Serum amyloid A regulates granulomatous inflammation in sarcoidosis through Toll-like receptor-2.

ABSTRACT:

Rationale

The critical innate immune mechanisms that regulate granulomatous inflammation in sarcoidosis are unknown. Because the granuloma-inducing component of sarcoidosis tissues has physicochemical properties similar to those of amyloid fibrils, we hypothesized that host proteins capable of forming poorly soluble aggregates or amyloid regulate inflammation in sarcoidosis.

Objectives

To determine the role of the amyloid precursor protein, serum amyloid A, as an innate regulator of granulomatous inflammation in sarcoidosis.

Methods

Serum amyloid A expression was determined by immunohistochemistry in sarcoidosis and control tissues and by ELISA. The effect of serum amyloid A on nuclear factor (NF)-kappaB induction, cytokine expression, and Toll-like receptor-2 stimula

SUBMITTER: Chen ES 

PROVIDER: S-EPMC2822973 | biostudies-literature | 2010 Feb

REPOSITORIES: biostudies-literature