Genetic deficiency of CD28 costimulatory molecule results in more severe Paracoccicioidomycosis (PCM) associated with decreased antibodies and cytokines production (2007)
- Authors:
- Autor USP: CALICH, VERA LUCIA GARCIA - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Imprenta:
- Publisher: Sociedade Brasileira de Imunologia
- Publisher place: Rio de Janeiro
- Date published: 2007
- Source:
- Título: Abstracts
- Conference titles: International Congress of Immunology
-
ABNT
FELONATO, M. e CALICH, Vera Lúcia Garcia. Genetic deficiency of CD28 costimulatory molecule results in more severe Paracoccicioidomycosis (PCM) associated with decreased antibodies and cytokines production. 2007, Anais.. Rio de Janeiro: Sociedade Brasileira de Imunologia, 2007. . Acesso em: 22 jan. 2026. -
APA
Felonato, M., & Calich, V. L. G. (2007). Genetic deficiency of CD28 costimulatory molecule results in more severe Paracoccicioidomycosis (PCM) associated with decreased antibodies and cytokines production. In Abstracts. Rio de Janeiro: Sociedade Brasileira de Imunologia. -
NLM
Felonato M, Calich VLG. Genetic deficiency of CD28 costimulatory molecule results in more severe Paracoccicioidomycosis (PCM) associated with decreased antibodies and cytokines production. Abstracts. 2007 ;[citado 2026 jan. 22 ] -
Vancouver
Felonato M, Calich VLG. Genetic deficiency of CD28 costimulatory molecule results in more severe Paracoccicioidomycosis (PCM) associated with decreased antibodies and cytokines production. Abstracts. 2007 ;[citado 2026 jan. 22 ] - Depletion of natural killer cells induces a more severe pulmonary paracoccidioidomycosis in athymic and euthymic BALB/C mice
- Mannose receptors play a different role in the activation of macrophages from resistant and susceptible mice to Paracoccidioides brasiliensis infection
- iNOS knock-out mice are not more susceptible to pulmonary paracoccidioidomycosis
- Role of CD4, CD8 T cells, IFN-gama and IL-12 in the protective immunity against murine pulmonary paracoccidioidomycosis (PCM)
- Paracoccidioides brasiliensis-TLR-4 interaction induces macrophage activation but results in more severe paracoccidioimycosis
- Suceptible and resistant mice to p. brasiliensis infection use an indoleamine 2,3-dioxygenase mechanism to control fungal growth
- Mannose receptors play a distinct role in the interaction of p. Brasiliensis cells with murine macrophages of resistant and susceptible.
- IL-10 deficiency determines a better fungicidal ability associated with overproduction of IFN-? and nitric oxide by Paracoccidioides brasiliensis infected macrophages
- Paracoccidioides brasiliensis infection determines dendritic cells to differentiate to the plasmocytoid subpopulation which induces a more severe pulmonary infection when transferred to resistant mice
- Nitric oxide but not treg cells plays a major immunoregulatory role in a pulmonary model of fungal infection
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