%0 Journal Article
%T Dynamics of Lymphocyte Populations during Trypanosoma cruzi Infection: From Thymocyte Depletion to Differential Cell Expansion/Contraction in Peripheral Lymphoid Organs
%A Alexandre Morrot
%A Juliana Barreto de Albuquerque
%A Luiz Ricardo Berbert
%A Carla Eponina de Carvalho Pinto
%A Juliana de Meis
%A Wilson Savino
%J Journal of Tropical Medicine
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/747185
%X The comprehension of the immune responses in infectious diseases is crucial for developing novel therapeutic strategies. Here, we review current findings on the dynamics of lymphocyte subpopulations following experimental acute infection by Trypanosoma cruzi, the causative agent of Chagas disease. In the thymus, although the negative selection process of the T-cell repertoire remains operational, there is a massive thymocyte depletion and abnormal release of immature CD4+CD8+ cells to peripheral lymphoid organs, where they acquire an activated phenotype similar to activated effector or memory T cells. These cells apparently bypassed the negative selection process, and some of them are potentially autoimmune. In infected animals, an atrophy of mesenteric lymph nodes is also observed, in contrast with the lymphocyte expansion in spleen and subcutaneous lymph nodes, illustrating a complex and organ specific dynamics of lymphocyte subpopulations. Accordingly, T- and B-cell activation is seen in subcutaneous lymph nodes and spleen, but not in mesenteric lymph nodes. Lastly, although the function of peripheral CD4+CD8+ T-cell population remains to be defined in vivo, their presence may contribute to the immunopathological events found in both murine and human Chagas disease. 1. Introduction Trypanosoma cruzi is the causative agent of Chagas disease affecting more than 10 million people in Latin America. The parasite is transmitted by feces of infected insect vectors belonging to the family Reduviidae [1¨C3]. After infection, the initial acute phase of the disease progresses to an asymptomatic indeterminate period with virtually undetectable parasitemia and a strong humoral and cellular anti-T. cruzi responses. Up to several years after the initial infection, approximately 20 to 30% of all infected individuals develop a chronic inflammatory disease primarily affecting the heart [2¨C4]. Although different mechanisms have been proposed to trigger this pathology, there is a growing body of evidence that parasite persistence is associated with a chronic inflammatory response, which is the primary cause of Chagas disease [5, 6]. Experimental models of T. cruzi infection have been widely used to study various aspects of the infection. Acute infection in mice leads to strong activation of innate and adaptive immune response [7, 8]. In the course of infection, there is a fine change in the dynamics on the size of lymphocyte populations that contributes to regional specificities of the immune response in central and peripheral lymphoid organs: while there is an expansion
%U http://www.hindawi.com/journals/jtm/2012/747185/