Absence of FcγRIII results in increased proinflammatory response in FcγRIII-KO cardiac recipients.

ABSTRACT:

Background

Alloantibody can contribute significantly to rejection of heart transplants by activation of complement and interactions with a variety of effector cells, including macrophages and monocytes through activating FcγRI, FcγRIII, FcγRIV, the inhibitory FcγRIIB and complement receptors. These receptors link cellular and humoral immunity by bridging the antibody specificity to effector cells. Activating FcγRs are also involved in serum amyloid P component (SAP)-mediated clearance of apoptotic bodies.

Methods

B10.A (H-2a) hearts were transplanted into wild-type (WT) or FcγRIII-knockout (KO) C57BL/6 (H-2b) mouse recipients. Levels of alloantibodies and SAP in the circulation were determined by flow cytometry and enzyme-linked immunosorbent assay, respectively. Intragraft

SUBMITTER: Erdinc Sunay MM 

PROVIDER: S-EPMC3795861 | biostudies-literature | 2013 Oct

REPOSITORIES: biostudies-literature