Diversidad socioeconómica regional de los flujos de migración interna en Brasil

Los niveles de pobreza en Brasil presentan una notable heterogeneidad espacial. Entre otros fenómenos, la migración puede tener cierto impacto en los niveles de pobreza regionales. Con estos antecedentes, se analiza la diversidad socioeconómica regional de los flujos migratorios en los siguientes casos: urbano-urbano, rural-urbano, urbano-rural y rural-rural dentro y entre los estados de Brasil. Para ello se utilizaron técnicas multivariables de análisis de clusters. Se observan algunas tendencias generales: entre mayor es el nivel socioeconomico hay mayores flujos urbano-urbano y de mayor distancia, mientras que entre menor es dicho nivel se dan más flujos rural-rural y de menor distancia. Más aún, los emigrantes más pobres se encuentran en los flujos con origen rural en y/o con destino a la región Noreste del país

CD8þT cells are not required for vaccine-induced immunity against Leishmania amazonensis in IL-12/23P40_/_ C57BL/6 mice.

Vaccine-induced protection against leishmaniasis is largely dependent on cell-mediated type 1 response and IL-12-driven IFN-g production. Surprisingly, our previous data showed that IL-12/23p40_/_ mice could be vaccinated against L. amazonensis and were able to produce limited amounts of IFN-g. Since the role of CD8þT in immunization against L. amazonensis is obscure, the aim of this study was to evaluate the effects of CD8þ cells in protection against L. amazonensis in IL-12/23p40_/_ mice. In order to deplete CD8þ cells, one group of vaccinated animals was treated with anti-CD8 mAb. Infection was followed for 8 weeks. The vaccinated CD8þ-depleted group developed smaller lesions than the non-depleted group. CD8 depletion did not affect tissue parasitism or antibody response against the parasite, and treated animals displayed milder inflammation and better tissue integrity. IFN-g production in spleen and draining lymph node was impaired in the depleted group, suggesting that CD8þ cells produced this cytokine in IL-12-independent vaccination. Such results suggest that this T cell subset contributes to augmented pathology in IL12/23p40_/_ mice vaccinated and challenged with L. amazonensis. Although these cells could produce some IFN-g the in the absence of IL-12, they do not affect the parasite tissue load

The influence of CD25+ cells on the generation of immunity to tumour cell lines in mice

CD25+ regulatory T cells comprise 5–10% of CD4+ T cells in naïve mice and have been shown in several in vivo murine models to prevent the induction of autoimmune disease and inflammatory disease. Since T cells, which mediate autoimmunity, can through recognition of self-antigens also target tumour cells, it was postulated that CD25+ regulatory cells would also inhibit the generation of immune responses to tumours. Depletion of these cells using CD25-specific monoclonal antibodies has indeed been shown to promote rejection of several transplantable murine tumour cell lines including melanoma, leukaemia and colorectal carcinoma. Results obtained using these models indicate that in the absence of regulatory cells, CD4+ T cells mediate tumour immunity, although the precise mechanisms through which these cells result in tumour rejection have not yet been elucidated. The target antigens recognized by these CD4+ T cells have also not yet been identified. Immunization of mice with tumour cells in the absence of CD25+ regulatory cells does, however, induce immunity against a variety of different tumour cell lines indicating that the target antigen(s) are shared amongst tumours of distinct histological origins. Since CD25+ regulatory cells have been identified in humans, the possibility that the cells inhibit immune responses to shared rejection antigens expressed by human tumours is worthy of investigation

An immunodominant MHC class II-restricted tumor antigen is conformation dependent and binds to the endoplasmic reticulum chaperone, calreticulin

There is accumulating evidence that CD4+ T cell responses are important in antitumor immunity. Accordingly, we generated CD4+ T cells against the murine CT26 colon cancer. Three of three independent CT26-specific CD4+ hybridomas were found to recognize the high m.w. precursor of the env gene product gp90. The CD4+ response was completely tumor specific in that the same glycoprotein expressed by other tumors was not recognized by the CT26-specific hybridomas. The recognition of gp90 by the hybridomas was strictly dependent on the conformation of gp90. Different procedures that disrupted the conformation of the glycoprotein, such as disulfide bond reduction and thermal denaturation, completely abrogated recognition of gp90 by all three hybridomas. In CT26 cells, but not in other tumor cells tested, a large proportion of gp90 was retained in the endoplasmic reticulum, mostly bound to the endoplasmic reticulum chaperone, calreticulin. Although calreticulin was not essential for the stimulation of the gp90-specific hybridomas, most of the antigenic form of gp90 was bound to it. The antigenicity of gp90 correlated well with calreticulin binding, reflecting the fact that specificity of binding of calreticulin to its substrate required posttranslational modifications that were also necessary for the generation of this tumor-specific CD4+ epitope