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The MHC class II transactivator (CIITA) mRNA stability is critical for the HLA class II gene expression in myelomonocytic cells.

Abstract：

:The human promyelocytic U937 cells express detectable levels of MHC class II (MHC-II) molecules. Treatment with 12-o--tetradecanoyl phorbol 13-acetate (TPA), inducing macrophage-like differentiation, produces a dramatic decrease of MHC-II expression as result of down-modulation of the activation of immune response gene 1 (AIR-1)-encoded MHC-II transactivator (CIITA). This event is specific, as MHC class I remains unaffected. Similar results are observed with U937 cells expressing an exogenous full-length CIITA. Molecular studies demonstrate that TPA treatment affects the stability of CIITA mRNA rather than CIITA transcription. Importantly, cis-acting elements within the distal 650 bp of the 1035-bp 3' untranslated region (3'UTR, nucleotides 3509-4543) are associated to transcript instability. Transcription inhibitors actinomycin D and 5,6-dichlororibofuranosyl benzimidazole, and the translation inhibitor cycloheximide significantly rescue the accumulation of CIITA mRNA in TPA-treated cells. A similar effect is also observed after treatment with staurosporine and the PKC-specific inhibitor GF109203X. The instability of CIITA mRNA produced by TPA in U937 cells is not seen in B cells. These results demonstrate the presence of an additional level of control of MHC-II expression in the macrophage cell lineage depending upon the control of CIITA mRNA stability, most likely mediated by differentiation-induced, 3'UTR-interacting factors which require kinase activity for their destabilizing function.

journal_name

Eur J Immunol

journal_title

European journal of immunology

authors

De Lerma Barbaro A,Procopio FA,Mortara L,Tosi G,Accolla RS

doi

10.1002/eji.200425378

keywords:

subject

Has Abstract

pub_date

2005-02-01 00:00:00

pages

603-11

issue

2

eissn

0014-2980

issn

1521-4141

journal_volume

35

pub_type

杂志文章

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