Intrinsic expression of Nod2 in CD4(+) T lymphocytes is not necessary for the development of cell-mediated immunity and host resistance to Toxoplasma gondii

Autor(es):Mostrar menos -

Caetano, Braulia C. ^[1] ; Biswas, Amlan ^[2] ; Lima-Junior, Djalma S. ^[3] ; Benevides, Luciana ^[4] ; Mineo, Tiago W. P. ^[4] ; Horta, Catarina V. ^[3] ; Lee, Kyoung-Hee ^[2] ; Silva, Joao S. ^[4] ; Gazzinelli, Ricardo T. ^[1] ; Zamboni, Dario S. ^[3] ; Kobayashi, Koichi S. ^{[5, 2]}

Afiliação do(s) autor(es)

^[1] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA - USA

^[2] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 - USA

^[3] Dept Cell Biol, Sao Paulo - Brazil

^[4] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Biochem & Immunol, Sao Paulo - Brazil

^[5] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02215 - USA

• Tipo de documento: Artigo Científico
• Fonte: European Journal of Immunology; v. 41, n. 12, p. 3627-3631, DEC 2011.
• Citações Web of Science: 26

Resumo

Nod2 belongs to the nucleotide-binding domain leucine-rich repeat family of proteins and senses bacterial cell wall components to initiate innate immune responses against various pathogens. Recently, it has been reported that T-cell-intrinsic expression of Nod2 promotes host defense against Toxoplasma gondii infection by inducing type 1 immunity. Here, we present results that demonstrate that Nod2 does not play a role in the defense against T. gondii infection. Nod2-deficient mice were fully capable of inducing Th1 immune responses and did not show enhanced susceptibility to infection. Upon TCR stimulation in vitro, Nod2-deficient CD4(+) T cells showed normal activation, IL-2 production, proliferation, and Th1/2 differentiation. Nod2 mRNA and protein were expressed in CD4(+) T and CD8(+) T cells at substantial levels. Therefore, Nod2, although expressed in CD4(+) T cells, does not have an intrinsic function in T-cell activation and differentiation. (AU)

• Processo FAPESP: 10/50959-4 - Determinação de loci e genes de camundongos responsáveis pela resistência natural à infecção por Trypanosoma cruzi
• Beneficiário: Dario Simões Zamboni
• Modalidade de apoio: Auxílio à Pesquisa - Regular