Chagasic Patients with Indeterminate Clinical Form of the Disease have High Frequencies of Circulating CD3+CD16–CD56+ Natural Killer T Cells and CD4+CD25High Regulatory T Lymphocytes
Chagasic Patients with Indeterminate Clinical Form of the Disease have High Frequencies of Circulating CD3+CD16–CD56+ Natural Killer T Cells and CD4+CD25High Regulatory T Lymphocytes
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具有不确定临床形式的恰加斯病患者具有高频率的循环 CD3+CD16–CD56+ 自然杀伤 T 细胞和 CD4+CD25 高调节性 T 淋巴细胞
DOI：
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发表时间：
2005
影响因子：
3.7
通讯作者：
Olindo de Assis Martins
中科院分区：
文献类型：
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作者：
D. Vitelli;R. Sathler;J. C. P. Dias;V. P. M. Pascoal;A. Teixeira;A. Teixeira;P. S. Lage;S. Elói;Rodrigo Corrêa;Olindo de Assis Martins
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+CD25high 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+CD25high and NKT regulatory cells (CD3+CD16–CD56+), associated with increased levels of circulating cytotoxic NK cells (CD3–CD16+CD56+ and CD3–CD16+CD56dim 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.
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影响因子：
4.4
作者：
L. Lanier;J. Phillips;J. Hackett;M. Tutt;V. Kumar
通讯作者：
L. Lanier;J. Phillips;J. Hackett;M. Tutt;V. Kumar
DOI：
10.1016/s0035-9203(01)90153-1
发表时间：
2001
影响因子：
2.2
作者：
d'AvilaReis,D;Lemos,EM;Silva,GC;Adad,SJ;McCurley,T;Correa-Oliveira,R;Machado,CR
通讯作者：
Machado,CR
影响因子：
32.4
作者：
Grossman, WJ;Verbsky, JW;Ley, TJ
通讯作者：
Ley, TJ
影响因子：
32.4
作者：
HUANG, JH;GETTY, RR;TYKOCINSKI, ML
通讯作者：
TYKOCINSKI, ML
影响因子：
32.4
作者：
Dittmer, U;He, H;Hasenkrug, KJ
通讯作者：
Hasenkrug, KJ