Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis.
Microbes Infect
; 6(6): 542-8, 2004 May.
Article
em En
| MEDLINE
| ID: mdl-15158187
ABSTRACT
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.
Buscar no Google
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Candida albicans
/
Candidíase
/
Glicoproteínas de Membrana
/
Citocinas
/
Receptores de Superfície Celular
/
Anticorpos Antifúngicos
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article