z-logo
open-access-imgOpen Access
Glucocorticoid‐mediated immunomodulation: hydrocortisone enhances immunosuppressive endogenous retroviral protein (p15E) expression in mouse immune cells
Author(s) -
FIEGL M.,
STRASSERWOZAK E.,
GELEY S.,
GSUR A.,
DRACH J.,
KOFLER R.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb08348.x
Subject(s) - immune system , biology , endogeny , glucocorticoid , immunology , messenger rna , gene , virus , gene expression , signal transduction , microbiology and biotechnology , virology , genetics , endocrinology
SUMMARY To define glucocorticoid (GC)‐regulated genes contributing to the anti‐inflammatory and immunosuppressive effects of GC, previous work from our laboratory revealed up‐regulation of transcripts from endogenous type B mouse mammary tumour virus (Mtv) and type C murine leukaemia virus (Emv) loci by high dose GC treatment of P388D1 macrophage‐like cells. This study demonstrates enhancement of expression from Mtv and Emv loci in P388D1 cells by more physiological hydrocortisone concentrations (1 μM), and shows direct transcriptional mode of regulation by blocking GC‐mediated signal transduction at different levels. Furthermore, we found up‐regulation of Emv mRNA steady‐state levels in murine lymphoid lineage cells (T‐like EL4 and BW5147 cells; B‐like X63 cells) upon GC treatment. The Emv transcripts shown by us to be GC‐up‐regulated encode for the transmembrane envelope protein TM/p15E which is highly conserved in several retroviruses. TM/p15E and the p15E‐like products found in humans exert immunosuppressive effects in different test systems. Thus, our findings raise the possibility that immunomodulation by GC might be mediated in part by enhanced expression of p15E(‐like) products.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here