In Honor of Elie Metchnikoff, a Nobel Prize Winner, Who Discovered Macrophages as Phagocyte Cells Involved in the Process of Innate Immunity

Dear Colleagues,

This Special Issue honors the discoverer of macrophages, Elie Metchnikoff, who observed these phagocytic cells in the process of innate immunity in 1882. Macrophages, which are formed from hematological progenitor cells (from yolk sac, fetal liver and bone marrow hematopoiesis), circulate in the blood and can migrate into tissues, are ubiquitous and differentially regulated in their function by tissue-specific and immunological transcription processes. Due to their versatile functions, several classes are known from which two main subtypes can be distinguished. M1 macrophages, which are typically activated via bacterial lipopolysaccharides and Th1 cytokines (interferons g+a), produce pro-inflammatory cytokines (interleukins IL-1/6/12/23, TNF-a), reactive oxygen (ROS) and nitrogen species (RNS), express the CC chemokine receptors CCR1/5 and are involved in the promotion of T-helper cells (Th1/17). M2 macrophages are anti-inflammatory, are activated via the Th2 cytokines IL-4/13 and produce the cytokines IL-10, tissue growth factor TGF-beta, chemokines (CCL17/18/22/24) and scavenger receptors (CD163, Stabilin-1). Macrophages serve important functions in immune response, development, tissue homeostasis e.g. wound healing and tissue repair. Activated fibroblasts are also directly involved in the recruitment of macrophages. The process of chemotaxis and migration of monocytes e.g. to the site of infection or injury occurs through the secretion of the chemokine monocyte chemoattractant protein-1 (MCP-1) that binds to the CC chemokine receptor 2 (CCR2) on the monocytes. After infection, the pro-inflammatory M1 phenotype of the macrophages is characteristic, leading to the fight against the invasive organisms through the production of ROS, RNS and TH1/17 cells. But it is precisely here that microorganisms show their ability to circumvent the immune response by influencing macrophage polarization and suppressing important functions such as phagocytic activity. But also the pro-inflammatory phenotype itself has to be switched off later because of the collateral tissue destruction. This occurs through apoptosis, or the re-polarization of macrophages into the anti-inflammatory phenotype. But these important functions of the macrophages can be disturbed in chronic diseases and autoimmune diseases, which includes atherosclerosis, asthma, fibrosis, inflammatory bowel disease, rheumatoid arthritis (RA), experimental autoimmune encephalomyelitis (EAE), multiple sclerosis (MS), autoimmune hepatitis, Crohn's disease and chronic demyelinating diseases of the central nervous system. The pathogenesis of these diseases is based on changes in the differentiation, polarization, re-polarization and activation of macrophages. In order to gain a better understanding of how novel therapies can be developed, the diversity of macrophage functions needs to be better understood.

Dr. Pierre Tennstedt
Guest Editor

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