| First Author | Villamón E | Year | 2004 |
| Journal | Microbes Infect | Volume | 6 |
| Issue | 6 | Pages | 542-8 |
| PubMed ID | 15158187 | Mgi Jnum | J:105414 |
| Mgi Id | MGI:3615053 | Doi | 10.1016/j.micinf.2004.02.015 |
| Citation | Villamon E, et al. (2004) 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 |
| abstractText | 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. |
