MDSCs use a complex molecular network to suppress T-cell immunity in a pulmonary model of fungal infection (2024)
- Authors:
- Autor USP: CALICH, VERA LUCIA GARCIA - ICB
- Unidade: ICB
- DOI: 10.3389/fcimb.2024.1392744
- Subjects: IMUNOLOGIA; PARACOCCIDIOIDES; PARACOCCIDIOIDOMICOSE; DERMATOPATIA PARASITÁRIA ANIMAL; MODELOS ANIMAIS DE DOENÇAS; CAMUNDONGOS; ANTÍGENOS DE FUNGOS; FÁRMACOS IMUNOSSUPRESSORES; INTERLEUCINA 10; TRANSDUÇÃO DE SINAL CELULAR; LINFÓCITOS T; PULMÃO; LECTINAS; IMUNOLOGIA CELULAR
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Frontiers in Cellular and Infection Microbiology
- ISSN: 2235-2988
- Volume/Número/Paginação/Ano: v. 14, art. 1392744, 20 p., 2024
- Este periódico é de acesso aberto
- Este artigo NÃO é de acesso aberto
-
ABNT
KAMINSKI, Valéria de Lima et al. MDSCs use a complex molecular network to suppress T-cell immunity in a pulmonary model of fungal infection. Frontiers in Cellular and Infection Microbiology, v. 14, p. 20 , 2024Tradução . . Disponível em: https://doi.org/10.3389/fcimb.2024.1392744. Acesso em: 24 fev. 2026. -
APA
Kaminski, V. de L., Borges, B. M., Santos, B. V. dos, Preite, N. W., Loures, F. V., & Calich, V. L. G. (2024). MDSCs use a complex molecular network to suppress T-cell immunity in a pulmonary model of fungal infection. Frontiers in Cellular and Infection Microbiology, 14, 20 . doi:10.3389/fcimb.2024.1392744 -
NLM
Kaminski V de L, Borges BM, Santos BV dos, Preite NW, Loures FV, Calich VLG. MDSCs use a complex molecular network to suppress T-cell immunity in a pulmonary model of fungal infection [Internet]. Frontiers in Cellular and Infection Microbiology. 2024 ; 14 20 .[citado 2026 fev. 24 ] Available from: https://doi.org/10.3389/fcimb.2024.1392744 -
Vancouver
Kaminski V de L, Borges BM, Santos BV dos, Preite NW, Loures FV, Calich VLG. MDSCs use a complex molecular network to suppress T-cell immunity in a pulmonary model of fungal infection [Internet]. Frontiers in Cellular and Infection Microbiology. 2024 ; 14 20 .[citado 2026 fev. 24 ] Available from: https://doi.org/10.3389/fcimb.2024.1392744 - cd28 costimulatory molecule deficiency in more severe paracoccidioides brasiliensis infection but protects mice from life-threatening immunopathology
- Paracoccidioides brasiliensis infection determines dentric cells to diferentiate to the plasmacytoid subpopulation which induces a more severe pulmonary infection when transfered to resistant mice
- The IDO-AhR axis controls Th17/Treg immunity in a pulmonary model of fungal infection
- TLR-2 is a negative regulator of TH17 cells and tissue pathology in a pulmonary model of fungal infection
- Absence of TLR2 results in less severe paracoccidioidomycosis but increased inflammatory response caused by PMN & TH17 cells
- Toll like receptors and the adaptor molecule MYD88 play an important role in pulmonary paracoccidioidomycosis
- TLR2 is a negative regulator of Th17 cells and tissue pathology in a pulmonary model of fungal infection
- Human alfa / beta and gama / delta t cells respond to proteins of the yeast form of paracoccidioides brasiliensis
- The immune response of high (H) and low responders (L) mice (selection III) and F1 (HIII x LIII) hybrids to paracoccidioides brasiliensis infection
- PMN leukocytes play a more prominent role in natural immunity of susceptible than resistant mice to pulmonary paracoccidiodomycosis
Informações sobre o DOI: 10.3389/fcimb.2024.1392744 (Fonte: oaDOI API)
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