Toll-like receptor 9 signaling is associated with immune responses to Trypanosoma brucei infection.
Int Immunopharmacol
; 134: 112250, 2024 Jun 15.
Article
en En
| MEDLINE
| ID: mdl-38749335
ABSTRACT
Trypanosoma brucei, a causative agent of human and animal trypanosomiasis, regularly switches its major surface antigen to avoid elimination by the immune system. Toll-like receptor 9 (TLR9) is a key modulator for resistance to host-infective trypanosomes; however, the underlying molecular mechanism remains indistinct. Thus, we first approached the issue using Tlr9-mutant mice that render them non-responsive to TLR9 agonists. After infection, T cells in the spleens of Tlr9-mutant mice were analyzed by flow cytometry and a reduction in CD8+, CD4+ T, and NKT cells was observed in Tlr9-mutant mice compared to WT mice. We further found that the responses of inflammatory cytokines in the sera were reduced in Tlr9-mutant mice after T. brucei infection. The underlying molecular mechanism was that T. b. brucei DNA activated TLR9, which consequently upregulated the expression of p38 and ERK/MAPK, resulting in host resistance to trypanosome infection. In conclusion, these findings provide novel insights into the TLR9-mediated host responses to trypanosome infection.
Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Trypanosoma brucei brucei
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Tripanosomiasis Africana
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Transducción de Señal
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Citocinas
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Receptor Toll-Like 9
Límite:
Animals
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Humans
Idioma:
En
Revista:
Int Immunopharmacol
Asunto de la revista:
ALERGIA E IMUNOLOGIA
/
FARMACOLOGIA
Año:
2024
Tipo del documento:
Article