Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.3389/fimmu.2017.00318

http://scihub22266oqcxt.onion/10.3389/fimmu.2017.00318
suck pdf from google scholar
C5360705!5360705!28382039
unlimited free pdf from europmc28382039    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi


Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
pmid28382039      Front+Immunol 2017 ; 8 (ä): ä
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Genetic and Epigenetic Determinants in Autoinflammatory Diseases #MMPMID28382039
  • Álvarez-Errico D; Vento-Tormo R; Ballestar E
  • Front Immunol 2017[]; 8 (ä): ä PMID28382039show ga
  • The concept of autoinflammation has evolved over the past 20?years, beginning with the discovery that mutations in the Mediterranean Fever (MEFV) gene were causative of Familial Mediterranean Fever. Currently, autoinflammatory diseases comprise a wide range of disorders with the common features of recurrent fever attacks, prevalence of hyperreactive innate immune cells, and signs of inflammation that can be systemic or organ specific in the absence of pathogenic infection of autoimmunity. Innate immune cells from the myeloid compartment are the main effectors of uncontrolled inflammation that is caused in great extent by the overproduction of inflammatory cytokines such as IL-1? and IL-18. Defects in several signaling pathways that control innate immune defense, particularly the hyperreactivity of one or more inflammasomes, are at the core of pathologic autoinflammatory phenotypes. Although many of the autoinflammatory syndromes are known to be monogenic, some of them are genetically complex and are impacted by environmental factors. Recently, epigenetic dysregulation has surfaced as an additional contributor to pathogenesis. In the present review, we discuss data that are currently available to describe the contribution of epigenetic mechanisms in autoinflammatory diseases.
  • ä


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box