Abstracts (complete list) - Wissenschaft Online

Susanne Berchtold, Edda Fahl, Mathias Hornef, Julia Geisel, Julia-Stefanie Frick, Erwin
Bohn
IFIT-2 – a putative novel negative regulator of
proinflammatory responses
Interferon-induced tetratricopeptide repeat protein (IFIT-) 2 is induced upon acute
infection with Yersinia enterocolitica in CD11b-positive cells of the spleen of mice as well
as in the colon of IL-2 deficient mice which develop inflammatory bowel disease. IFIT-2
is induced by type II and type I interferons or indirectly by LPS in an IFN dependent
manner. Recently it was reported that mouse IFIT2 (P54) affects protein synthesis by
interaction with the translation initiation factor eIF3c. Therefore we speculated that this
gene could represent a negative regulator of host responses by down regulating protein
synthesis. To address the role of IFIT2, stably transfected RAW 264.7 macrophages
were established overexpressing IFIT-2. These cells were viable and showed similar
proliferation as control cells. IFIT-2 overexpression did not alter LPS triggered p38, ERK,
JNK and IκB phosphorylation indicating that IFIT-2 does not affect LPS mediated signal
transduction. Overexpression of IFIT-2 in RAW 264.7 macrophages reduced LPS induced
protein expression in a selective manner at a posttranscriptional level. Thus, TNF-
&alpha, IL-6 and MIP-2 secretion but not protein expression of IFIT-1 or early growth
reponse 1 were affected by IFIT-2. IFIT-2 may thereforee represent a novel negative
regulator of proinflammatory responses.