Minimal role for the alternative pathway in complement activation by HIT immune complexes.

ABSTRACT:

Background

Anti-platelet factor 4 (PF4)/heparin immune complexes that cause heparin-induced thrombocytopenia (HIT) activate complement via the classical pathway. Previous studies have shown that the alternative pathway of complement substantially amplifies the classical pathway of complement activation through the C3b feedback cycle.

Objectives

These studies sought to examine the contributions of the alternative pathway to complement activation by HIT antibodies.

Methods

Using IgG monoclonal (KKO) and/or patient-derived HIT antibodies, we compared the effects of classical pathway (BBK32 and C1-esterase inhibitor [C1-INH]), alternative pathway (anti-factor B [fB] or factor D [fD] inhibitor) or combined classical and alternative pathway inhibition (soluble complement re

SUBMITTER: Barnes AP 

PROVIDER: S-EPMC9938942 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature