Intravenous immunoglobulins modulate neutrophil activation and vascular injury through FcγRIII and SHP-1.

ABSTRACT:

Rationale

Intravascular neutrophil recruitment and activation are key pathogenic factors that contribute to vascular injury. Intravenous immunoglobulin (IVIG) has been shown to have a beneficial effect in systemic inflammatory disorders; however, the mechanisms underlying IVIG's inhibitory effect on neutrophil recruitment and activation are not understood.

Objective

We studied the mechanisms by which IVIG exerts protection from neutrophil-mediated acute vascular injury.

Methods and results

We examined neutrophil behavior in response to IVIG in vivo, using real-time intravital microscopy. We found that an antibody that blocks both FcγRIII and its inhibitory receptor counterpart, FcγRIIB, abrogated the inhibitory effect of IVIG on leukocyte recruitment and heterotypic r

SUBMITTER: Jang JE 

PROVIDER: S-EPMC3351009 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature