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Regulation of T lymphocyte apoptotic markers is associated to cell activation during the acute phase of dengue.

Abstract：

:Dengue fever, a public health problem in Brazil, may present severe clinical manifestations as result of an increased vascular permeability and coagulation disorders. T cell activation is a critical event for an effective immune response against infection, including the production of cytokines. We aim to reveal mechanisms that modulate the virus-cell interaction, with an emphasis on cell death. Apoptosis is involved in lymphocyte homeostasis, contributes to the clearance of virus-infected cells but also may play a role in the pathogenesis. Phosphatidylserine exposure on CD8T lymphocytes from dengue patients support early apoptotic processes and loss of genomic integrity, observed by DNA fragmentation in T lymphocytes and indicating late apoptosis. These T cells express activation and cytotoxic phenotypes as revealed by CD29 and CD107a upregulation. Higher frequencies of CD95 were detected in T lymphocytes mainly in those with the cytotoxic profile (CD107a+) and lower levels of anti-apoptotic molecule Bcl-2, suggesting that both CD4+ and CD8+ T cell subsets are more susceptible to apoptosis during acute dengue. The analysis of apoptosis-related protein expression profile showed that not only molecules with pro- but also those with anti-apoptotic functions are overexpressed, indicating that survival mechanisms could be possibly protecting cells against apoptosis caused by viral, immune, oxidative and/or genotoxic stresses. These observations led us to propose that in dengue patients there is an association between T cell susceptibility to apoptosis and the activation state. The mechanisms for understanding the immunopathogenesis during dengue infection are discussed.

journal_name

Immunobiology

journal_title

Immunobiology

authors

Torrentes-Carvalho A,Marinho CF,de Oliveira-Pinto LM,de Oliveira DB,Damasco PV,Cunha RV,de Souza LJ,de Azeredo EL,Kubelka CF

doi

10.1016/j.imbio.2013.11.002

subject

Has Abstract

pub_date

2014-05-01 00:00:00

pages

329-40

issue

5

eissn

0171-2985

issn

1878-3279

pii

S0171-2985(13)00204-0

journal_volume

219

pub_type

杂志文章

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