Dear Les Ander

Nice Q.

Check these interesting articles:

Chapter Regulation of IFN-γ Expression

Article Regulation of interferon-γ gene expression by nuclear factor...

Article Regulation of interferon-y gene expression. J Interferon Cytokine Res

As I reviewed, a number of transcription factors are involved in the interferon-gamma expression:

- T-bet

- RUNX1,3

- NFAT

- NFkB

- AP-1-CREB- ATF family members

- IL-12, IL-15, IL-18

- IFN-a

- heterotrimeric transcription factor complex known as ISGF3 between Stat1 and IFN-regulatory factor 9

I wish I’ve not overlooked any factor.

Best Wishes

Farzad Taghizadeh-Hesary

Les Ander

The cytokine IFN-g belongs to the family of interferons, which are closely related by their ability to protect cells from viral infections. Based on several criteria, the IFN molecules have been divided into two distinct classes. The first class is named type I IFN and includes the IFN-a and IFN-b molecules, which are the classical interferons induced in response to viral infections. The second class is solely composed by IFN-g (also termed type II or immune IFN), which is not related to the type I IFN at both the genetic and the protein levels. Although IFN-g displays most of the biologic activities that have been described to the other IFN, it has a lower specific antiviral activity, but presents more immunomodulatory properties than the type I interferons (Farrar & Schreiber 1993).

Both human and mouse IFN-g genes generate a unique 1.2 kb mRNA that encodes an amino acid polypeptide of 166 and 134 residues, respectively (Boehm et al. 1997). Two polypeptide chains self-associate in an antiparallel fashion, producing a molecule that exhibits a twofold axis of symmetry with an apparent molecular weight of 34 kDa (Farrar & Schreiber 1993, Bach et al. 1997). Only the dimer displays biologic activity, possibly because it is the only conformation of the molecule that can induce IFN-g receptor (IFN-gR) dimerization (Farrar & Schreiber 1993). For a long time, the production of IFN-g has been considered to be restricted to activated natural killer (NK) cells, CD4+ T helper-1 (Th1) cells, and CD8+ T cytotoxic cells (Farrar & Schreiber 1993, Boehm et al. 1997). However, we now know that these cells are the most potent, but not the only sources of IFN-g. Several studies have identified additional IFN-g-secreting cell types, including gd T cells, NKT cells, macrophages, dendritic cells, naive CD4+ T cells, and even B cells (Frucht et al. 2001, Szabo et al. 2003).