Immunomodulation in systemic lupus erythematosus: induction of M2 population in monocyte-derived macrophages by pioglitazone.

Lupus

PubMedID: 28457196

Mohammadi S, Saghaeian-Jazi M, Sedighi S, Memarian A. Immunomodulation in systemic lupus erythematosus: induction of M2 population in monocyte-derived macrophages by pioglitazone. Lupus. 2017;961203317701842.
Macrophages have recently gained attention in systemic lupus erythematosus (SLE) pathogenesis for their role in the anti-inflammatory clearance of apoptotic cells. The M1/M2 polarization of macrophages improves efferocytic capability. Peroxisome proliferator-activated receptor ? is proposed to function in the expansion of the M2 subpopulation. Pioglitazone is a peroxisome proliferator-activated receptor ? agonist with a variety of anti-inflammatory effects. In this paper, we investigated the ex vivo alterations of monocyte-derived macrophages of 15 newly diagnosed SLE patients and 10 normal subjects triggered by apoptotic cells among SLE patients following pioglitazone treatment. The phagocytosis capacity of macrophages and M1/M2 polarization (CD86/CD163) was evaluated. The supernatants were also analyzed for the expression of interleukin (IL)-10, IL-12, transforming growth factor ß1 and TNF-a. The mRNA expression of IL-1ß and mannose receptor C-type 1 were also quantified among treated and non-treated monocyte-derived macrophages. We found that efferocytosis is defective among monocyte-derived macrophages of SLE patients and might be a major underlying mechanism involved in the sustained inflammation. Pioglitazone could enhance alternative activation of monocyte-derived macrophages and consequently immunomodulation in these patients.