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


10.1016/j.immuni.2016.01.003

http://scihub22266oqcxt.onion/10.1016/j.immuni.2016.01.003
suck pdf from google scholar
C4838571!4838571 !26850657
unlimited free pdf from europmc26850657
    free
PDF from PMC    free
html from PMC    free

Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26850657 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215

suck abstract from ncbi

pmid26850657
      Immunity 2016 ; 44 (4 ): 821-32
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • MicroRNAs 24 and 27 Suppress Allergic Inflammation and Target a Network of Regulators of T Helper 2 Cell-Associated Cytokine Production #MMPMID26850657
  • Pua HH ; Steiner DF ; Patel S ; Gonzalez JR ; Ortiz-Carpena JF ; Kageyama R ; Chiou NT ; Gallman A ; de Kouchkovsky D ; Jeker LT ; McManus MT ; Erle DJ ; Ansel KM
  • Immunity 2016[Apr]; 44 (4 ): 821-32 PMID26850657 show ga
  • MicroRNAs (miRNAs) are important regulators of cell fate decisions in immune responses. They act by coordinate repression of multiple target genes, a property that we exploited to uncover regulatory networks that govern T helper-2 (Th2) cells. A functional screen of individual miRNAs in primary T cells uncovered multiple miRNAs that inhibited Th2 cell differentiation. Among these were miR-24 and miR-27, miRNAs coexpressed from two genomic clusters, which each functioned independently to limit interleukin-4 (IL-4) production. Mice lacking both clusters in T cells displayed increased Th2 cell responses and tissue pathology in a mouse model of asthma. Gene expression and pathway analyses placed miR-27 upstream of genes known to regulate Th2 cells. They also identified targets not previously associated with Th2 cell biology which regulated IL-4 production in unbiased functional testing. Thus, elucidating the biological function and target repertoire of miR-24 and miR-27 reveals regulators of Th2 cell biology.
  • |Animals [MESH]
  • |Asthma/*immunology [MESH]
  • |Base Sequence [MESH]
  • |Cell Differentiation/genetics/immunology [MESH]
  • |Cells, Cultured [MESH]
  • |Disease Models, Animal [MESH]
  • |Female [MESH]
  • |Inflammation/immunology [MESH]
  • |Interleukin-4/*biosynthesis/immunology [MESH]
  • |Lymphocyte Activation/immunology [MESH]
  • |Male [MESH]
  • |Mice [MESH]
  • |Mice, Knockout [MESH]
  • |MicroRNAs/*genetics [MESH]
  • |Multigene Family/genetics [MESH]
  • |Sequence Analysis, RNA [MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box