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Psoriasis is an inflammatory disease that is initiated by pathogenic T cells within skin lesions that correlates with hyperproliferation of keratinocytes and the release of cytokines and damage-associated molecular pattern molecules into the circulation (Wang and Jin, 2020). Exposure to damage-associated molecular patterns and low levels of cytokines and chemokines shift neutrophils from a quiescent to a primed state characterized by increased sensitivity to subsequent stimulation that induces amplified adhesive and effector function at sites of tissue inflammation (Miralda et al, 2017).
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Garcia et al. (2023) studied this question.
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