There is only one class II interferon, interferon gamma. Interferon gamma is produced by T lymphocytes when stimulated with antigens or mitogens. Interferon gamma binds to a distinct receptor, the interferon gamma receptor (IFNGR) consisting of the two subunits IFNGR1 (previously α chain) and IFNGR2 (previously β chain or accessory factor).
Interferon-gamma, which is dimeric in solution, crystallizes with two dimers related by a noncrystallographic twofold axis in the asymmetric unit. The protein is primarily alpha helical, with six helices in each subunit that comprise approximately 62 percent of the structure; there is no beta sheet. The dimeric structure of human interferon-gamma is stabilized by the intertwining of helices across the subunit interface with multiple intersubunit interactions. (Fig. 1)
Interferon gamma is critical for innate and adaptive immunity against viral and intracellular bacterial infections and for tumor control. Interferon gamma is an important activator of macrophages.
The tuberculin skin test was the only test for detecting latent tuberculosis (TB) infection, until another new TB infection test method was developed, interferon gamma release assays (IGRAs). The Interferon gamma (IFN-γ) release assays (IGRA) are in vitro assays measuring the interferon gamma release of sensitized T-cells after exposure to M. tuberculosis antigens. Interferon gamma release assays (IGRAs) are based on the ability of the Mycobacterium tuberculosis antigens for early secretory antigen target 6 (ESAT-6) and culture filtrate protein 10 (CFP-10) to stimulate host production of interferon-gamma. New IGRAs show considerable promise and have excellent specificity. Additional studies are needed to better define their performance in high-risk populations and in serial testing. Longitudinal studies are needed to define the predictive value of IGRAs.