Answers are grounded in this paper and cite their sources.
Background: Psoriasis is a systemic, immune-mediated, inflammatory skin disease in which T cells have been found to play a significant role. The phenotypic and functional properties of circulating CD8 T cells in the pathogenesis of the disease are still ill-defined. Objective: This study aimed to assess changes in the phenotype, activation status and mediator release of CD8 T cells in the peripheral blood of patients with mild-to-moderate psoriasis. Methods: TCR-independent (phorbol 12-myristate 13-acetate (PMA) plus ionomycin (ION)) or TCR-dependent (anti-CD3/CD28) activation by flow cytometry. Results: Patients with psoriasis exhibited reduced circulating CD8 memory T cell frequency compared to healthy controls. Additionally, although CD8 T cell subsets showed similar levels of the skin homing marker CCR4, they demonstrated a significant upregulation of B- and T-lymphocyte attenuator (BTLA) expression compared to healthy individuals. Upon CD8 T cell activation, IL-17A and IL-17F were expressed at low and comparable levels in psoriasis patients and healthy controls. In contrast, CD69, IFNγ, and Granzyme B were significantly decreased in anti-CD3/CD28-activated CD8 T cell subsets. PASI scores positively correlated with IFNγ-producing CD8 T memory cells and negatively with TNF-producing CD8- T cell subsets. Conclusion: Patients with mild-to-moderate psoriasis showed a significant decrease in CD8 T memory cells and reduced release of cytotoxic mediators by CD8 T cells. Thus, this indicates that psoriasis impacts the functionality of circulating CD8 T cells.
No takes yet. Share an insight, caveat, or question.
Chen et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: