2008 PBL Cat_mech_r.qxd:PBL Catalog.mech 11/29/07 1:50 PM Page 6
Application Note
Stat2 dependent regulation of MHC class II expression (continued)
Results
Initial analysis of Stat2 knockout fibroblasts demonstrated an absolute defect analysis of Stat1-Stat2 double knockout macrophages determined that
in IFN-α dependent target gene expression (5). Extension of these studies to analogous to IFN-γ, the aberrant ability of IFN-α to induce MHC II was
macrophages revealed that IFN-α failed to induce MHC II expression in wild dependent on Stat1 (Fig. 1B; (7)). These observations suggest that Stat2
type (WT) macrophages, a signature IFN-γ response (see Fig. 1A). Yet, IFN-α normally serves to suppress IFN-I dependent MHC II expression, in WT
potently stimulated MHC II expression in Stat2-/- macrophages. Subsequent macrophages.
Figure 1: MHC II expression on macrophages.
Figure 1
(A)Nonelicted peritoneal (left) or BM (right) macrophages (CD11b
+
,
CD11c
-
) from wild-type (WT) and homozygous Stat2 knockout
(Stat2
-/-
) mice were stained with anti-mouse I-A
b
or isotype matched
control (dotted line), before (thin line) and after treatment with either
IFN-α
A/D
(1000 U/ml, 72 h; indicated with light gray) or with IFN-γ
(66 U/ml; 72 h; indicated with dark gray), fixed and then harvested
for FACS.
(B) Nonelicted peritoneal macrophages from Stat1
-/-
/Stat2
-/-
were
stained with anti-mouse I-A
b
and analyzed as outlined in panel A. Data
in both panels are representative of at least three independent
experiments.
PBLInterferonSource Toll Free: 1 877- PBL-8881
6
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