Analysis of Signals Leading to Differentiation of Immature HL-60 after Administration of IL-4
Treatment of acute myeloid leukaemia (AML) cells with differentiation agents leads not only to the acquisition of normal phenotypes but also contributes to the understanding of special immuno-haematology issues. For instance, induction of HLA-DR antigens on human promyelocytic leukaemia HL-60 cells...
Saved in:
| Main Author: | |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S096293519400058X |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | Treatment of acute myeloid leukaemia (AML) cells with
differentiation agents leads not only to the acquisition of normal
phenotypes but also contributes to the understanding of special
immuno-haematology issues. For instance, induction of HLA-DR
antigens on human promyelocytic leukaemia HL-60 cells by
interleukin-4 (IL-4) is of pivotal importance in immunology not
only because class II expression is prerequisite to antigen
recognition and response but also because IL-4 participates in a
plethora of inflammatory or non-inflammatory reactions. At the same
time, the same observation coupled with an increase in Mac-1, mature
monocyte marker, is revealing ways to haematologists for converting
malignant cases to normal situations. Based on previous reports that
HLA-DR induction by IL-4 in the HL-60 system is mediated via the
G-protein system (p21ras), this study was undertaken in order to
define the intermediate signalling steps followed by this agent from
the moment it is added to cultures to the differentiated cellular
form obtained. It is proposed that IL-4 increases p21ras which in turn
suppresses the HL-60 cells' p34cdc2 constitutive expression. This
inhibition appears to be responsible for the subsequently.observed
cessation ofgrowth. Concomitant to decreased cellular proliferation,
HI-DR antigen expression increases, a finding that matches the
initially mentioned induction of p21ras since its inhibition abolishes HI-DR upregulation. |
|---|---|
| ISSN: | 0962-9351 1466-1861 |