Immunology and Infection by Protozoan Parasites

Copyright © 2015 Edecio Cunha-Neto et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Protozoan infection is the cause of diseases of high morbidity and mortality. Most are non-self-limiting chronic infections and neglected diseases; emergent antimicrobial-resistant strains pose a substantial problem; for many of them treatment either is highly toxic or has limited effectiveness. Vaccine development is still a formidable task and there is no licensed vaccine for human protozoan infection. The key to the control of protozoan infection is the understanding of the host immune response to protozoan parasites, which will guide the development of effective vaccines and immunother-apeutic agents. In this special issue, there are important studies on the immunology of T. cruzi infection, tegumentary and visceral leishmaniasis, malaria, and toxoplasmosis, both in patients and in animal models, which promote the understanding of immunopathological/immunoprotective parameters in these diseases. The reviews by J. M. ´ Alvarez and colleagues and by E. Cunha-Neto and C. Chevillard cover fundamental findings, mechanisms, and questions concerning the immune response and pathology of mouse and human disease. In this line, L. G. Nogueira and colleagues characterize the myocardial expression of transcriptional factors involved in effector CD4+ T cell differentiation and the characteristic cytokines produced by the distinct lymphocyte subsets and demonstrate a profound predominance of local Th1 response. L. C. J. Abel and coworkers characterized the proinflammatory effects of glicophosphatidyl inositol-anchored T. cruzi mucin (GPI-mucins) on human immune cells. It was observed that IL-12 production by GPI-mucins was dependent on IFN-í µí»¾ and CD40-CD40L interactions. F. C. Dias and colleagues investigated the HLA-G expression in tissues and HLA-G 147 3 í® í° UTR polymorphic site typing in patients presenting Chagas disease and the role of the mouse functional homolog in T. cruzi infection. F. Vorraro and colleagues studied the susceptibility to T. cruzi of mouse strains previously selected based on inflammatory and antibody responses to complex antigens. Q. Miao and M. Ndao review the potential impact of T. cruzi infection on the status of host lipid metabolism. The role of lipid mediators in T. cruzi infection is explored in two research articles. A. M. C. Canavaci and colleagues revisit the pathological role of 5-lipoxygenase in the acute infection of mice and A. D. Malvezi and coworkers investigate the role of cyclooxygenase …