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Recombinant Human Interferon-gamma (IFNy)
(Cat. No.: C014)
Background:
The major interferon produced by mitogenically or antigenically stimulated lymphocytes. It is structurally different from type I interferon and its major activity is immunoregulation. It has been implicated in the expression of class II histocompatibility antigens in cells that do not normally produce them, leading to autoimmune disease. Interferon gamma is produced mainly by T-cells and natural killer cells activated by antigens, mitogens, or alloantigens. It is produced by lymphocytes expressing the surface antigens CD4 and CD8. The synthesis of IFN-gamma is induced, among other things, by Interleukin-2, FGF-basic, and EGF.
Description:
Recombinant Human Interferon gamma produced in E. coli is a single, non-glycosylated, polypeptide chain containing 144 amino acids and having a molecular mass of 16879 Dalton.
Quality Control:
Biological activity: The specific activity as determined in a viral resistance assay using VSV-WISH cells was found to be greater than 1.5 x 107 IU/ mg.
Purity: Greater than 95% as determined by
(a) Analysis by SEC-HPLC.
(b) Analysis by reducing and non-reducing SDS-PAGE Silver Stained gel.
Molecular weight: 16.8KD+/-10% determined by reduced SDS-PAGE.
Isoelectric Point: the main zone between 8.1~9.1 analysis by IEF.
Residual DNA: less than 300ng/mg analysis by solid phase blot.
UV scan: the maximal absorption wave is 280+/-3nm.
Amino-Acid Sequence: The sequence of the first fifteen N-terminal amino acids was determined and was found to be Gln-Asn-Pro-Tyr-Val-Lys-Glu-Ala-Glu-Asn-Leu-Lys-Lys- Tyr-Phe.
Residual host cell protein: less than 0.1% analysis by ELISA.
Endotoxin: Less than 1ng/µg (1IEU/µg) determined by LAL test.
Formulation: The protein was lyophilized after extensive dialysis from a concentrated (1mg/ml) solution in 10mM sodium Phosphate buffer pH=7.4+/-0.1.
Storage: Lyophilized rHuIFN-gamma although stable at room temperature for 3 weeks, should be stored desiccated below -18oC. Upon reconstitution rHuIFN-gamma should be stored at 4oC between 2-7 days and for future use below -18oC. For long-term storage it is recommended to add a carrier protein (0.1% HSA or BSA).
Please avoid freeze-thaw cycles.
Reconstitution: It is recommended to reconstitute the lyophilized rHuIFN-gamma in sterile 18MΩ-cm H2O not less than 100µg/ml, which can then be further diluted to other aqueous solutions.
Latest Publications:
1: PLoS ONE 2009 ;Vol 4(1)
The impact of HIV infection and CD4 cell count on the performance of an interferon gamma release assay in patients with pulmonary tuberculosis.
[Abstract] BACKGROUND: The performance of the tuberculosis specific Interferon Gamma Release Assays (IGRAs) has not been sufficiently documented in tuberculosis- and HIV-endemic settings. This study evaluated the sensitivity of the QuantiFERON TB-Gold In-Tube (QFT-IT) in patients with culture confirmed pulmonary tuberculosis (PTB) in a TB- and HIV-endemic population and the effect of HIV-infection and CD4 cell count on test performance. METHODOLOGY/PRINCIPAL FINDINGS: 161 patients with sputum culture confirmed PTB were subjected to HIV- and QFT-IT testing and measurement of CD4 cell count. The QFT-IT was positive in 74% (119/161; 95% CI: 67-81%). Sensitivity was higher in HIV-negative (75/93) than in HIV-positive (44/68) patients (81% vs. 65%, p = 0.02) and increased
with CD4 cell count in HIV-positive patients (test for trend p = 0.03). 23 patients (14%) had an indeterminate result and this proportion decreased with increasing CD4 cell count in HIV-positive patients (test for trend p = 0.03). Low CD4 cell count (<300 cells/microl) did not account for all QFT-IT indeterminate nor all negative results. Sensitivity when excluding indeterminate results was 86% (95% CI: 81-92%) and did not differ between HIV-negative and HIV-positive patients (88 vs. 83%, p = 0.39). CONCLUSIONS/SIGNIFICANCE: Sensitivity of the QFT-IT for diagnosing active PTB infection was reasonable when excluding indeterminate results and in HIV-negative patients. However, since the test missed more than 10% of patients, its potential as a rule-out test for active TB disease is limited.
Furthermore, test performance is impaired by low CD4 cell count in HIV-positive patients and possibly by other factors as well in both HIV-positive and HIV-negative patients. This might limit the potential of the test in populations where HIV-infection is prevalent.
2: J Immunol 2009 Feb;Vol 182(3)
The Adaptor Molecule Signaling Lymphocytic Activation Molecule-Associated Protein (SAP) Regulates IFN-{gamma} and IL-4 Production in V{alpha}14 Transgenic NKT Cells via Effects on GATA-3 and T-bet Expression.
[Abstract] NKT cells comprise a rare regulatory T cell population of limited TCR diversity, with most cells using a Valpha14Jalpha18 TCR. These cells exhibit a critical dependence on the signaling adapter molecule, signaling lymphocytic activation molecule-associated protein (SAP), for their ontogeny, an aspect not seen in conventional alphabeta T cells. Prior studies demonstrate that SAP enhances TCR-induced activation of NF-kappaB in CD4(+) T cells. Because NF-kappaB is required for NKT cell development, SAP might promote the ontogeny of this lineage by signaling to NF-kappaB. In this study, we demonstrate that forced expression of the NF-kappaB target gene, Bcl-x(L), or inhibitory NF-kappaB kinase beta, a catalytic subunit of the IkappaB kinase complex essential for
NF-kappaB activation, fails to restore NKT cell development in sap(-/-) mice, suggesting that SAP mediates NKT cell development independently of NF-kappaB. To examine the role of SAP in NKT cell function, we generated NKT cells in sap(-/-) mice by expressing a transgene encoding the Valpha14Jalpha18 component of the invariant TCR. These cells bound alpha-galactosylceramide-loaded CD1d tetramers, but exhibited a very immature CD24(+)NK1.1(-) phenotype. Although sap(-/-) tetramer-reactive cells proliferated in response to TCR activation, they did not produce appreciable levels of IL-4 or IFN-gamma. The reduction in cytokine production correlated with the near absence of GATA-3 and T-bet, key transcription factors regulating cytokine expression and maturation of NKT cells. Ectopic expression of
GATA-3 partially restored IL-4 production by the NKT cells. Collectively, these data suggest that by promoting GATA-3 and T-bet expression, SAP exerts control over NKT cell development and mature NKT cell cytokine production.
3: J Immunol 2009
Feb;Vol 182(3)
MicroRNA-513 regulates B7-H1 translation and is involved in IFN-gamma-induced B7-H1 expression in cholangiocytes.
[Abstract] Biliary epithelial cells (cholangiocytes) respond to proinflammatory cytokines such as IFN-gamma and actively participate in the regulation of biliary inflammatory response in the liver. B7-H1 (also known as CD274 or PD-L1) is a member of the B7 costimulatory molecules and plays a critical immunoregulatory role in cell-mediated immune responses. In this study, we show that resting human cholangiocytes in culture express B7-H1 mRNA, but not B7-H1 protein. IFN-gamma induces B7-H1 protein expression and alters the microRNA (miRNA) expression profile in cholangiocytes. Of those IFN-gamma-down-regulated miRNAs, we identified microRNA-513 (miR-513) with complementarity to the 3'-untranslated region of B7-H1 mRNA. Targeting of the B7-H1 3'-untranslated region by
miR-513 results in translational repression. Transfection of cholangiocytes with an antisense oligonucleotide to miR-513 induces B7-H1 protein expression. Additionally, transfection of miR-513 precursor decreases IFN-gamma-induced B7-H1 protein expression and consequently influences B7-H1-associated apoptotic cell death in cocultured Jurkat cells. Thus, miR-513 regulates B7-H1 translation and is involved in IFN-gamma-induced B7-H1 expression in human cholangiocytes, suggesting a role for miRNA-mediated gene silencing in the regulation of cholangiocyte response to IFN-gamma.
4: J Immunol 2009 Feb;Vol 182(3)
Differentiated human alveolar type II cells secrete antiviral IL-29 (IFN-lambda1) in response to influenza A infection.
[Abstract] Alveolar type II epithelial cells (ATIIs) are one of the primary targets for influenza A pneumonia. The lack of a culture system for maintaining differentiated ATIIs hinders our understanding of pulmonary innate immunity during viral infection. We studied influenza A virus (IAV)-induced innate immune responses in differentiated primary human ATIIs and alveolar macrophages (AMs). Our results indicate that ATIIs, but not AMs, support productive IAV infection. Viral infection elicited strong inflammatory chemokine and cytokine responses in ATIIs, including secretion of IL-8, IL-6, MCP-1, RANTES, and MIP-1beta, but not TNF-alpha, whereas AMs secreted TNF-alpha as well as other cytokines in response to infection. Wild-type virus A/PR/8/34 induced a greater cytokine
response than reassortant PR/8 virus, A/Phil/82, despite similar levels of replication. IAV infection increased mRNA expression of IFN genes IFN-beta, IL-29 (IFN-lambda1), and IL-28A (IFN-lambda2). The major IFN protein secreted by type II cells was IL-29 and ATIIs appear to be a major resource for production of IL-29. Administration of IL-29 and IFN-beta before infection significantly reduced the release of infectious viral particles and CXC and CC chemokines. IL-29 treatment of type II cells induced mRNA expression of antiviral genes MX1, OAS, and ISG56 but not IFN-beta. IL-29 induced a dose-dependent decrease of viral nucleoprotein and an increase of antiviral genes but not IFN-beta. These results suggest that IL-29 exerts IFN-beta-independent protection in type II cells through direct
activation of antiviral genes during IAV infection.
Domain Info
GeneBank Entry:
NM_000619
Protein Accession No.:
NP_000610
Protein Sequence:
MQDPY VKEAE NLKKY FNAGH SDVAD NGTLF LGILK NWKEE SDRKI MQSQI VSFYF KLFKN FKDDQ SIQKS VETIK EDMNV KFFNS NKKKR DDFEK LTNYS VTDLN VQRKA IHELI QVMAE LSPAA KTGKR KRSQM LFRGR RASQ
Transcript Info
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*NOTE: ALL PRODUCTS ARE FOR RESEARCH USE ONLY |
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