STAT6 and the regulation of CD23 expression in B-chronic lymphocytic leukemia.

Abstract:

:High CD23 expression is a hallmark of B-CLL cells. It is lost during in vitro culture and can be reinduced by IL-4, albeit to a lower extent than in normal B cells. To elucidate the events controlling CD23 expression in B-CLL cells, the IL-4 mediated induction of STAT6 was investigated. Western-blot analysis demonstrated that B-CLL cells contain comparable amounts of STAT6. Electrophoretic mobility shift assays (EMSA) showed no constitutive nuclear translocation of STAT6. IL-4 induced the translocation of STAT6 in B-CLL cells from all 22 patients investigated. The increase was transient, dose and time dependent without a distinct difference between B-CLL cells and non-malignant B cells. However, in contrast to normal B lymphocytes no strict correlation between CD23 expression and STAT6 activation was detected in B-CLL. Therefore further signalling pathways and transcription factors in addition to STAT6 have to be activated to explain the high expression of CD23 in B-CLL cells. For example, STAT1 which is induced by IFN-gamma and binds to the classical STAT6 site. It might be involved in the strong induction of CD23 on B-CLL cells after cotreatment with IL-4 and IFN-gamma, while in non-malignant B lymphocytes IFN-gamma leads to a reduction of IL-4 mediated CD23 expression.

journal_name

Leuk Res

journal_title

Leukemia research

authors

Kneitz C,Goller M,Seggewiss R,Yaman A,Serfling E,Tony HP

doi

10.1016/s0145-2126(99)00191-5

keywords:

subject

Has Abstract

pub_date

2000-04-01 00:00:00

pages

331-7

issue

4

eissn

0145-2126

issn

1873-5835

pii

S0145212699001915

journal_volume

24

pub_type

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