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Single cell mapping identifies a distinct platelet-phenotype in psoriatic type III inflammation
Katharina S Kommoss1,2, Sinduya Krishnarajah3,4, Tabea Bieler1,5
1Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.
The understanding of platelet biology is expanding beyond their well-established role in thrombosis and hemostasis to encompass their functions in inflammation. To gain insights into the phenotype and possible platelet-subgroups in the context of type III inflammation, high-parametric single cell spectral flow cytometry was applied to a prospectively followed cohort of psoriasis patients undergoing systemic therapy. By focusing on the activation profile of platelets and their interaction with immune cells, we identify cell-surface proteins CD32+CD154+ and TLR2+TLR4+, distinguishing unique platelet subsets in psoriasis patients. These subsets demonstrate regression over the course of systemic therapy. Notably, these platelet phenotypes and frequencies differ from those of healthy controls, and patients with atopic dermatitis (AD), a type II inflammation-driven disease. Our data highlight a specific platelet phenotype responding acutely to the respective inflammatory context. This finding warrants further investigation into platelets as a diagnostic tool in inflammatory conditions, necessitating future insight into the function of these subsets across disease etiologies.
The understanding of platelet biology is expanding beyond their well-established role in thrombosis and hemostasis to encompass their functions in inflammation. To gain insights into the phenotype and possible platelet-subgroups in the context of type III inflammation, high-parametric single cell spectral flow cytometry was applied to a prospectively followed cohort of psoriasis patients undergoing systemic therapy. By focusing on the activation profile of platelets and their interaction with immune cells, we identify cell-surface proteins CD32+CD154+ and TLR2+TLR4+, distinguishing unique platelet subsets in psoriasis patients. These subsets demonstrate regression over the course of systemic therapy. Notably, these platelet phenotypes and frequencies differ from those of healthy controls, and patients with atopic dermatitis (AD), a type II inflammation-driven disease. Our data highlight a specific platelet phenotype responding acutely to the respective inflammatory context. This finding warrants further investigation into platelets as a diagnostic tool in inflammatory conditions, necessitating future insight into the function of these subsets across disease etiologies.
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