Psoriasis, an incurable immune-mediated inflammatory skin illness, greatly affects patients’ physical and emotional health. Genetics, epigenetics, environmental variables, and unbalanced immune cells such as T cells, dendritic cells (DCs), and keratinocytes cause psoriasis. The immune system plays a major role in psoriasis, yet it lacks well-defined antigens, autoimmune genetic risk factors, and particular antibodies. Psoriasis is an autoinflammatory illness due to molecular and cellular features like neutrophils in skin lesions and innate immune system stimulation. High-molecular-weight protein complexes known as autoinflammatory inflammasomes frequently occur in autoinflammatory diseases, genetic disorders characterized by recurring fever, higher acute-phase reactants, and organ inflammation. Immune cells organize these inflammasomes in their cytoplasm. They start inflammatory processes like making mature IL-1β, IL-18, caspase-1, and pyroptosis. Recent research has focused on immune response triggers rather than autoimmune psoriasis. Researchers have specifically linked NLRP1, NLRP3, and AIM2 inflammasomes to psoriasis. Identifying activators, inhibitors, genetic susceptibility regions, and inflammasome-related genes in psoriasis provides useful insights. This systematic review gathers recent and thorough research on inflammasomes and psoriasis to better understand this complex skin disorder’s pathogenesis.
Sharma et al. (Mon,) studied this question.