IFNGR2 antibody
- Known as:
- IFNGR2 (anti-)
- Catalog number:
- orb5501
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- IFNGR2 antibody
Related genes to: IFNGR2 antibody
- Gene:
- IFNGR2 NIH gene
- Name:
- interferon gamma receptor 2
- Previous symbol:
- IFNGT1
- Synonyms:
- AF-1
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: IFNGR2 antibody
Related articles to: IFNGR2 antibody
- Mendelian susceptibility to mycobacterial disease (MSMD) is a rare type of inborn error of immunity (IEI) characterized by increased vulnerability to mycobacterial infection. Evolvement of secondary hemophagocytic lymphohistiocytosis (HLH), a life-threatening condition where hemophagocytosis is seen either in the bone marrow, the spleen or lymph node has been recently recognized in this rare disease. Herein we illustrate the role of lymph node cytology in alerting clinicians to the possibility of evolving HLH in a case of MSMD. A 4-month old male infant presented with genetically confirmed MSMD with homozygous mutation in IFNGR2 (+). He received anti tubercular treatment and best supportive care. At 22 months he presented again with generalized lymphadenopathy, massive splenomegaly, bicytopenia and high grade fever. The cervical node FNAC showed, in addition to ill formed granulomas and acid-fast bacilli, features of hemophagocytosis with engulfed intact lymphocytes, neutrophils, and RBCs within macrophages. A concern for secondary HLH was raised by the cytopathologists and further lab investigations recommended. The patient was clinically monitored for any further morbidity. Since HLH is increasingly being reported as an infectious complication in IEI a high index of suspicion will help in its early detection in MSMD. Lymph node FNAC is a quick and easy tool in diagnosing the same. - Source: PubMed
Publication date: 2026/07/22
Soni DeeptiMukhopadhyay SramanaPanwar HemlataJain SuramyaWalke VaishaliChaudhary NarendraMaheshwari Mahesh - In mammals, IFN-γ acts as a critical cytokine that triggers intracellular signaling by binding to specific IFNGR1 and IFNGR2 receptors. Unlike mammals, teleosts possess two members of type II IFN genes (IFN-γ and IFN-γrel), two IFNGR1 paralogs (CRFB13 and CRFB17) and a single IFNGR2 homolog (CRFB6). Despite the identification of type II IFN receptors in multiple fish species, the molecular features, expression profiles and signaling-associated function remain limited. In this study, three type II interferon receptor genes, AjCRFB6, AjCRFB13 and AjCRFB17 were identified in Japanese eel, Anguilla japonica. All three receptors possess typical conserved structural domains of class II cytokine receptors. Phylogenetic analysis assigned them to respective teleost CRFB subfamilies. These three genes displayed broad tissue expression, with predominant abundance in immune-related spleen, trunk kidney and liver tissues. Following Poly(I:C) stimulation, AjCRFB6 and AjCRFB13 generally showed significant upregulation from 6 hpi in the liver, trunk kidney and spleen, maintaining elevated expression at most subsequent time points, while AjCRFB17 exhibited a distinct expression pattern from AjCRFB6 and AjCRFB13, with a generally downregulated or unchanged expression trend across most tested time points. It was revealed that AjIFN-γ initiates downstream ISGs transcription and STAT1 phosphorylation through AjCRFB6+AjCRFB13 or AjCRFB6+AjCRFB13+AjCRFB17, whereas all AjCRFB17-containing complexes confer responsiveness to AjIFN-γrel. Furthermore, co-immunoprecipitation assays revealed that AjSTAT1 specifically interacts with AjCRFB13 and AjCRFB17, but not with AjCRFB6. These results provide a reference for further exploring the potential roles of type II IFN receptors in teleost immunity and signaling. - Source: PubMed
Publication date: 2026/07/15
Su ShengnanLin ChangjiZeng ZhanzhuangLi DongliXu JisongXiong JingPang HuanyingHuang WenshuLiang Ying - Interferon (IFN)-resistant cell clones 3Cl8 and 3γR8, isolated from wild-type Friend erythroleukemia cells 745A were characterized to identify the resistance defect. The 3Cl8 cell clone is resistant to type I IFNs and sensitive to type II IFN, whereas 3γR8, derived from 3Cl8, is resistant to both type I and II IFNs. Here, we report that no activation of the JAK-STAT pathway is detected after IFN treatment of resistant cells. Interestingly, the absence of major transcripts of the IFNAR2 receptor chain has been observed in type I IFN-resistant cells, and a point mutation relative to the IFNGR2 receptor chain (β chain) has been identified in type II IFN-resistant cells, inducing a frameshift leading to premature termination of translation. In addition, we have identified a new polymorphism of the murine IFNAR1 chain and possibly the presence of a murine IFNAR2b transmembrane, non-transducing chain in 745A cells, similar to that observed in humans and differing from previous reports on other murine systems. - Source: PubMed
Publication date: 2026/06/30
Percario Zulema AntoniaMangino GiorgioRaponi AriannaFratini EmilianoVaccari GabrieleGiannessi FlaviaFiorucci GiannaCervelli ManuelaRomeo GiovannaAffabris Elisabetta - Diabetic kidney disease (DKD) is a major microvascular complication of diabetes, with microcirculatory dysfunction and immune injury as its core pathological features. Extracellular vesicles (EVs) act as key mediators of intercellular communication, but it remains unclear whether EV-encapsulated microRNAs (miRNAs) are involved in the crosstalk between endothelial cells (ECs) and monocytes in DKD. - Source: PubMed
Publication date: 2026/06/11
Jing JiaxingAn JiashengChen XiangmeiCong BinYu WentaoGao Weijuan - Interferon-gamma (IFN-γ) serves as an inflammatory cytokine essential for modulating innate and cell-mediated immune responses by associating with a receptor complex composed of IFNGR1 and IFNGR2. In this research, the entire cDNA of IFNGR2 from Nibea albiflora was cloned and functionally analyzed (referred to as NaIFNGR2), with the complete cDNA sequence measuring 924 bp and encoding 307 amino acids. The phylogenetic analysis and multiple sequence alignment revealed a significant similarity of NaIFNGR2 with homologous sequences found in other bony fish, especially within the FNⅢ domain and the transmembrane region. Real-time PCR analysis revealed that NaIFNGR2 was consistently expressed across all examined tissues, including the head-kidney, spleen, liver, kidney, gill, muscle, and blood, with the highest levels found in the gills. Following stimulation with Polyinosinic-polycytidylic acid (Poly (I:C)), Vibrio alginolyticus, or Vibrio parahaemolyticus, the mRNA levels of NaIFNGR2 showed an increase in a time-dependent manner. Subcellular localization studies indicated that NaIFNGR2 resided on the cell membrane and NaIFN-γ, once synthesized within the cell, was transported to the membrane to interact with NaIFNGR2. Additionally, NaIFNGR1 and NaIFNGR2 were completely co-localized on the cell membrane, which was consistent with the findings that NaIFNGR1 and NaIFNGR2 could form a heterodimeric complex. Being treated with the NaIFN-γ recombinant protein, both alone and in combination with LPS, various concentrations of NaIFN-γ were non-toxic to the growth of RAW 264.7 macrophages and significantly promoted their proliferation. The expression levels of IL-1β, IL-6, and TNF-α proteins were markedly upregulated in a concentration- and time-dependent manner following 24 and 48 h of combined stimulation. Furthermore, the secretion of nitric oxide (NO) was significantly increased after 36 and 48 h of stimulation, highlighting the regulatory effect of NaIFN-γ on macrophages and its influence on the inflammatory response. Collectively, the findings indicated that the NaIFN-γ ligand-receptor system was present in N. albiflora and played a crucial role in the immune response to pathogenic bacterial infections, enhancing our comprehension of the function of IFN-γ within the immunomodulatory processes of teleosts. - Source: PubMed
Publication date: 2026/04/27
Yuan HanbingLiu YongxinZhou XuXu DongdongChi ChangfengLü ZhenmingLiu Huihui