Functions of MAP3Ks in antiviral immunity

Abstract

Immune signal transduction is crucial to the body’s defense against viral infection. Recognition of pathogen-associated molecular patterns by pattern recognition receptors (PRRs) activates the transcription of interferon regulators and nuclear factor-κB (NF-κB); this promotes the release of interferons and inflammatory factors. Efficient regulation of type I interferon and NF-κB signaling by members of the mitogen-activated protein (MAP) kinase kinase kinase (MAP3K) family plays an important role in antiviral immunity. Elucidating the specific roles of MAP3K activation during viral infection is essential to develop effective antiviral therapies. In this review, we outline the specific regulatory mechanisms of MAP3Ks in antiviral immunity and discuss the feasibility of targeting MAP3Ks for the treatment of virus-induced diseases.

NF-κB p65 and TCF-4 interactions are associated with LPS-stimulated IL-6 secretion of macrophages

“…The NF-κB transcription factor plays a key role in regulating the immune response to infection in mammalian cells [ 10 , 11 ]. It is found in an inactive state in the cytoplasm, bound to its inhibitor IκB (Inhibitor of κB).…”

Aloe-derived nanovesicles attenuate inflammation and enhance tight junction proteins for acute colitis treatment

“…Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is a chronic inflammation of the digestive tract characterized by diarrhea, acute pain, weight loss, and ulceration. 1 It also increases the risk of developing malignancies, including colon cancer. 2 Despite the steadily increasing incidence rate worldwide, the cause of IBD has not been clearly established; 3 it is considered a multifactorial disease associated with genetics, gut microbiota, dietary environments, and the immune network.…”

“…During IBD progress, free radicals, including nitric oxide, and pro-inflammatory cytokines, including TNF-β, IL-1β, IL-6, IL-12, IL-23, IL-17, and IFN-γ, are upregulated in the local gastrointestinal (GI) tract. 1 These result in the decreased expression of tight junction (TJ) and adherent junction (AJ) proteins, which incur a leaky gut in IBD. 5,6 Accordingly, various medicines, including 5-aminosalicylate, steroids (prednisolone, budesonide), and immunomodulators (azathiopurine, mercaptiopurine, methotrexate, and cyclosporine) have been used as maintenance drugs to mitigate the pathogenic symptoms of IBD.…”