Rheumatoid arthritis, systemic lupus erythematosus and primary Sjögren’s syndrome shared megakaryocyte expansion in peripheral blood
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  • Published on:
    Correspondence on “Rheumatoid arthritis, systemic lupus erythematosus and primary Sjogren's syndrome shared megakaryocyte expansion in peripheral blood” by Wang, Y. et al
    • Hui Wu, PhD The Eighth Affiliated Hospital of Sun Yat-sen University
    • Other Contributors:
      • Hongxing Wang, PhD
      • Yi Zhang, Professor

    With great interest, we read the article by Wang Y et al., which suggested that Megakaryocytes (MKs) expansion might contribute to the pathogenesis of Rheumatoid Arthritis (RA)1. MKs are large, polyploid cells that originate from hematopoietic stem cells (HSC) and give rise to platelets. However, the authors fall short in recognizing the role of MK-derived platelets in RA.
    Wang Y et al. identified increased MKs in peripheral blood of RA using single-cell RNA sequencing and flow cytometry approaches. They provide clues that MKs act as specific endogenous antigen-presenting cells (APCs), triggering the initial autoimmune T cell for RA pathogenesis1. Of note, novel evidence suggests that MKs derived from bone marrow (BM), lung2 and liver3, instead serve as immunomodulatory or secretory cells4. The generation of platelets is the primary function of MKs.
    Indeed, many characteristics and roles of platelets inherit from MKs. For example, once activated, platelets present antigens via MHC class I molecules (MHC-I) derived from parent MKs5; in this way, the immunogenic information can be conveyed to platelets. Similarly, platelets can also act as an essential immune effector in RA6. An array of platelet surface receptors is responsible for activation, adhesion, and thrombus formation via initiating a complex network of signaling pathways in the presence of ligands. In addition, it is well known that ligands for platelet receptors such as collagen, fibrinogen, serotonin,...

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    Conflict of Interest:
    None declared.