Interferons (IFNs) are natural glycoproteins belonging to the cytokine superfamily and are produced by the cells of the immune system of most vertebrates in response to challenges by foreign agents such as viruses, parasites, and tumor cells. Interferon-beta (IFN beta) is an extracellular protein mediator of host defense and homeostasis. IFN beta has well-established direct antiviral, antiproliferative, and immunomodulatory properties. Recombinant IFN beta is approved for the treatment of relapsing-remitting multiple sclerosis. The recombinant IFN beta protein has the theoretical potential to either treat or causes autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks. It is the most widely prescribed disease-modifying therapy for multiple sclerosis (MS). Large-scale clinical trials have established the clinical efficacy of IFN beta in reducing relapses and slowing disease progression in relapsing-remitting MS. IFN beta therapy was shown to be comparably beneficial for opticospinal MS (OSMS) and conventional MS in Japanese. IFN beta is effective in reducing relapses in secondary progressive MS and may have a modest effect in slowing disability progression. In addition to the common antiviral activity, IFN beta also induces increased production of the p53 gene product which promotes apoptosis and thus has a therapeutic effect against certain cancers. The role of IFN-beta in bone metabolism could warrant its systematic evaluation as a potential adjunct to therapeutic regimens of osteolytic diseases. Furthermore, IFN beta might play a beneficial role in the development of chronic progressive CNS inflammation.
Interferons (IFNs) are natural glycoproteins belonging to the cytokine superfamily and are produced by the cells of the immune system of most vertebrates in response to challenges by foreign agents such as viruses, parasites, and tumor cells. Interferon-beta (IFN beta) is an extracellular protein mediator of host defense and homeostasis. IFN beta has well-established direct antiviral, antiproliferative, and immunomodulatory properties. Recombinant IFN beta is approved for the treatment of relapsing-remitting multiple sclerosis. The recombinant IFN beta protein has the theoretical potential to either treat or causes autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks. It is the most widely prescribed disease-modifying therapy for multiple sclerosis (MS). IFN beta is effective in reducing relapses in secondary progressive MS and may have a modest effect in slowing disability progression. In addition to the common antiviral activity, IFN beta also induces increased production of the p53 gene product which promotes apoptosis and thus has a therapeutic effect against certain cancers. The role of IFN-beta in bone metabolism could warrant its systematic evaluation as a potential adjunct to therapeutic regimens of osteolytic diseases. Furthermore, IFN beta might play a beneficial role in the development of chronic progressive CNS inflammation.
The cluster of differentiation (CD) system is commonly used as cell markers in immunophynotyping. Different kinds of cells in the immune system can be identified through the surface CD molecules which associating with the immune function of the cell. There are more than 320 CD unique clusters and subclusters have been identified. Some of the CD molecules serve as receptors or ligands important to the cell through initiating a signal cascade which then alter the behavior of the cell. Some CD proteins do not take part in cell signal process but have other functions such as cell adhesion. CD119 (cluster of differentiation 119), also known as IFNGR1 ( interferon gamma receptor 1), is part of the heterodimeric gamma interferon receptor which consists of IFNGR1 (CD119) and IFNGR2. The IFNGR1 gene encodes the ligand-binding chain (alpha) of the interteron receptor while IFNGR gene encodes the non-ligand binding partner. The ability of the interferon-γ was achieved through binding to the interferon receptor CD119. After binding, the products of activated T-lymphocytes interferon-γ exerts antiviral activity, growth inhibitory effect, and several immune- regulatory activities on a variety of cell types.
The tetrameric receptor complex for IFNγ consists of two subunits, IFNGR1 (IFNγ Rα) and IFNGR2 (IFNγ Rβ), through which the dimeric IFN-γ exerts its biological functions, including antiviral, antiproliferation and immune-modulatory activity in mammals. Both IFNGR1 and IFNGR2 are single transmembrane proteins belonging to the class II cytokine family. FNGR1, widely expressed in most host cells, is essential for IFNγ binding, receptor trafficking, and signal transduction. IFNGR1 possesses an intracellular Janus tyrosine kinase (JAK) 1 binding site, a signal transducer and activator of transcription 1 (STAT1) binding site. The resulting STAT1 homodimers translocate from the cytoplasm to the nucleus and bind to the interferon-gamma activated sequence (GAS) promoter to induce expression of downstream interferon stimulated genes (ISGs).
Interferon gamma receptor beta chain (IFNgammaR2), also known as IFNGR2, belongs to the type II cytokine receptor family, whose deficiency is a cause of autosomal recessive mendelian susceptibility to mycobacterial disease (MSMD), also known as familial disseminated atypical mycobacterial infection. This accessory factor is an integral part of the IFN-gamma signal transduction pathway and is likely to interact with GAF, JAK1, and/or JAK2. IFNGR2 is a component of the IFNgamma receptor complex along with the IFNgammaR alpha chain (IFNGR1), and is a new Bax suppressor. The C-terminal fragment (cytoplasmic domain) of IFNgammaR2 is expressed in human cancer cell lines of megakaryocytic cancer (DAMI), breast cancer (MDA-MD-468), and prostate cancer (PC3 cells). The Th1 cytokine IFNgamma, acting through its heterodimeric receptors, IFNgammaR1 and IFNgammaR2, in the induction/proliferation of Th1 cells, might suppress the Th2 responses that may underlie atopic asthma. IFNGR2 has always been seen as a key mechanism for shielding T lymphocytes from the antiproliferative effects of the IFNgamma-signal transducer and activator of transcription 1 (STAT1) pathway.
Lascia la tua email e seleziona le aree che vuoi seguire per ricevere novita di prodotto, approfondimenti tecnici e promozioni piu pertinenti.
Puoi scegliere le macro-aree Life Science e Diagnostica oppure le singole specializzazioni.
Seleziona uno o piu ambiti di interesse per ricevere comunicazioni piu utili e mirate.
Aggiornamenti su ricerca, strumentazione e applicazioni per il mondo Life Science.
Novita, approfondimenti e promozioni per laboratori diagnostici e flussi operativi.
2025 TEMA Ricerca - All Rights Reserved.
