Mechanism of formation of human IgE-binding factors (soluble CD23): III. Evidence for a receptor (Fc epsilon RII)-associated proteolytic activity.
Mechanism of formation of human IgE-binding factors (soluble CD23): III. Evidence for a receptor (Fc epsilon RII)-associated proteolytic activity.
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DOI:
10.1084/jem.172.3.693
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发表时间:
1990-09-01
期刊:
影响因子:
--
通讯作者:
Delespesse G
中科院分区:
文献类型:
--
作者:
Letellier M;Nakajima T;Pulido-Cejudo G;Hofstetter H;Delespesse G
There is mounting evidence that Fc epsilon RII (CD23) and its soluble fragments (IgE-binding factors [BFs] or soluble CD23) have pleiotropic activities. IgE-BFs are formed mainly by the proteolytic cleavage of surface Fc epsilon RII; they are first released as 37- and 33-kD unstable molecules that are subsequently transformed into 25-kD IgE- BFs. In this study, purified and radioiodinated 37-kD IgE-BFs as well as 45-kD Fc epsilon RII were used as substrates to identify the proteases leading to the formation of 25-kD IgE-BFs. These substrates generate 25-kD IgE-BFs when incubated with several Fc epsilon RII- bearing cells, including CHO1-7 cells (transfected with Fc epsilon RII cDNA); by contrast Fc epsilon RII- cells, including CHO control cells, have no effect. Highly purified unlabeled native 37-kD and recombinant 29-kD IgE-BFs also cleave labeled 45-kD Fc epsilon RII into 25-kD IgE- BFs. The proteolytic activity of these purified IgE-BFs is specifically removed by immunoprecipitation with an antibody against IgE-BFs. These data strongly suggest that Fc epsilon RII and some of its soluble fragments play an active role in the proteolytic mechanism generating IgE-BFs. They are supported by the observation that IgE-BFs released by CHO1-7 cells are cleaved exactly at the same sites as B cell-derived IgE-BFs. Taken collectively, the results are compatible with an autoproteolytic process.
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DOI:
10.1016/0167-5699(86)90184-2
发表时间:
1986-01-01
期刊:
IMMUNOLOGY TODAY
影响因子:
--
作者:
CAPRON, A;DESSAINT, JP;TONNEL, AB
通讯作者:
TONNEL, AB
DOI:
10.1073/pnas.82.24.8325
发表时间:
1985-12-01
影响因子:
11.1
作者:
DORSCHHASLER, K;KEIL, GM;KOSZINOWSKI, UH
通讯作者:
KOSZINOWSKI, UH
影响因子:
5.4
作者:
GORDON, J;CAIRNS, JA;GUY, GR
通讯作者:
GUY, GR
影响因子:
3.6
作者:
LETELLIER, M;SARFATI, M;DELESPESSE, G
通讯作者:
DELESPESSE, G
影响因子:
5.4
作者:
ARMITAGE, RJ;GOFF, LK
通讯作者:
GOFF, LK