High-dose intravenous immunoglobulin does not reduce the numbers of circulating CD14 +CD16 ++ monocytes in patients with inflammatory disorders

摘要

With great interest we have read the paper of Siedlar et al. [1], in which a new mechanism of action of intravenous immunoglobulins (IVIg) is presented. This mechanism includes a reduction of the numbers of "pro-inflammatory" CD14~+CD16~++ monocytes and suppression of their TNF-alpha production. Modulating the numbers of CD14~+CD16~++ monocytes is of particular clinical importance in inflammatory diseases (e.g. sepsis, hemophagocytic syndrome and Kawasaki disease), where the numbers of this subset are dramatically increased. Therefore, the authors suggest that declining the numbers of CD14~+CD16~++ monocytes may contribute to the anti-inflammatory effects of high-dose IVIg treatment (1-2 g/kg) in patients with inflammatory conditions. However, the study of Siedlar et al. [1] was not performed in patients receiving the "anti-inflammatory" dose of 1-2 g/kg, but in patients with common variable immunodeficiency (CVID) that received a replacement dose of 0.4 g/kg IVIg.