The monoclonal antibody 5G11 reacts with the mouse lymphotoxin beta-receptor (LTbetaR), a member of the tumor necrosis factor (TNF) family. This receptor can be activated by its functional ligands lymphotoxin-alpha1-beta2 (LT-alpha1beta2) and LIGHT and is critically involved in controlling bacterial infections. In Mycobacterium infection, its role is related to bactericidal granuloma formation in the spleen, macrophage differentiation and the maintenance of the appropriate Th1/Th2 cytokine balance. In CMV infection, LTbetaR signaling induces the expression of IFN-beta in infected fibroblasts, resulting in viral stasis. LTbetaR plays an important role in lymphoid organogenesis and tumor development. The receptor is expressed on fibroblasts and stromal cells and at low levels in some myeloid cell lines. In the adult animal, the LTbetaR seems to be necessary for maintaining the splenic architecture and aspects of Ig formation and B cell follicular structure. When the LT-alpha1beta2/LTbetaR pathway is disrupted by genetic deletion, mice completely lack Peyer’s patches. Also, LTbetaR induces cell death in some adenocarcinoma tumor lines in the presence of IFNgamma.The monoclonal antibody 5G11 directed against the mouse LTbetaR is able to activate the LTbetaR in an agonistic way and induces NFkappaB activation and secretion of MIP-2 and IL-6 in mouse fibroblast cells. Therefore, the monoclonal antibody 5G11 can be used to gain more insight into the expression pattern of the LTbetaR and also to investigate molecular mechanisms induced by LTbetaR activation.