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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Cutting Edge: Nucleotide-Binding Oligomerization Domain 1-Dependent Responses Account for Murine Resistance against Trypanosoma cruzi Infection

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Author(s):
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Silva, Grace K. ; Gutierrez, Fredy R. S. [1] ; Guedes, Paulo M. M. [1] ; Horta, Catarina V. ; Cunha, Larissa D. ; Mineo, Tiago W. P. [1] ; Santiago-Silva, Juliana [1] ; Kobayashi, Koichi S. [2, 3] ; Flavell, Richard A. [4, 5] ; Silva, Joao S. [1] ; Zamboni, Dario S. [6]
Total Authors: 11
Affiliation:
[1] Univ Sao Paulo, Dept Biochem & Immunol, Med Sch Ribeirao Preto, BR-14049900 Ribeirao Preto, SP - Brazil
[2] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 - USA
[3] Harvard Univ, Sch Med, Dept Canc Immunol, Boston, MA 02115 - USA
[4] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06510 - USA
[5] Yale Univ, Sch Med, Dept Immunol, New Haven, CT 06510 - USA
[6] Univ Sao Paulo, Dept Cell Biol, Med Sch Ribeirao Preto, FMRP USP, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 6
Document type: Journal article
Source: JOURNAL OF IMMUNOLOGY; v. 184, n. 3, p. 1148-1152, FEB 1 2010.
Web of Science Citations: 68
Abstract

An effective innate immune recognition of the intracellular protozoan parasite Trypanosoma cruzi is critical for host resistance against Chagas disease, a severe and chronic illness that affects millions of people in Latin America. In this study, we evaluated the participation of nucleotide-binding oligomerization domain (Nod)like receptor proteins in host response to T cruzi infection and found that Nod1-dependent, but not Nod2-dependent, responses are required for host resistance against infection. Bone marrow-derived macrophages from Nod1(-/-) mice showed an impaired induction of NF-kappa B-dependent products in response to infection and failed to restrict T cruzi infection in presence of IFN-gamma. Despite normal cytokine production in the sera, Nod1(-/-) mice were highly susceptible to T cruzi infection, in a similar manner to MyD88(-/-) and NO synthase 2(-/-) mice. These studies indicate that Nod1-dependent responses account for host resistance against T cruzi infection by mechanisms independent of cytokine production. The Journal of Immunology, 2010, 184: 1148-1152. (AU)