Neutrophils are now recognized as major components of the response to Toxoplasma gondii by their contribution to parasite elimination by a number of mechanisms. This article focuses on recent advances in the understanding of the mechanisms of migration, cytokine release, and formation of extracellular traps by neutrophils during toxoplasmosis.
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Caspase-1 in Cx3cr1-expressing cells drives an IL-18-dependent T cell response that promotes parasite control during acute Toxoplasma gondii infection.
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Inflammasome activation is a robust innate immune mechanism that promotes inflammatory responses through the release of alarmins and leaderless cytokines, including IL-1α, IL-1β, and IL-18. Various stimuli, including infectious agents and cellular stress, cause inflammasomes to assemble and activate caspase-1. Then, caspase-1 cleaves targets that lead to pore formation and leaderless cytokine activation and release.
View Article and Find Full Text PDFThe emerging role of in periodontal diseases and underlying mechanisms.
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Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address:
Toxoplasma gondii (T. gondii), an obligate intracellular parasite, is considered as an opportunistic infection and causes toxoplasmosis in humans and animals. Congenital toxoplasmosis can influence pregnancy and cause mild to severe consequences for the fetal and neonatal.
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Background: Infection with the protozoan parasite Toxoplasma gondii leads to the formation of lifelong cysts in neurons that can have devastating consequences in the immunocompromised. In the immunocompetent individual, anti-parasitic effector mechanisms and a balanced immune response characterized by pro- and anti-inflammatory cytokine production establishes an asymptomatic infection that rarely leads to neurological symptoms. Several mechanisms are known to play a role in this successful immune response in the brain including T cell production of IFNγ and IL-10 and the involvement of CNS resident cells.
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Laboratory of Biology and Toxicology - BIOTOX, Regional University of Cariri - URCA, Crato, 63105-000, Ceará, Brazil.
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