Product: Interferon gamma Antibody
Catalog: DF6045
Source: Rabbit
Application: WB, IHC
Reactivity: Human, Mouse, Rat
Mol.Wt.: 19-25kDa; 19kD(Calculated).
Uniprot: P01579
RRID: AB_2838015

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Interferon gamma Antibody detects endogenous levels of total Interferon gamma.
Cite Format: Affinity Biosciences Cat# DF6045, RRID:AB_2838015.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


IFG; IFI; IFN gamma; IFN, immune; IFN-gamma; IFNG; IFNG_HUMAN; Immune interferon; Interferon gamma;



Released primarily from activated T lymphocytes.

Interferons (IFNs) appear both locally and systematically early after viral infection and participate in limiting the spread of infection. They also affect cell differentiation, growth, surface antigen expression and immunoregulation (1). There are three naturally occurring interferons: α, β and γ. IFN-α is derived from lymphoblastic tissue and has a number of therapeutic applications in the treatment of various human cancers and diseases of viral origin. Recombinant IFN-α from both natural and synthetic genes binds to a common cell surface receptor and induces antiviral activity in a variety of cell lines. When binding to discrete cell surface receptors on target cells, IFN-α induces rapid changes in Jak/Stat phosphorylation, which initiates the Jak/Stat signaling pathway (2). IFN-α signaling also involves production of DAG without an increased intracellular free calcium concentration and the subsequent activation of calcium-independent isoforms of PKC (β and ε) (3). All IFN-α signaling pathways lead to final alterations of gene expression, which mediate their pleiotropic biologic activities. IFN-γ, also known as type II interferon, is produced mainly in activated T lymphocytes and natural killer cells (4) and has broad effects on various cells of the immune system. Many signaling proteins including IL-2, FGF, and EGF induce the synthesis of IFN-γ.

PTMs - P01579 As Substrate

Site PTM Type Enzyme
N48 N-Glycosylation
S74 Phosphorylation
S92 Phosphorylation
S107 Phosphorylation
N120 N-Glycosylation

Research Backgrounds


Produced by lymphocytes activated by specific antigens or mitogens. IFN-gamma, in addition to having antiviral activity, has important immunoregulatory functions. It is a potent activator of macrophages, it has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of the type I interferons.


Proteolytic processing produces C-terminal heterogeneity, with proteins ending alternatively at Gly-150, Met-157 or Gly-161.

Subcellular Location:


Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Released primarily from activated T lymphocytes.

Subunit Structure:



Belongs to the type II (or gamma) interferon family.

Research Fields

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TGF-beta signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Jak-STAT signaling pathway.   (View pathway)

· Genetic Information Processing > Folding, sorting and degradation > Proteasome.

· Human Diseases > Endocrine and metabolic diseases > Type I diabetes mellitus.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Systemic lupus erythematosus.

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Human Diseases > Immune diseases > Allograft rejection.

· Human Diseases > Immune diseases > Graft-versus-host disease.

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Antigen processing and presentation.   (View pathway)

· Organismal Systems > Immune system > Natural killer cell mediated cytotoxicity.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)


1). Chen X et al. ILT4 inhibition prevents TAM- and dysfunctional T cell-mediated immunosuppression and enhances the efficacy of anti-PD-L1 therapy in NSCLC with EGFR activation. Theranostics 2021 Jan 19;11(7):3392-3416. (PubMed: 33537094) [IF=11.600]

Application: IHC    Species: human    Sample: tumor cells

Figure 4. | ILT4 in EGFR-activated tumor cells impaired the proliferation and cytotoxicity of T cells. (A-B) High ILT4 expression in tumor cells of NSCLC tissues was correlated with decreased infiltration and IFN-γ generation in CD3+ T cells detected by IHC analysis. (A) Images of ILT4 expression, T cell infiltrates, and IFN-γ levels, brown granules represent positive staining.

2). Yarong Du et al. The Reduced Oligomerization of MAVS Mediated by ROS Enhances the Cellular Radioresistance. OXID MED CELL LONGEV 2020 Mar 4;Article ID 2167129 [IF=7.310]

3). Tu W et al. Acupoint application inhibits nerve growth factor and attenuates allergic inflammation in allergic rhinitis model rats. J Inflamm (Lond) 2020 Feb 10;17:4 (PubMed: 32063751) [IF=6.283]

Application: IF/ICC    Species: rat    Sample: mast cells

Fig. 3| Effect of AAT on the expression of NGF、IL-4 and IFN-γ protein in nasal mucosa of AR rats. . c The effects of Acupoint Application Therapy on mast cells localization of IFN-γ with Olympus microscope. The values represent the mean± S.E.M (n=3/group). Compared with M group, Significant differences *P<0.05, **P<0.01, ***P<0.001; compared with 1HG group, Significant differences# P< 0.05, ## P<0.01, ### P<0.001; AAT, Acupoint Application Therapy; AR, allergic rhinitis; NGF, nerve growth factor;1HH, prescription NO.2 mixed with Honey; 1HG, prescription NO.1 mixed with fresh Ginger Juice; M group, model group; C group, control group

4). Song Y et al. Caveolin-1 protects against DSS-induced colitis through inhibiting intestinal nitrosative stress and mucosal barrier damage in mice. Biochem Pharmacol 2020 Jul 14;114153. (PubMed: 32679126) [IF=6.100]

Application: IHC    Species: mouse    Sample: colon

Fig. 2. |Down-regulation of Cav-1 in the colon tissue and accompany with the increase of INOS and NO levels after DSS administration. (a) Western blot analysis for detecting Cav-1, Bcl-2, P-Stat3 and Stat3 expression incolon tissues and quantified in a bar graph. (b) Immunofluorescence analysis for detecting Cav-1 and the macrophage-specific marker F4/80 expression in the colon tissue.. (e, f) Immunohistochemistry analysis for inflammatory factors TNF-α and IFN-γ.

5). Wang M et al. Berberine combined with cyclosporine A alleviates acute graft-versus-host disease in murine models. Int Immunopharmacol 2020 Feb 9;81:106205 (PubMed: 32050154) [IF=5.714]

Application: WB    Species: Mice    Sample: liver and intestinal tissues

Fig. 3. BBR and the concomitant treatment of BBR and CsA reduced the inflammatory response and oxidative stress in liver and intestine of GVHD models. The changes of inflammatory cytokines IFN-γ, TNF-α, IL-6 and IL-17 in liver (A, C, E and G) and intestine (B, D, F and H) by western blot analysis. The contents of ROS and MDA in liver (I, K) and intestine (J, L). Data are represented as means ± SD (n = 6). **p < 0.01 versus the control. #p < 0.05 and ##p < 0.01 versus the GVHD group. &p < 0.05 and &&p < 0.01 versus the GVHD + BBR group. † p < 0.05 and ††p < 0.01 versus the GVHD + CsA group.

6). Xie F et al. Costunolide Improved Dextran Sulfate Sodium-Induced Acute Ulcerative Colitis in Mice Through NF-κB, STAT1/3, and Akt Signaling Pathways. Int Immunopharmacol 2020 May 12;84:106567. (PubMed: 32413737) [IF=5.714]

Application: IHC    Species: mouse    Sample: colon

Fig. 4. |Costunolide suppressed DSS-induced expression of pro-inflammatory cytokines in mice. RT-qPCR assay showed the effect of costunolide on the mRNA expression of IL-1β, IL-6, TNF-α, and IFN-γ (A). IHC analysis displayed the effect of costunolide on the protein expression of IL-1β (B), IL-6 (C), TNF-α (D), and IFN-γ(E).

7). Huang J et al. Palovarotene Can Attenuate Heterotopic Ossification Induced by Tendon Stem Cells by Downregulating the Synergistic Effects of Smad and NF-κB Signaling Pathway following Stimulation of the Inflammatory Microenvironment. Stem Cells Int 2022 Apr 28;2022:1560943. (PubMed: 35530413) [IF=5.131]

Application: IHC    Species: Rat    Sample: tendon stem cells (TSCs)

Figure 6 In vitro experimental further verifies the effects of palovarotene and Smad and NF-κB signaling pathways in HO. In immunohistochemistry, the positive rate of inflammation such as TNF-α, TGF-β, IFN-γ, IL-1β, and MMP-9 was increased (a), as well as p65, ID1, p-SMAD1/5, and osteogenic genes, concluding OCN and SOX9 (b). Scale bar = 25 μm. (c) Immunofluorescence and quantitative analysis against Smad5. Scale bar = 25 μm. Data are means ± SD (n = 3) ∗p < 0.05 and ∗∗p < 0.01. #p < 0.05 and ##p < 0.01. (d) The mRNA expression, Western blot analysis of tendon tissues, and relevant quantitative analysis of p65, ID1, OCN, and SOX9. Data are means ± SD (n = 3). ∗p < 0.05 and ∗∗p < 0.01. #p < 0.05 and ##p < 0.01.

8). Dou B et al. Blood HDAC4 Variation Links With Disease Activity and Response to Tumor Necrosis Factor Inhibitor and Regulates CD4+ T Cell Differentiation in Ankylosing Spondylitis. Front Med (Lausanne) 2022 May 6;9:875341. (PubMed: 35602496) [IF=5.091]

9). Liang X et al. GOLM1 is related to the inflammatory/immune nature of uveal melanoma and acts as a promising indicator for prognosis and immunotherapy response. Front Genet 2022 Nov 18;13:1051168. (PubMed: 36468024) [IF=4.599]

10). Yang Z et al. ILT4 in Colorectal Cancer Cells Induces Suppressive T Cell Contexture and Disease Progression. Onco Targets Ther 2021 Jul 20;14:4239-4254. (PubMed: 34321889) [IF=4.345]

Application: IHC    Species: Human    Sample: TILs

Figure 5 ILT4 in CRC cells was inversely correlated with IFN-γ production in TILs. (A and B) IHC analysis showed that CRC tissues with high ILT4 expression displayed lower IFN-γ levels in TILs, compared with the CRC tissues with low ILT4 expression. (A) Representative imaging of ILT4 and IFN-γ levels in CRC tissues and (B) the statistical results in 145 patients. Scale bar: 20μm. (C) High IFN-γ levels in TILs were correlated with decreased lymph node involvement and earlier tumor stage, compared with the IFN-γ-low group. The medium proportion of IFN-γ+ cells in TILs was used to discriminate IFN-γ-low and -high groups. (D) High IFN-γ expression in TILs was correlated with superior patient OS. The cutoff value for high and low IFN-γ was as described in (C). (E and F) IHC analysis showed that high ILT4 expression in CRC cells predicted declined IFN-γ+ TIL frequency in the tumor center (E) but not in the invasive margin (F). The cutoff score for high and low ILT4 groups was the same as in Figure 1C. (G) The frequency of IFN-γ+ TILs was positively correlated with CD8+ T but not CD4+ T cell density by IHC analysis. (H) IFN-γ expression was positively correlated with CD8 levels in CRC tissues by analyzing TCGA database. The online tool GEPIA was used to analyze the correlation between IFN-γ and CD8 levels. (I) Patients with high ILT4 and low IFN-γ levels showed more advanced lymph node involvement, perineural invasion, and tumor stage than those in the ILT4-low IFN-γ-high group. (J) High ILT4 in combination with low IFN-γ levels predicted poor patient OS relative to the ILT4-low IFN-γ-high counterpart. *p<0.05; **p<0.01; ***p<0.001.

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