Coordinate activation of inflammatory gene networks, @entity133 and neonatal death in XXXX deficient @entity19 .

@entity32 @entity944 @entity19 @entity635 @entity16 @entity133 @entity1129 @entity72968 @entity3804 @entity12100
Gene expression can be regulated by chromatin modifiers, transcription factors and proteins that modulate DNA architecture. Among the latter, AT-hook transcription factors have emerged as multifaceted regulators that can activate or repress broad A/T-rich gene networks. Thus, alterations of AT-hook genes could affect the transcription of multiple genes causing global cell dysfunction. Here we report that targeted deletions of @entity19 @entity72968 , a hypothetical @entity1129 factor, sensitize @entity19 to pathogen-induced @entity32 and cause @entity944 . Compared with wild-type littermates, @entity72968 KO @entity19 appeared weak, failed to thrive and most died by postnatal day 10. Systemic @entity32 , predominantly in the lungs, was accompanied by enhanced leukocyte infiltration and @entity133 . Cytologic, immunohistochemical and molecular analyses revealed @entity3804 (+)Gr1(+) neutrophils as major tissue infiltrators, neutrophilic granule protein, cathelin-related antimicrobial peptide and @entity12100 as neutrophil-specific chemoattracting factors, @entity635 and interferon-y as proinflammatory mediators, and matrix metalloprotease 9 as a plausible proteolytic trigger of @entity16 . @entity72968 KO bone marrow transplants in wild-type recipients reproduced the severe pathogen-induced reactions and confirmed the involvement of neutrophils in acute @entity32 . Moreover, promoter/reporter experiments showed that @entity72968 could act as a gene repressor. Our results support the concept of coordinated pathway-specific gene regulation functions modulating the intensity of inflammatory responses, reveal neutrophils as prominent mediators of acute @entity32 and suggest mechanisms underlying the triggering of acute and potentially fatal immune reactions.
