Explorar Audiolivros. Os mais vendidos Escolhas dos editores Todos os audiolivros. Explorar Revistas. Escolhas dos editores Todas as revistas. Explorar Podcasts Todos os podcasts. Explorar Documentos. Enviado por Jorge Afiune. Denunciar este documento. Pesquisar no documento. LTs etc. Luis Lopes. Teresa Campos. Johnys Berton. Regina Gdedge. Mafalda Ramos. Renan Germano. Brendha Louyse Sanres.
Yvonne Klimesch. Marjorie Dantas. Clara Justinno. Sandra Soares. Larissa Lyra. Alexia Branco de Souza. Rafael Rezende. Hugo Oliveira. Carolina Alexandra. Caroline Mereles. Karen Caetano.
Cynthia Muniz. Mais de Jorge Afiune. Jorge Afiune. Populares em Health. Adriana Tavares. Ruben Roa. Samuel Josex. Luiz Eduardo. Cristiano Stigirt. Lucas Silveira. Jose Kalilodoka Nelito. Aline Von Der Goltz Vianna. Catarina Santangelo. Everton Silva. At the first week splenic eosinophilia concomitant with raised IL5 after infection, there was evidence of fungal destruc- production Calich and Kashino, ; Meloni-Bm- tion and control of its proliferation in both animal neri et al.
The production of Nishimura, , demonstrating the important role P. Further evidence of the protec- optimal clearance of the fungus from tissues of mice tive effect of natural immunity came from the resist- infected with P.
Moreover, the experiments Burger et al. Our results also indicate that, early in the dis- b. Thus, the majority of P. In 43 and also the A mice, P. The al. T cells in the course of pulmonary PCM L.
Cano We have also carried out some studies on the par- and V. Calich, manuscript in preparation. A mice after P. Depletion of sis infection L. Cano, S. Kashino, R.
Calich, unpublished observations. However, these cells that this cell subpopulation is not necessary to con- appear to be involved in the later control of the pul- trol pulmonary infections caused by isolates of low monary infection, hampering the escape of fungal virulence.
These remained unaffected. A mice. Since we used much animals was associated with a sustained production lower doses of mAb, other protocols using higher of IFIVy, and the unexpected superior ability of sus- amounts of anti-IL4 should be tested in our experi- ceptible animals to control fungal growth in the mental model. In both mouse strains, neutralization of et al.
Wolf, Genetics Institute, fold the already high number of fungal cells in the Boston was administered i. This finding ble BIO. A mice which were tested at weeks 4 and 8 clearly showed the critical role played by IFNy in after i. This treatment markedly inhibited host resistance against P.
Histopatholog- lesions of Bl0. A animals. This packed epithelioid cells and a restricted number of finding is consistent with a pulmonary model of fungi were replaced by a fungus-rich diffuse inflam- Cryptococcus neofonnans infection where the pro- mation obliterating the normal pulmonary structure.
To better understand the immunoregulatory In murine PCM, the protective effect of IL12 was mechanismsinvolved in susceptibility to pulmonary detected at week 8 after infection and was associated PCM, B A animals were in vivo depleted of lL4, a with decreased levels of type 2 cytokines IL4 and cytokine which favours Th2 development Reiner ILlO present in the lungs.
Unexpectedly, the pul- and Lockesley, ; Seder and Paul, A mice which period. Over the past few years, it has become clear presented the same severe disseminated disease as that IL12 is the principal cytokine in inducing Thl their untreated infected counterparts. In addition, responsesthrough its ability to elicit IFNy procluc- IL4 neutralization did not change the predominant tion by T lymphocytes and NK cells Trinchieri, secretion of type 2 cytokines in the lungs, and In our experimental protocol, however, ephemerally lowered the levels of IL10 present in increased production of IFNy was not observed after the spleen.
Also, no significant differences were 4 and 8 weeks of infection, but measurements of noted in the pulmonary histopathological features cytokines at earlier periods of infection will prob- Armda et al.
These findings suggest that ably help to elucidate this issue. In parallel with the low- isms, in which abrogation of endogenous IL4 leads ered levels of pulmonary lL4, a diminished produc- susceptible hosts to a healing phenotype Romani et tion of IgGl-specific antibodies was observed in al.
In another experi- lLtreated mice. A similar finding was S. At the optimal time for development of a reported for mice systemically infected with C. The i. In sup- Surprisingly, the animals challenged i. A mice immune response developed following S. Armda and inoculation led to opposite disease outcomes, V. The abil- depending on the route of challenge Arruda et al. The lower mortality observed after P. In conclusion, to our know- S. A animals can indeed develop a protective immunity The S.
This pathogenic fungi such as C. Both susceptible and resistant mice inoculated with P. Despite the the higher mortality, the s. A ani- not show an increased fungal load in the examined mals presented significantly higher DTH responses organs. Furthermore, BIO. A ani- anergic in terms of DTH reactions like their i. Interestingly, BIO. In this model in the i. A IL10 points out the deleterious effects of type 2 mice was associated with a high production of IgA-, cytokines Calich and Kashino, Our results clearly show sities of ligands and costimulatory molecules, that the immunoregulatory mechanisms, which determine the phenotype of responding T cells account for the lack of stable cell-mediated immu- Gajewski et al.
Purified splenic B cells stimulate opti- routes of infection, are absent or less evident in the mal proliferation of Th2 cells while adherent spleen infection induced by the S.
A Since BIO. A mice do not present any intrinsic functional dichotomy of APC was also found by deficiency in the ability to develop an effective cel- Schmitz et al. Thus, the site of the immune response T-cell-mediated immunity and activation of B cells and the route of entry of antigen could play a criti- lead to severe disease outcome.
Along this line, different patterns duction of high levels of specific antibodies are of immune response to P. However, the pro- tion by diverse routes could be the result of distinct duction of certain immunoglobulin isotypes such as APC interacting with T cells leading to the preferen- IgG2a correlates with protective immunity. In addi- tial activation of type 1 or type 2 subpopulations tion, most P.
One but some fungal components can directly activate can speculate that in the protection model of PCM B cells. However, secretion of IL12 and mediated immunity which leads to a benign disease IFNy is protective, while the dominance or early and self-healing ; in the exacerbation model secretion of IL10 or TGFP is associated with sus- s. In addition, there is evidence Although it is very attractive, this hypothesis does that T-cell activation occurs by both class-I and not clearly explain the differences in responses class-II-restricted pathways.
Nevertheless, since suscep- ulate expansion of the fungal population during the tible mice were found to be much more reactive to early phases of infection, indicating an important P. A mice infected i. Mendes h Several parameters indicate that susceptible Jr. Calich and C. Vaz, unpublished data. Concluding remarks i Susceptibility can be circumvented by immune Our experimental murine model appears to intervention, for instance, by the administration of mimic human PCM, with resistant mice reproducing IL12 or by previous S.
The studies employing these mouse murine model of PCM provided new instruments strains with polarized behaviour, submitted to infec- for a better comprehension of the immunopatho- tion by several routes and to immunomanipulations, genesis of this deep mycosis. Furthermore, the enabled us to improve our knowledge of the host- increasing knowledge of the immunological mech- parasite relationship in this mycosis.
The main con- anisms which confer resistance to PCM, as well as clusions or inferences so far obtained are: to other mycotic infections, opens new perspectives a Resistance to P. Calich, V. Lacaz, C. CRC Press Inc. Arruda, C. Singer-Vermes, L. Bava, A. Lymphocyte subpopulations and cytokine , Mechanisms of host resistance to Paracoc- production in paracoccidioidomycosis patients.
Torres-Rodrigues pp. Prous Science Ed. Biagioni, L. Marques, S. A, Mota, N. Cruz, M. France, C. Lacaz, A. Del Negro Burger, E. Histopathology of Deepe, G. Fava Netto, C. OPaulo, 18, Nishimura, K. Mycopath- V. Toews, G. Gajewski, T. Studies with a highly vir- Garcia, N.
Salsa- , Immunization of mice by intracutaneous maggiore. Reskallah-Iwasso, M. Orme, I. Immu- Kawakami, K. IL protects mice against pulmonary and dissemi- Romani, L. Mosci, P. Cell, 80,
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