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Chagasic Patients with Indeterminate Clinical Form of the Disease have High Frequencies of Circulating CD3 + CD16 – CD56 + Natural Killer T Cells and CD4 + CD25 High Regulatory T Lymphocytes
Author(s) -
VitelliAvelar D. M.,
SathlerAvelar R.,
Dias J. C. P.,
Pascoal V. P. M.,
TeixeiraCarvalho A.,
Lage P. S.,
ElóiSantos S. M.,
CorrêaOliveira R.,
MartinsFilho O. A.
Publication year - 2005
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2005.01668.x
Subject(s) - cytotoxic t cell , immunophenotyping , immunology , biology , immune system , cd16 , cd8 , natural killer t cell , il 2 receptor , context (archaeology) , cd3 , cd38 , t cell , antigen , microbiology and biotechnology , in vitro , stem cell , cd34 , genetics , paleontology
Several studies have demonstrated that different clinical manifestations of human Chagas' disease are associated with distinct and complex host–parasite relationships directly involving the immune system. In this context, it has been proposed that tissue damage might be more severe in the absence of regulatory mechanisms that involve both innate and adaptive immune responses. Herein, we describe a descriptive phenotypic profile focusing on the frequency of major regulatory T cells [CD4 + CD25 high and natural killer T (NKT) lymphocytes] in different clinical forms of Chagas' disease. Ex vivo immunophenotyping of whole blood demonstrated that the indeterminate clinical form displays a higher frequency of both CD4 + CD25 high and NKT regulatory cells (CD3 + CD16 – CD56 + ), associated with increased levels of circulating cytotoxic NK cells (CD3 – CD16 + CD56 + and CD3 – CD16 + CD56 dim NK cells). By contrast, the increased percentage of activated CD8 + HLA‐DR + T‐cell subset was exclusively associated with severe clinical forms of Chagas' disease. We hypothesize that regulatory T cells may be able to control the deleterious cytotoxic activity in the indeterminate clinical form by inhibiting the activation of CD8 + HLA‐DR + T cells. The lack of regulated populations in cardiac and digestive clinical forms could account for impaired immune response that culminates in strong cytotoxic activity and tissue damage.