Interleukin-1 links autoimmune and autoinflammatory pathophysiology in mixed-pattern psoriasis

RODOLFO KÖLLIKER FRERS; TAMARA KOBIEC; MATILDE OTERO-LOSADA; MARÍA INÉS HERRERA , LUCAS DANIEL UDOVIN (*), TAMARA KOBIEK , CAMILLA GUIMARÃES COSTA TABOSA, BIANCA ROSSETI PICININ ARRUDA VIEIRA, JUAN PABLO LUACES , FRANCISCO CAPANI; LUCAS UDOVIN; CARLOS F. KUSNIER; FRANCISCO CAPANI

MEDIATORS OF INFLAMMATION

HINDAWI PUBLISHING CORPORATION

Año: 2021

0962-9351

Autoinflammatory and autoimmune diseases are characterized by an oversensitive immune systemwith loss of the physiological endogenous regulation, involving multifactorial self-reactivepathological mechanisms of mono or polygenic nature.Failure in regulatory mechanisms triggers a complex network of dynamic relationships betweeninnate and adaptive immunity, leading to coexistent autoinflammatory and autoimmune processes.Sustained exposure to a trigger or a genetic alteration at the level of the receptors of the naturalimmune system may lead to abnormal activation of the innate immune system, adaptive systemactivation, loss of self-tolerance, and systemic inflammation.The IL-1 family members critically activate and regulate innate and adaptive immune responses´diversity and plasticity in autoimmune and/or autoinflammatory conditions.The IL-23 / IL-17 axis is key in the communication between innate immunity (IL-23-producing myeloidcells) and adaptive immunity (Th17- and IL-17-expressing CD8 + T cells). In psoriasis, thesecytokines are decisive to the different clinical presentations, whether as plaque psoriasis (psoriasisVulgaris), generalized pustular psoriasis (pustular psoriasis), or mixed forms. These forms reflect agradient between autoimmune pathophysiology with predominant adaptive immune response andautoinflammatory pathophysiology with predominant innate immune response.