The interferon-inducible HIN-200 gene family in apoptosis and inflammation: Implication for autoimmunity

Abstract

The Ifi-200/HIN-200 gene family encodes highly homologous human (IFI16, myeloid cell nuclear differentiation antigen, absent in melanoma 2, and IFIX) and murine proteins (Ifi202a, Ifi202b, Ifi203, Ifi204, Ifi205, and Ifi206), which are induced by type I and II interferons (IFN). These proteins have been described as regulators of cell proliferation and differentiation and, more recently, several reports have suggested their involvement in both apoptotic and inflammatory processes. The relevance of HIN-200 proteins in human disease is beginning to be clarified, and emerging experimental data indicate their role in autoimmunity. Autoimmune disorders are sustained by perpetual activation of inflammatory process and a link between autoimmunity and apoptosis has been clearly established. Moreover, the interferon system is now considered as a key player in autoimmune disorders such as systemic lupus erythemathosus, systemic sclerosis, and Sjögren's syndrome, and it is therefore conceivable to hypothesize that HIN-200 may be among the pivotal mediators of IFN activity in autoimmune disease. In particular, the participation of HIN-200 proteins in apoptosis and inflammation could support their potential role in autoimmunity.

Keywords::

• HIN-200
• IFI-200
• apoptosis
• inflammation
• autoimmunity

Declaration of interest: This work was supported by grants Special Project Oncology “Compagnia di San Paolo,” MIUR (“Program 40%” to S. L.), Ricerca Sanitaria Finalizzata 2007 (to S. L.) and 2008 (to M. M., M. G., and S. L.), and Fondazione CRT – “Progetto Alfieri” to S. L. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.