjahr

2019

Quelle

MEDLINE

Beschreibungen/Notizen

• Rheumatoid arthritis (RA) is an autoimmune disease in which a variety of circulating pro-inflammatory cells and dysregulated molecules are involved in disease aetiology and progression. Platelets are an important cellular element in the circulation that can bind several dysregulated molecules (such as collagen, thrombin and fibrinogen) that are present both in the synovium and the circulation of patients with RA. Platelets not only respond to dysregulated molecules in their environment but also transport and express their own inflammatory mediators, and serve as regulators at the boundary between haemostasis and immunity. Activated platelets also produce microparticles, which further convey signalling molecules and receptors to the synovium and circulation, thereby positioning these platelet-derived particles as strategic regulators of inflammation. These diverse functions come together to make platelets facilitators of cellular crosstalk in RA. Thus, the receptor functions, ligand binding potential and dysregulated signalling pathways in platelets are becoming increasingly important for treatment in RA. This Review aims to highlight the role of platelets in RA and the need to closely examine platelets as health indicators when designing effective pharmaceutical targets in this disease. Platelets mediate inflammatory responses by facilitating immune cell crosstalk and participating in inflammatory signalling cascades. In this Review, the authors discuss the emerging role of platelet signalling pathways in the pathogenesis of rheumatoid arthritis. Key points Platelets have important immune effector functions in rheumatoid arthritis (RA). Platelet signalling pathways are dysregulated in the presence of pro-inflammatory molecules such as collagen, thrombin, fibrinogen and cytokines. Increased (pro-inflammatory) platelet signalling causes platelets to develop antigen-presenting functions and results in dysregulated intercellular aggregation and pathological clot formation. Activated platelets and their thrombo-inflammatory function in RA represent an important risk factor for thrombosis and cardiovascular comorbidities. Activated platelets produce pro-inflammatory microparticles that are present both in the circulation and in the synovium; these microparticles function in systemic inflammatory processes in RA. In an individualized medicine approach, platelet structure and biochemical markers of inflammation would be used during diagnosis and platelet activity monitored during treatment to track immune responses in RA.