C57BL/6NCya-Ifng^em1/Cya

Ifng, also known as Interferon gamma, is a cytokine that plays a crucial role in the immune system. It enhances immune function, for example, by promoting the activation of immune cells such as macrophages. It is involved in both innate and adaptive immune responses and is associated with pathways like the JAK-STAT signaling pathway [2].

In autism spectrum disorder (ASD), real-time PCR showed significant up-regulation of IFNG in children with ASD compared to controls, suggesting a functional disruption in the IFNG/IFNG-AS1 regulatory network, which may contribute to the chronic inflammatory aspect of ASD [1]. In colon adenocarcinoma (COAD), IFNG was significantly correlated with tumor immunotherapy biomarkers, and high IFNG expression was associated with longer disease-free survival. Also, autophagy and IFNG were related to cisplatin chemosensitivity, indicating IFNG might be a potential targeted therapy for cisplatin-resistant colon cancer [3]. Polymorphisms in IFNG were associated with tuberculosis in the Tibetan population, with certain alleles acting as protective or risk factors [4,6]. In pancreatic cancer, CDK1/2/5 inhibition can overcome IFNG-mediated adaptive immune resistance, turning a 'cold' tumor microenvironment into a 'hot' one [5]. In atopic dermatitis, high and low IFNG-expressing subgroups were characterized, corresponding to intrinsic and extrinsic AD classifications, which may be considered for evaluating therapeutic efficacy in the future [7].

In conclusion, Ifng is essential in immune-related biological processes. Its dysregulation is implicated in various diseases including ASD, COAD, tuberculosis, pancreatic cancer, and atopic dermatitis. Studies using different research models, though not specifically KO/CKO mouse models in the provided references, have helped to understand its role in these disease conditions, providing insights into potential therapeutic strategies.

References:

1. Fallah, Hamid, Sayad, Arezou, Ranjbaran, Fatemeh, Ghafouri-Fard, Soudeh, Taheri, Mohammad. 2019. IFNG/IFNG-AS1 expression level balance: implications for autism spectrum disorder. In Metabolic brain disease, 35, 327-333. doi:10.1007/s11011-019-00510-4. https://pubmed.ncbi.nlm.nih.gov/31728886/

2. Benci, Joseph L, Johnson, Lexus R, Choa, Ruth, Kambayashi, Taku, Minn, Andy J. . Opposing Functions of Interferon Coordinate Adaptive and Innate Immune Responses to Cancer Immune Checkpoint Blockade. In Cell, 178, 933-948.e14. doi:10.1016/j.cell.2019.07.019. https://pubmed.ncbi.nlm.nih.gov/31398344/

3. Yue, Taohua, Cai, Yunlong, Zhu, Jing, Wang, Pengyuan, Rong, Long. 2023. Autophagy-related IFNG is a prognostic and immunochemotherapeutic biomarker of COAD patients. In Frontiers in immunology, 14, 1064704. doi:10.3389/fimmu.2023.1064704. https://pubmed.ncbi.nlm.nih.gov/36756126/

4. Wu, S-Q, Ding, X-J, Yang, Q-L, Wang, M-G, He, J-Q. . IFNG and IFNGR1 polymorphisms are associated with tuberculosis: a case-control study. In European review for medical and pharmacological sciences, 26, 8777-8787. doi:10.26355/eurrev_202212_30549. https://pubmed.ncbi.nlm.nih.gov/36524496/

5. Huang, Jin, Chen, Pan, Liu, Ke, Kang, Rui, Tang, Daolin. 2020. CDK1/2/5 inhibition overcomes IFNG-mediated adaptive immune resistance in pancreatic cancer. In Gut, 70, 890-899. doi:10.1136/gutjnl-2019-320441. https://pubmed.ncbi.nlm.nih.gov/32816920/

6. Wu, Shouquan, Wang, Yu, Zhang, Miaomiao, Wang, Minggui, He, Jian-Qing. 2019. Genetic variants in IFNG and IFNGR1 and tuberculosis susceptibility. In Cytokine, 123, 154775. doi:10.1016/j.cyto.2019.154775. https://pubmed.ncbi.nlm.nih.gov/31310896/

7. Wasserer, Sophia, Jargosch, Manja, Mayer, Kristine E, Eyerich, Kilian, Lauffer, Felix. 2024. Characterization of High and Low IFNG-Expressing Subgroups in Atopic Dermatitis. In International journal of molecular sciences, 25, . doi:10.3390/ijms25116158. https://pubmed.ncbi.nlm.nih.gov/38892346/