@Article{,
AUTHOR = {Thomas Hehlgans, Peter Müller, Peter Stopfer, Daniela N. Männel},
TITLE = {Activation of the lymphotoxin-beta receptor induces NFκB-dependent interleukin-6 and MIP-2 secretion in mouse fibrosarcoma cells},
JOURNAL = {European Cytokine Network},
VOLUME = {14},
YEAR = {2003},
NUMBER = {2},
PAGES = {103--107},
URL = {http://www.techscience.com/ECN/v14n2/66543},
ISSN = {1952-4005},
ABSTRACT = {Activation of the lymphotoxin beta-receptor (LTβR), a member of the tumor necrosis factor
receptor family, plays a crucial role in lymphoid organogenesis and tumor development. Lymphotoxin a1b2
(LTa1b2) and LIGHT have been identified as membrane anchored ligands for the LTβR. While LTβR is expressed
on a wide range of cell types e.g. fibroblasts and monocytes, the ligands are expressed only on activated
lymphocytes and NK cells. In order to characterize LTβR expression and the biological consequences of LTβR
activation rat anti-mouse LTβR monoclonal antibodies were generated. These antibodies recognized a mouse
LTβR-Ig fusion protein as well as endogenous LTβR on a variety of mouse fibroblast and fibrosarcoma cell lines.
Specificity was demonstrated by the lack of binding to LTβR-deficient embryonic fibrobasts. Competitive binding
studies revealed that three different epitopes were recognized by the monoclonal antibodies. Two of the
monoclonals activated the LTβR and induced activation of NFκB and secretion of MIP-2 and IL-6 in L929 mouse
fibroblast cells. MIP-2 and IL-6 secretion was NFκB-dependent because IκB-transfected cells released signifi-cantly
reduced amounts of both mediators.},
DOI = {}
}