Influence of chemokines on the endothelial permeability and cellular transmigration during dengue.

Abstract:

:During a pathogenic infection, an inflammatory process is triggered in which several inflammatory mediators, such as cytokines, chemokines, growth factors, complement system components, nitric oxide, and others induce integrity alteration on the endothelial barrier. Chemokines are responsible for regulating leukocyte trafficking under homeostatic conditions as well as activating immune system cells under inflammatory conditions. They are crucial molecules in the early stages of infection, leading to the recruitment of immune cells, namely neutrophils, monocytes, natural killer (NK) cells, natural killer T cells (NKT), dendritic cells (DC), T lymphocytes and all cells expressing chemokine receptors for inflammatory sites. Other functions, such as collagen production, tissue repair, a proliferation of hematopoietic precursors and angiogenesis, are also performed by these molecules. Chemokines, amongst inflammatory mediators, play a key role in dengue immunopathogenesis. Dengue fever is a disease caused by the dengue virus (DENV). It is characterized by a broad spectrum of clinical manifestations ranging from asymptomatic cases to mild and severe symptomatic ones. As for the latter, the appearance of hemorrhagic manifestations and changes in vascular permeability may lead the patient to develop cavitary effusions, organ involvement, and even death. As chemokines exert an influence on various homeostatic and inflammatory processes, acting vigorously on vascular endothelial activation and cell migration, the main purpose of this chapter is to discuss the influence of chemokines on the alteration of endothelial permeability and migration of T lymphocytes in DENV infection.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Cipitelli MDC,Amâncio Paiva I,Badolato-Corrêa J,de-Oliveira-Pinto LM

doi

10.1016/j.imlet.2019.06.001

subject

Has Abstract

pub_date

2019-08-01 00:00:00

pages

88-97

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(19)30125-7

journal_volume

212

pub_type

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