| First Author | Nayak L | Year | 2013 |
| Journal | Am J Pathol | Volume | 182 |
| Issue | 5 | Pages | 1696-704 |
| PubMed ID | 23499374 | Mgi Jnum | J:195343 |
| Mgi Id | MGI:5478651 | Doi | 10.1016/j.ajpath.2013.01.029 |
| Citation | Nayak L, et al. (2013) Kruppel-like factor 2 is a transcriptional regulator of chronic and acute inflammation. Am J Pathol 182(5):1696-704 |
| abstractText | Although myeloid cell activation is requisite for an optimal innate immune response, this process must be tightly controlled to prevent collateral host tissue damage. Kruppel-like factor 2 (KLF2) is a potent regulator of myeloid cell proinflammatory activation. As an approximately 30% to 50% reduction in KLF2 levels has been observed in human subjects with acute or chronic inflammatory disorders, we studied the biological response to inflammation in KLF2(+/-) mice. Herein, we show that partial deficiency of KLF2 modulates the in vivo response to acute (sepsis) and subacute (skin) inflammatory challenge. Mechanistically, we link the anti-inflammatory effects of KLF2 to the inhibition of NF-kappaB transcriptional activity. Collectively, the observations provide biologically relevant insights into KLF2-mediated modulation of these inflammatory processes that could potentially be manipulated for therapeutic gain. |
