ifn-γ

IFN-γ Antagonist 1 (AYCRDGKIGPPKLDIRKEEKQI), an interferon γ (IFN γ) antagonist, effectively inhibits IFN-γ induced HLR DR antigen expression in Colon 205 cells, demonstrating an IC50 of approximately 35 μM. This compound shows promise for applications in immune regulation [1].

IFN-γ Antagonist 1 (AYCRDGKIGPPKLDIRKEEKQI) acetate, an interferon γ (IFN γ) antagonist, effectively inhibits the expression of HLR DR antigen in Colon 205 cells induced by IFN-γ, with an IC50 of approximately 35 μM. This compound holds promise for applications in immune regulation [1].

Interphotoreceptor retinoid-binding protein (1-20) (IRBP1-20), a dodecapeptide fragment of retinoid-binding protein 3, plays a crucial role in pigment regeneration by facilitating the transport of retinol and retinal between photoreceptor cells and the retinal pigment epithelium. It has been utilized to provoke autoimmune uveoretinitis in C57BL/6 mice, possessing the H-2b haplotype. Furthermore, IRBP1-20 at a concentration of 3 µM enhances the secretion of IL-4, IL-5, and IL-6 from primary mouse spleen lymphocytes. Immunization and subsequent rechallenge with IRBP1-20 lead to increased ear swelling, inflammation of ocular blood vessels, infiltration by immune cells, damage to the photoreceptor layer, and retinal detachment in IFN-γ-deficient mice.

HOXB7 (8-25), a peptide fragment derived from homeobox B7 (HOXB7)—a key controller of cell growth and oncogene activator—facilitates antigen presentation when pulsed onto dendritic cells obtained from human peripheral blood mononuclear cells (PBMCs). This process promotes the activation and interferon-gamma (IFN-γ) production by CD4+ helper T cells, triggering targeted and broad-spectrum antitumor responses.

TPP-1, a peptide inhibitor, targets the interaction between programmed cell death protein 1 (PD-1) and its ligand (PD-L1), binding specifically to PD-L1 with a dissociation constant (Kd) of 94.67 nM. At a concentration of 20 µM, TPP-1 effectively counteracts the PD-L1-induced suppression of IFN-γ production in anti-CD3-stimulated isolated human CD4+ T cells. Furthermore, TPP-1 demonstrates significant efficacy in reducing tumor volume in a mouse xenograft model of HL-60 leukemia. This model involved HL-60 cells co-cultured with anti-CD3-activated isolated human CD4+ T cells, with TPP-1 administration at a dosage of 4 mg/kg showing notable antitumor activity.

EGFRvIII peptide, a synthetic peptide mirroring the EGFRvIII fusion junction—a tumor-specific, perpetually active EGFR variant missing amino acids 6-273 of the wild-type—binds to HLA-A*0201-positive T2 cells under MHC class I at 25 µg/ml. It enables antigen presentation in dendritic cells from human peripheral blood mononuclear cells (PBMCs), thus activating CD8+ cytotoxic T lymphocytes and prompting IFN-γ production. Administered at 15 µg/animal with the TLR5 agonist flagellin B, EGFRvIII peptide elevates CD8+ T cell numbers, lowers regulatory T cells (Tregs) in the brain, diminishes tumor volume, and extends survival in a GL261 glioblastoma mouse model.

CFP10 (71–85) is an immunologically active peptide that induces IFN-γ production and cytotoxic T lymphocyte (CTL) activity in CD4+ and CD8+ T cells from individuals with diverse MHC class II and I expression profiles.

Interphotoreceptor retinoid-binding protein (651-670) (IRBP651-670), a peptide fragment of retinoid-binding protein 3 (also known as IRBP), plays a crucial role in the visual cycle by facilitating the transport of retinol and retinal between photoreceptor cells and the retinal pigment epithelium. This transport is essential for the regeneration of pigments necessary for vision. When administered at a dose of 300 µg/animal, IRBP651-670 induces autoimmune uveoretinitis in C57BL/6 mice, a model possessing the H-2b haplotype. This immunization leads to increased levels of ocular cytokines including IL-1β, IL-6, IL-17, TNF-α, and IFN-γ, promotes immune cell infiltration into the eye, and results in photoreceptor cell damage.

PD-1 PD-L1 inhibitory peptide C8 disrupts the PD-1 PD-L1 interaction, leading to the activation of CD8+ and CD4+ T cells and an increase in IFN-γ secretion. In mouse models, PD-1 PD-L1 inhibitory peptide C8 has demonstrated antitumor activity.

NFAT inhibitor. Inhibits LPS or LPS plus IFN-γ-induced IL-12 p40, IL-12 p70, IL-23 and TNF secretion from bone marrow-derived macrophages (BMDMs). Also attenuates NO production and Nos2 mRNA expression in LPS-stimulated BMDMs. Improves symptoms in a mouse

MBP (83-99) is an immunodominant epitope recognized by MBP-specific T cell lines, which stimulates both cell proliferation and IFN-γ secretion in T cells [1] [2].

Influenza NP (311-325) is a biologically active peptide consisting of amino acids 311 to 325 from the influenza virus nucleoprotein (NP). As a bona fide MHC class II-restricted epitope, it is critical for studying host immune responses during viral infection, inducing robust gamma interferon (IFN-gamma) production in intracellular cytokine assays without stimulating CD8 T-cells in mice. The presence of Glutamine (Q) or Glutamic acid (E) at the N-terminus can lead to spontaneous formation of Pyroglutamyl (pGlu) peptides, enhancing peptide stability against gastrointestinal proteases. These peptides are considered a normal variant and included in peptide purity measurements in HPLC analysis.

Tkip is a specific inhibitor of JAK2. It binds to the autophosphorylation site of JAK2, thereby inhibiting JAK2 autophosphorylation and the phosphorylation of the IFN-γ receptor subunit IFNGR-1. Tkip can suppress the antiviral activity of IFN-γ and the expression of MHC class I molecules. Tkip is applicable in studies related to the IFN-γ signaling pathway.

YH32367 (ABL105) is a bispecific antibody targeting HER2 and 4-1BB. It induces the secretion of IFN-γ, resulting in the death of tumor cells when co-cultured with hPBMC and HER2-expressing tumor cells. YH32367 demonstrates notable antitumor activity.