Are the innate and adaptive immune systems setting hypertension on fire?

Autor(es)

Bomfim, Gisele F. ; Rodrigues, Fernanda Luciano ; Carneiro, Fernando S.

• Tipo de documento: Artigo de Revisão
• Fonte: PHARMACOLOGICAL RESEARCH; v. 117, p. 377-393, MAR 2017.
• Citações Web of Science: 14

Resumo

Hypertension is the most common chronic cardiovascular disease and is associated with several pathological states, being an important cause of morbidity and mortality around the world. Low-grade inflammation plays a key role in hypertension and the innate and adaptive immune systems seem to contribute to hypertension development and maintenance. Hypertension is associated with vascular inflammation, increased vascular cytokines levels and infiltration of immune cells in the vasculature, kidneys and heart. However, the mechanisms that trigger inflammation and immune system activation in hypertension are completely unknown. Cells from the innate immune system express pattern recognition receptors (PRR), which detect conserved pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPS) that induce innate effector mechanisms to produce endogenous signals, such as inflammatory cytokines and chemokines, to alert the host about danger. Additionally, antigen-presenting cells (APC) act as sentinels that are activated by PAMPs and DAMPs to sense the presence of the antigen/neoantigen, which ensues the adaptive immune system activation. In this context, different lymphocyte types are activated and contribute to inflammation and end-organ damage in hypertension. This review will focus on experimental and clinical evidence demonstrating the contribution of the innate and adaptive immune systems to the development of hypertension. (C) 2017 Elsevier Ltd. All rights reserved. (AU)

• Processo FAPESP: 15/21976-1 - Controle autonômico cardiovascular em camundongos knockout para receptores toll-like 9 com hipertensão induzida por angiotensina II.
• Beneficiário: Fernanda Luciano Rodrigues
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 10/17362-4 - Mecanismos da disfunção erétil na insuficiência cardíaca
• Beneficiário: Fernando Silva Carneiro
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores
• Processo FAPESP: 16/11988-5 - Contribuição do NLRP3 para o efeito pró-inflamatório da ET-1 em células de músculo liso do corpo cavernoso: relevância na função erétil.
• Beneficiário: Fernando Silva Carneiro
• Modalidade de apoio: Auxílio à Pesquisa - Regular