Following gastric bypass surgery in morbidly obese diabetic patients, MMP-9 and NOM levels dropped, along with the expression of six asthma-related genes including the key factors, interleukin 4, LIGHT, lymphotoxin
beta and interleukin 33 in parallel with weight loss and improvements in the status of their diabetes.
Essential role of nuclear factor (NF)-[kappa]B-inducing kinase and inhibitor of [kappa]B (I[kappa]B) kinasea in NF-[kappa]B activation through lymphotoxin
[beta] receptor, but not through tumor necrosis factor receptor I.
and tumor necrosis factor-alpha production by myelin basic protein-specific T cell clones correlates with encephalitogenicity.
, RANKL (receptor activator of nuclear factor kappa B ligand), and intracellular kinases].
Th1 cells secrete IL-2, IFN-[gamma], and lymphotoxin
, and are primarily associated with macrophage activation and delayed-type hypersensitivity.
Selmaj K, Raine CS, Cannella B, Brosnan CF: Identification of lymphotoxin
and tumor necrosis factor in multiple sclerosis lesions.
Enbrel binds to lymphotoxin
and TNF-alpha, blocking its interaction with cell surface TNF receptors, thus preventing synovial inflammation.
In contrast, the noncanonical NF-[kappa]B-activating pathway is activated by B-cell activating factor (BAFF) , lymphotoxin
[beta] (LT[beta]) , CD40 ligand , CD27 ligand , human T-cell leukemia virus (HTLV) , and Epstein-Barr virus (EBV)  and it relies on IKK[alpha] and causes activation of NF-[kappa]B2/RelB complexes by inducing the proteolytic processing of the NF-[kappa]B2/p100 precursor.
Inflectra (infliximab) is a chimeric human-murine monoclonal antibody that binds with high affinity to both soluble and transmembrane forms of TNF alpha but not to lymphotoxin
beta receptor and atherosclerosis: observations from the Dallas Heart Study.
To measure the effects of microbes and immunity, the researchers compared normal mice with mice that have a genetic defect that renders them unable to produce lymphotoxin
, a molecule that helps to regulate interactions between the immune system and bacteria in the bowel.
However, the lymphotoxin
[beta] receptor (LT[beta]R) in stromal cells induces processing of p100 via an alternative pathway, which leads to the delayed and sustained liberation of p50-RelB and p52-RelB complex (14).