Antigen-dependent Proliferation of CD4+ CD25+ Regulatory T Cells In Vivo

The failure of CD25+ regulatory T cells (Tregs) to proliferate after T cell receptor (TCR) stimulation in vitro has lead to their classification as naturally anergic. Here we use Tregs expressing a transgenic TCR to show that despite anergy in vitro, Tregs proliferate in response to immunization in vivo. Tregs also proliferate and accumulate locally in response to transgenically expressed tissue antigen whereas their CD25− counterparts are depleted at such sites. Collectively, these data suggest that the anergic state that characterizes CD25+ Tregs in vitro may not accurately reflect their responsiveness in vivo. These observations support a model in which Treg population dynamics are shaped by the local antigenic environment

Cooperative Roles of CTLA-4 and Regulatory T Cells in Tolerance to an Islet Cell Antigen

Adoptive transfer of ovalbumin (OVA)-specific T cells from the DO.11 TCR transgenic mouse on a Rag−/− background into mice expressing OVA in pancreatic islet cells induces acute insulitis and diabetes only if endogenous lymphocytes, including regulatory T cells, are removed. When wild-type OVA-specific/Rag−/− T cells, which are all CD25−, are transferred into islet antigen–expressing mice, peripheral immunization with OVA in adjuvant is needed to induce diabetes. In contrast, naive CTLA-4−/−/Rag−/− OVA-specific T cells (also CD25−) develop into Th1 effectors and induce disease upon recognition of the self-antigen alone. These results suggest that CTLA-4 functions to increase the activation threshold of autoreactive T cells, because in its absence self-antigen is sufficient to trigger autoimmunity without peripheral immunization. Further, CTLA-4 and regulatory T cells act cooperatively to maintain tolerance, indicating that the function of CTLA-4 is independent of regulatory cells, and deficiency of both is required to induce pathologic immune responses against the islet self-antigen

Attempts to Identify Wildlife Reservoirs of Rabies in Indonesia

Penyakit rabies telah dikenal di Indonesia sejak tahun 1889, dan mengingat tidak adanya data yang diteliti mengenai penderita rabies, maka perlu dilakukan suatu penelitian. Penelitian dilakukan oleh NAMRU-2 bersama Departemen Kesehatan dari tahun 1970-1972 untuk menentukan pengaruh penyakit-penyakit Zoonotic yang endemic pada penduduk yang tidak immune yang sering berpindah ke hutan atau tempat yang tidak ada penduduknya. Penelitian di lakukan pada beberapa daerah pegunungan Jawa Barat, Jawa Timur, Lampung, Maluku, Kalimantan Tengah, Timor dan Sulawesi Tengah. Hasil penelitian menunjukkan bahwa dari 328 binatang yang diperoleh dari 28 berbagai daerah di Indonesia setelah diadakan pemeriksaan dengan metode fluorecent antibody technique {fat) dan inokuler pada tikus putih ternyata tidak ditemukan virus rabies. Binatang-binatang yang ditemukan tersebut dan kebiasaan hidupnya di lukiskan secara terperinci pada hasil penelitian ini

CD4 T cell activation as a predictor for treatment failure in Ugandans with Plasmodium falciparum malaria.

Host immunity plays an important role in response to antimalarial therapy but is poorly understood. To test whether T cell activation is a risk factor for antimalarial treatment failure, we studied CD4(+) and CD8(+) T cell activation in 31 human immunodeficiency virus-negative Ugandan patients 5-37 years of age who were treated for uncomplicated Plasmodium falciparum malaria. Increased CD4(+) T cell activation, as indicated by co-expression of HLA-DR and CD38, was an independent risk factor for treatment failure (hazard ratio = 2.45, 95% confidence interval = 1.02-5.89, P = 0.05) in multivariate analysis controlling for age, baseline temperature, and pre-treatment parasite density. The results provide insight into the role of cellular immunity in response to antimalarial therapy and underscore the need to investigate the mechanisms behind immune activation