1991
DOI: 10.1159/000235332
|View full text |Cite
|
Sign up to set email alerts
|

IgG Anti-IgE Autoantibodies in Immunoregulation

Abstract: Human sera contain anti-IgE autoantibodies with diverse biological functions in vitro. Opposite functions can be shown for triggering of IgE-mediated histamine release from human basophils in terms of anaphylactogenic or nonanaphylactogenic autoantibodies. Furthermore, autoantibodies are either capable of removing IgE from the surface of CD23-positive cells of binding more IgE to such cells. A similar dichotomy seems also to exist for the effect of autoantibodies on human IgE mRNA synthesis as well as IL-4-ind… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
8
0

Year Published

1993
1993
2002
2002

Publication Types

Select...
9
1

Relationship

2
8

Authors

Journals

citations
Cited by 23 publications
(8 citation statements)
references
References 4 publications
0
8
0
Order By: Relevance
“…Autoantibodies have been documented as either anaphylactogenic or not [9], We have also shown that the phenomenon of basophil releasability is probably related to a certain type o f anti-IgE (blocking or triggering) binding to cytophilic IgE [10], In addition. anti-IgE antibodies purified from complexes have been shown to both inhibit and in crease binding of IgE to the low-affinity receptor for IgE (FceRII also known asCD23).…”
Section: Introductionmentioning
confidence: 75%
“…Autoantibodies have been documented as either anaphylactogenic or not [9], We have also shown that the phenomenon of basophil releasability is probably related to a certain type o f anti-IgE (blocking or triggering) binding to cytophilic IgE [10], In addition. anti-IgE antibodies purified from complexes have been shown to both inhibit and in crease binding of IgE to the low-affinity receptor for IgE (FceRII also known asCD23).…”
Section: Introductionmentioning
confidence: 75%
“…Mast cells and basophils, in fact, are activated not only by IgE interaction with their receptor (direct anaphylaxis), but also by anti-IgE and anti-FcεRIα antibodies (''reverse type'' anaphylaxis) (11). It is clear that some of these autoantibodies could modulate the immune responses inhibiting IgE bound to their receptor, or, as occurs for some CIU cases, triggering the receptor to induce mediator release (13). It is clear that some of these autoantibodies could modulate the immune responses inhibiting IgE bound to their receptor, or, as occurs for some CIU cases, triggering the receptor to induce mediator release (13).…”
Section: Discussionmentioning
confidence: 99%
“…All other antibodies were anaphylactogenic although to different degrees. Our nonanaphylatogenic antibody (BSW17, [27]) also very ef fectively inhibited the binding of IgE of FceRI [28], How ever, further analysis clearly showed that this antibody nevertheless was capable of recognizing surface IgE but was obviously not capable of crosslinking IgE. Further more, in subsequent receptor dissociation studies we could show that this antibody was in addition capable of removing surface IgE [28], Thus, it represented a real 'de sensitizing' antibody.…”
Section: Anti-lge Antibody and Ige-binding To Fcerimentioning
confidence: 99%