Interferon-gamma (IFN-γ) is a type of protein known as a cytokine, produced primarily by T cells and natural killer (NK) cells, key components of the immune system. It is part of the Type II class of interferons and plays a central role in stimulating and modulating immune response to various pathogens (1).

Production of IFN-γ is usually induced in response to specific antigens or pathogen-associated molecular patterns (PAMPs), leading to the activation of T cells and NK cells. This process is regulated through a complex signaling cascade involving several types of immune cells and molecules, such as Interleukin-12 (IL-12) (2).

Once released, IFN-γ acts upon its specific receptors present on the surface of various immune cells. These receptors are called interferon-gamma receptors (IFNγR), which, once bound by IFN-γ, initiate a signaling cascade that results in the activation of a transcription factor called STAT1 (Signal Transducer and Activator of Transcription 1) (3). STAT1 translocates into the nucleus and regulates the expression of several genes involved in immune responses, thereby modulating cellular functions.

IFN-γ has several effects on the immune system:

Antiviral Activity: IFN-γ enhances the body’s response to viral infections by promoting the production of proteins that inhibit viral replication (4). This cytokine can also boost the activity of cytotoxic T lymphocytes and NK cells, promoting the destruction of virus-infected cells (5).

Antitumor Activity: IFN-γ has been found to inhibit the proliferation of various types of cancer cells and to promote apoptosis (controlled cell death). This effect is achieved through both direct action on tumor cells and by enhancing the cytotoxic activity of NK cells and T cells (6).

Immunoregulation: IFN-γ is a crucial cytokine for Th1 cell differentiation, which are a subset of T cells that play an essential role in cellular immunity against intracellular pathogens. It also inhibits the differentiation of Th2 cells and regulatory T cells, thus skewing the immune response towards a Th1 phenotype. Furthermore, IFN-γ enhances the expression of MHC (Major Histocompatibility Complex) class I and II molecules on the surface of various cells, promoting antigen presentation and subsequent activation of T cells (7).

Anti-inflammatory Activity: In some contexts, IFN-γ has an anti-inflammatory role, as it can inhibit the production of pro-inflammatory cytokines and chemokines, reducing inflammation and tissue damage (8).

Interferon-gamma is a critical modulator of immune responses, participating in antiviral, antitumor, immunoregulatory, and anti-inflammatory actions. Its importance is evident in patients with defects in IFN-γ production or signaling, who suffer from recurrent and severe infections, highlighting its central role in host defense (9).

If you have any questions about the Berkeley Formula Diindolylmethane (DIM) Supplement & Immune System Booster, please feel free to contact our customer service department at 877-777-0719 (9AM-5PM M-F PST) and our representatives will be happy to answer any questions that you may have. We will be glad to share with you why the Berkeley Formula is the DIM supplement of choice by nutritional scientists, medical professionals and biomedical investigators worldwide.

References:

Billiau, A., & Matthys, P. (2009). Interferon-gamma: a historical perspective. Cytokine & growth factor reviews, 20(2), 97-113.
Okamura, H., Tsutsui, H., Komatsu, T., Yutsudo, M., Hakura, A., Tanimoto, T., … & Nakanishi, K. (1995). Cloning of a new cytokine that induces IFN-γ production by T cells. Nature, 378(6552), 88-91.
Platanias, L. C. (2005). Mechanisms of type-I- and type-II-interferon-mediated signalling. Nature Reviews Immunology, 5(5), 375-386.
Der, S. D., Zhou, A., Williams, B. R., & Silverman, R. H. (1998). Identification of genes differentially regulated by interferon alpha, beta, or gamma using oligonucleotide arrays. Proceedings of the National Academy of Sciences, 95(26), 15623-15628.
Biron, C. A., Nguyen, K. B., Pien, G. C., Cousens, L. P., & Salazar-Mather, T. P. (1999). Natural killer cells in antiviral defense: function and regulation by innate cytokines. Annual review of immunology, 17(1), 189-220.
Zaidi, M. R., & Merlino, G. (2011). The two faces of interferon-γ in cancer. Clinical Cancer Research, 17(19), 6118-6124.
Schroder, K., Hertzog, P. J., Ravasi, T., & Hume, D. A. (2004). Interferon-γ: an overview of signals, mechanisms and functions. Journal of leukocyte biology, 75(2), 163-189.
Nathan, C. F., Murray, H. W., Wiebe, M. E., & Rubin, B. Y. (1983). Identification of interferon-γ as the lymphokine that activates human macrophage oxidative metabolism and antimicrobial activity. The Journal of experimental medicine, 158(3), 670-689.
Jouanguy, E., Altare, F., Lamhamedi, S., Revy, P., Emile, J. F., Newport, M., … & Casanova, J. L. (1996). Interferon-γ–receptor deficiency in an infant with fatal bacille Calmette–Guérin infection. New England Journal of Medicine, 335(26), 1956-1961.

If you have any questions about the Berkeley Formula Diindolylmethane (DIM) Supplement & Immune System Booster, please feel free to contact our customer service department at 877-777-0719 (9AM-5PM M-F PST) and our representatives will be happy to answer any questions that you may have. We will be glad to share with you why the Berkeley Formula is the DIM supplement of choice by nutritional scientists, medical professionals and biomedical investigators worldwide.