| Grant number: | 07/00035-8 |
| Support Opportunities: | Regular Research Grants |
| Start date: | August 01, 2007 |
| End date: | July 31, 2009 |
| Field of knowledge: | Agronomical Sciences - Veterinary Medicine - Animal Pathology |
| Principal Investigator: | Beatriz Rossetti Ferreira |
| Grantee: | Beatriz Rossetti Ferreira |
| Host Institution: | Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
| City of the host institution: | Ribeirão Preto |
Abstract
Ticks are blood-sucking arthropods parasites of vertebrate hosts that transmit a variety of infectious agents to men and domestic animals. During their feeding ticks inoculate saliva in the attachment site that contains diverse compounds with anti-haemostatic, anti-inflammatory and immuno-modulatory properties which facilitate their feeding and propagation. Recent research indicates that one of the feasible mechanisms through which saliva exerts its immunomodulation is by the inhibition of the host’s dendritic cell (DCs) activity. DCs are professional antigen presenting cells that detect and activate the immune response against diverse pathogens and/or its products. Several tick antigens can be recognized for the DCs through receptors "toll-like" (TLRs). Once activated these receptors induce the maturation of DCs, phenomenon characterized by the increase of co-stimulatory molecule expression and production of pro-inflammatory cytokines, such as IL-12. In our previous studies, Rhipicephalus sanguineus tick saliva reduced the expression of co-stimulatory molecules (CD40, CD80 and CD86) and inhibited the production of IL-12 by lipopolysaccharide (LPS)-stimulated DCs. Knowing that the maturation of LPS-induced DCs is resultant of TLR4 stimulation with subsequent induction of an intracellular signaling cascade that culminates in co-stimulatory molecule expression and production of IL-12 the objective of this study is to investigate the effect of R. sanguineus tick saliva on the activation of the signaling cascade and on the expression of TLR4 in DCs of mice. (AU)
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