6533b7d1fe1ef96bd125cd8e

RESEARCH PRODUCT

Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis

Didier FradeliziM. Luisa GilJosé-enrique O'connorDaniel GozalboM.luisa FerrándizPatricia RoigEva Villamón

subject

Chemokinemedicine.medical_treatmentImmunologyReceptors Cell SurfaceMicrobiologyMicrobiologyInterferon-gammaMiceCandida albicansmedicineAnimalsCandida albicansAntibodies FungalMice KnockoutToll-like receptorMembrane GlycoproteinsInnate immune systembiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisbiology.organism_classificationDisseminated CandidiasisInterleukin-12Immunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLTLR2Infectious DiseasesCytokineImmunoglobulin GImmunologybiology.proteinCytokines

description

Previous work by our group showed that Toll-like receptor 2 (TLR2) is essential for activation of innate immunity, playing a major role in the response of macrophages to Candida albicans, triggering cytokine and chemokine expression, and therefore TLR2 -/- mice are more susceptible to systemic primary candidiasis. In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the development of the acquired humoral response; and (iii) the production of Th1 cytokines IFN-gamma, IL-12 and TNF-alpha. Our results indicate that, although TLR2 -/- mice have a very impaired production of Th1 cytokines compared with control mice, they are equally capable of mounting a specific humoral response to the fungus and developing a vaccine-induced resistance.

yearjournalcountryeditionlanguage
2004-05-01Microbes and Infection
https://doi.org/10.1016/j.micinf.2004.02.015