An inflammatory triangle in Sarcoidosis: PPAR-γ, immune microenvironment, and inflammation.

INTRODUCTION

Sarcoidosis is an inflammatory disorder characterized by granuloma formation in several organs. Sarcoidosis patients experience higher inflammatory responses resulting in pulmonary fibrosis. Although the precise mechanisms have not been well elucidated, the relationship between the immune system activation and inflammatory status is pivotal in the pathogenesis of sarcoidosis.

AREAS COVERED

Peroxisome proliferator-activated receptor (PPAR) includes the transcription factors involved in cell metabolism, proliferation, and immune response. In the alveolar macrophages of patients with sarcoidosis, the reduced activity and a decreased level of PPAR-γ have been shown. In this study, we discuss how reducing the level of PPAR-γ could lead to increased inflammation and immune responses in patients with sarcoidosis.

EXPERT OPINION

Lack of PPAR-γ may contribute to the development of a suitable milieu for the formation of immune-associated pulmonary granuloma. Reduced levels of PPAR-γ in sarcoidosis could result from over-activation of the immune system and elevated inflammatory responses, as well. Due to the anti-inflammatory function of PPAR-γ, identifying the relation between PPAR-γ, sarcoidosis development, and inflammatory state could be essential to identify the appropriate therapeutic targets. The synthesis of PPAR-γ agonists or PPAR-γ ligands may be an effective step toward the treatment of sarcoidosis patients in the future.