HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pfueller, S. L. Articles by Lüscher, E. F. Search for Related Content PubMed Articles by Pfueller, S. L. Articles by Lüscher, E. F.

The Effects of Aggregated Immunoglobulins on Human Blood Platelets in Relation to Their Complement-Fixing Abilities¹

I. Studies of Immunoglobulins of Different Types

From the Theodor Kocher Institute, University of Berne, Berne, Switzerland

Abstract

Human immunoglobulin (IgG) coupled with bis-diazo-benzidine (BDB-IgG) is capable of causing a release reaction from platelets in a manner similar to heat-aggregated IgG or antigen-antibody complexes. Various organic solvents, e.g., ethanol and acetone, also produce platelet-stimulating complexes. All these aggregated immunoglobulins caused the fixation of complement (C), although not strictly in parallel to their ability to cause the platelet release reaction.

Myeloma proteins from the subclasses IgG1, IgG2 and IgG3, but not IgG4 or IgA, bind C, while all IgG subclasses, including IgG4, stimulate platelets. IgG3 proteins cause a poor release reaction but bind C well.

The release reaction induced by human BDB-IgG is inhibited by monomeric IgG but not by bovine IgG or albumin. Partially purified C1 and purified Clq also inhibit the release reaction. The presence of Ca²⁺ is not required for any of these effects.

It is concluded that for an aggregated immunoglobulin to stimulate platelets it is not necessary that it activate the complement enzymes in the classical way, but that either it may interact with a cell-bound Clq-like receptor, or the immunoglobulin possesses distinct, but closely situated, sites for platelet and C activation.

Footnotes

¹ This work was supported by the "Schweizerischer Nationalfonds zur Förderung der wissenschaftlichen Forschung."

² This author wishes to acknowledge a travel grant from the Postgraduate Medical Foundation, University of Sydney, Australia.

This article has been cited by other articles:

				N. Li Platelet-lymphocyte cross-talk J. Leukoc. Biol., May 1, 2008; 83(5): 1069 - 1078. [Abstract] [Full Text] [PDF]

				D. Brent Kerns, P. A. Frymoyer, R. T. Kopecky, D. Tice, M. F. Fillinger, D. Bruch, and R. A. Schwartz Is Heparin-Induced Platelet Activation an Unrecognized Cause of Thrombosis in Chronic Dialysis Patients? Vascular and Endovascular Surgery, July 1, 1992; 26(6): 487 - 493. [Abstract] [PDF]