IFN-? is constitutively expressed by cells of the reproductive tract and is inefficiently secreted by fibroblasts and cell lines.

ABSTRACT: Type-I interferons (IFNs) form a large family of cytokines that primarily act to control the early development of viral infections. Typical type-I IFN genes, such as those encoding IFN-? or IFN-? are upregulated by viral infection in many cell types. In contrast, the gene encoding IFN-? was reported to be constitutively expressed by cells of the female reproductive tract and to contribute to the protection against vaginal infections with herpes simplex virus 2 and Chlamydia muridarum. Our data confirm the lack of induction of IFN-? expression after viral infection and the constitutive expression of IFN-? by cells of the female but also of the male reproductive organs. Interestingly, when expressed from transfected expression plasmids in 293T, HeLa or Neuro2A cells, the mouse and human IFN-? precursors were inefficiently processed and secretion of IFN-? was minimal. Analysis of chimeric constructs produced between IFN-? and limitin (IFN-?) showed that both the signal peptide and the mature moiety of IFN-? contribute to poor processing of the precursor. Immunofluorescent detection of FLAG-tagged IFN-? in transfected cells suggested that IFN-? and chimeric proteins were defective for progression through the secretory pathway. IFN-? did not, however, act intracellularly and impart an antiviral state to producing cells. Given the constitutive expression of IFN-? in specialized cells and the poor processing of IFN-? precursor in fibroblasts and cell lines, we hypothesize that IFN-? secretion may require a co-factor specifically expressed in cells of the reproductive organs, that might secure the system against aberrant release of this IFN.

SUBMITTER: Hermant P 

PROVIDER: S-EPMC3739789 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature