Genetic deficiency of CD28 leads to a more severe pulmonary paracoccidioidomycosis (PCM) at the chronic phase of infection (2006)
- Authors:
- Autor USP: CALICH, VERA LUCIA GARCIA - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Abstract: Introduction : It has been accepted that two signals are necessary for an adequate activation of the immune system. The first signal is the cognitive interaction between the TCR receptor on T lymphocytes and peptide presented by MHC molecules of APC cells. The balance between accessory molecules on T cells and APC has been considered the second signal. The interaction CD28 molecules of T lymphocytes with APC B7 molecules results in T cell activation, proliferation and subsequent differentiation into effector or memory cells. As the main protective mechanism to PCM is mediated by T cell immunity, the purpose of this work was to investigate the role of the costimulatory signal mediated CD28 molecules in the innate and adaptative phases of immunity induced by P.brasiliensis (Pb) infection. Methods: Wild type (WT) and CD28KO C57BL/6 (KO) mice were i.t. infected with 1x106 yeast cells of Pb 18. Mice were sacrificed 72h, 2 and 10 weeks after infection and the severity of the disease determined by organ CFU counts (means ± standard errors) and analyzed by Student's t test. Antibodies were measured by ELISA.Results: At 72h post infection both mice strains showed similar fungal burdens in the lungs parenchyma (KO 4,01± 0,34 log10 and WT 4,11± 0,23 log10). At the same time point, no differences were observed in fungal loads recovered from bronchoalveolar lavage fluids of KO (3,60 ± 0,31 log10 and WT 3,65 ± 0,09 log10) mice. Again, atweek 2 after infection no differences were detected between fungal loads of KO (5,32 ± 0,10 log10 and WT 4,96 ± 0,14 log10) mice. However, by week 10 KO mice (5,67 ± 0,19 log10) presented increased pulmonary fungal burdens in comparison with WT mice (4,58 ± 0,30 log10). At this period of infection an impressive difference in antibody production was detected. WT mice produced significantly increased levels of total IgG, IgG1, IgG2a and IgG2b specific isotypes (p<0,001). Conclusions: Our results suggest that the CD28 molecule is not important at acute phase of murine PCM, while at the chronic phase this molecule seems to be essential to the control of humoral immunity and severity of PCM.
- Imprenta:
- Source:
- Título do periódico: Abstracts
- Conference titles: Meeting of the Brazilian Society for Immunology
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ABNT
FELONATO, M e CALICH, Vera Lúcia Garcia. Genetic deficiency of CD28 leads to a more severe pulmonary paracoccidioidomycosis (PCM) at the chronic phase of infection. 2006, Anais.. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo, 2006. . Acesso em: 23 abr. 2024. -
APA
Felonato, M., & Calich, V. L. G. (2006). Genetic deficiency of CD28 leads to a more severe pulmonary paracoccidioidomycosis (PCM) at the chronic phase of infection. In Abstracts. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo. -
NLM
Felonato M, Calich VLG. Genetic deficiency of CD28 leads to a more severe pulmonary paracoccidioidomycosis (PCM) at the chronic phase of infection. Abstracts. 2006 ;[citado 2024 abr. 23 ] -
Vancouver
Felonato M, Calich VLG. Genetic deficiency of CD28 leads to a more severe pulmonary paracoccidioidomycosis (PCM) at the chronic phase of infection. Abstracts. 2006 ;[citado 2024 abr. 23 ] - Role of IL-12 in the innate immunity of athymic and euthymic balb/c mice with paracoccidioidomycosis: effect of local and systemic il-12 neutralization
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- Exarcebation of murine paracoccidioidomycosis induces type 2 cytokines, whereas the protective model of the disease is associated to both, type 1 and type 2 T cell responses
- Effect of in vivo depletion of T CD4 cells in the pulmonary infection of susceptible (B10.A) and resistance (A/J) mice to P. brasiliensis infection
- Leucócitos polimorfonucleares (PMN) não exercem papel protetor na fase adquirida da imunidade contra a infecção com Paracoccidioides brasiliensis
- Role of CD4, CD8 T cells, IFN-gama and IL-12 in the protective immunity against murine pulmonary paracoccidioidomycosis (PCM)
- The immune response of high (H) and low responders (L) mice (selection III) and F1 (HIII x LIII) hybrids to paracoccidioides brasiliensis infection
- Pulmonary paracoccidioidomycosis (PCM) in IL-10 knock-out (KO) mice
- CD28 costimulatory molecule deficiency results in more severe Paracoccidioides brasiliensis infection but protects mice from life-threatening immunopathology
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