Formyl peptide receptor polymorphisms: 27 most possible ways for phagocyte dysfunction


Citar

Texto integral

Acesso aberto Acesso aberto
Acesso é fechado Acesso está concedido
Acesso é fechado Somente assinantes

Resumo

Formyl peptide receptors (FPRs) expressed by mammalian myeloid cells are the important part of innate immunity. They belong to the seven-transmembrane domain class of receptors coupled to heterotrimeric GTP-binding proteins. Binding of the receptor with a wide spectrum of exogenous and endogenous ligands triggers such defensive phagocyte reactions as chemotaxis, secretory degranulation, and respiratory burst, keeping a balance of inflammatory and antiinflammatory processes in the organism. The association between single nucleotide polymorphisms in the gene of FPR1 receptor resulting in disruption of the receptor structure and the development of certain pathologies accompanied with inflammation, such as aggressive periodontitis, macular degeneration, and even gastric cancer (Maney, P., and Walters, J. D. (2009) J. Periodontol., 80, 1498-1505; Liang, X. Y., et al. (2014) Eye, 28, 1502-1510; Otani, T., et al. (2011) Biochem. Biophys. Res. Commun., 405, 356-361) has been shown. In this review, we matched the missense mutation of formyl-peptide receptors with their known functional domains and classified them according to their potential significance in pathology.

Sobre autores

S. Skvortsov

Kazan State Medical Academy, Branch Campus of the Federal State Budgetary Educational Institution of Further Professional Education “Russian Medical Academy of Continuing Professional Education”

Email: aida.gabdoulkhakova@gmail.com
Rússia, Kazan, 420012

A. Gabdoulkhakova

Kazan State Medical Academy, Branch Campus of the Federal State Budgetary Educational Institution of Further Professional Education “Russian Medical Academy of Continuing Professional Education”; Kazan (Volga Region) Federal University

Autor responsável pela correspondência
Email: aida.gabdoulkhakova@gmail.com
Rússia, Kazan, 420012; Kazan, 420000


Declaração de direitos autorais © Pleiades Publishing, Ltd., 2017

Este site utiliza cookies

Ao continuar usando nosso site, você concorda com o procedimento de cookies que mantêm o site funcionando normalmente.

Informação sobre cookies