![]() ![]() Therefore, IFN-γ activity is a double edged sword and immune regulatory mechanisms strive to strike a delicate balance between infection control and disease pathology in this regard. Aberrant production of IFN-γ has been linked with autoimmunity and alterations in gut flora. Hyper-activity of both IFN-γ and IL-18 can exacerbate pathogenesis in Burkholderia infections. Over-activity of IFN-γ has been reported to cause excessive tissue damage, necrosis and inflammation and may contribute to disease pathology. Undoubtedly, such an important immune mediator is under stringent regulatory control. IFN-γ increases the efficiency of immune system by enhancing its competence to deliver anti-microbial effector functions. Thus, IFN-γ is a robust protective effector molecule mediating protection against a wide array of pathogenic entities. ![]() Enhanced anti-bacterial and immune protective effects simultaneous with pro-inflammatory responses leading to protection of epithelial monolayers from pathogen mediated injury are also conferred by IFN-γ during Staphylococcus aureus infections. Natural Killer (NK) cell -mediated IFN-γ production can successfully limit Hepatitis C virus proliferation in HIV+ (Human Immunodeficiency Virus) patients. The protective benefits of IFN-γ can also been seen in the context of viral infections, as enhanced survival of neurons infected with varicella zoster virus is observed post IFN-γ treatment. The presence of IFN-γ is of absolute necessity in combating mycobacterial infections through its ability to regulate various protective functions and sustain both CD4+ and CD8+ cell activity. Release of IFN-γ by the CD4+ helper T cell population contributes to necessary effector cell activation and the generation of antibody mediated responses to Chlamydia infections. For example, the role of IFN-γ in endowing protection against Chlamydial infections is quite immense. Immunity to several pathogens is mainly governed by IFN-γ activity. Additionally, cancer cells are destroyed by IFN-γ activity via induction of an anti-proliferative state. It can serve to amplify antigen presentation through antigen presenting cells (APCs) by enhancing antigen recognition via cognate T-cell interaction, increase the production of Reactive Oxygen Species (ROS) and Reactive Nitrogen Intermediates (RNIs) and induce anti-viral responses. IFN-γ, being the central effector of cell mediated immunity, can coordinate a plethora of anti-microbial functions. In this regard, IFN-γ has a critical role in recognizing and eliminating pathogens. The human immune system is evolved to eradicate or contain any pathogenic challenge and eliminate self-altered cancerous cells. Thus, IFN-γ mediated host-pathogen interactions are critical for our understanding of disease mechanisms and these aspects also manifest enormous therapeutic importance for the annulment of various infections and autoimmune conditions. ![]() As a counter strategy, many virulent pathogenic species have devised ways to thwart IFN-γ endowed immune-protection. The functional implications of its biological activity in several infectious diseases and autoimmune pathologies are also discussed. In this review, we attempt to elucidate the biological functions and physiological importance of this versatile cytokine. The importance of IFN-γ is further reinforced by the fact that mice possessing disruptions in the IFN-γ gene or its receptor develop extreme susceptibility to infectious diseases and rapidly succumb to them. Consequently, IFN-γ stimulated cells display altered expression of many such target genes which mediate its downstream effector functions. Microarray data has unraveled numerous genes whose transcriptional regulation is influenced by IFN-γ. leads to initiation of a cascade of pro-inflammatory responses. A complex interplay between immune cell activity and IFN-γ through coordinated integration of signals from other pathways involving cytokines and Pattern Recognition Receptors (PRRs) such as Interleukin (IL)-4, TNF-α, Lipopolysaccharide (LPS), Type-I Interferons (IFNS) etc. It can exhibit its immunomodulatory effects by enhancing antigen processing and presentation, increasing leukocyte trafficking, inducing an anti-viral state, boosting the anti-microbial functions and affecting cellular proliferation and apoptosis. A key player in driving cellular immunity, IFN-γ is capable of orchestrating numerous protective functions to heighten immune responses in infections and cancers. ![]()
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