Abstract
Macrophages, a kind of innate immune cells, derive from monocytes in circulation and play a crucial role in the innate and adaptive immunity. Under the stimulation of the signals from local microenvironment, macrophages generally tend to differentiate into two main functional phenotypes depending on their high plasticity and heterogeneity, namely, classically activated macrophage (M1) and alternatively activated macrophage (M2). This phenomenon is often called macrophage polarization. In pathological conditions, chronic persistent inflammation could induce an aberrant response of macrophage and cause a shift in their phenotypes. Moreover, this shift would result in the alteration of macrophage polarization in some vascular dermatoses; e.g., an increase in proinflammatory M1 emerges from Behcet's disease (BD), psoriasis, and systemic lupus erythematosus (SLE), whereas an enhancement in anti-inflammatory M2 appears in infantile hemangioma (IH). Individual polarized phenotypes and their complicated cytokine networks may crucially mediate in the pathological processes of some vascular diseases (vascular dermatosis in particular) by activation of T cell subsets (such as Th1, Th2, Th17, and Treg cells), deterioration of oxidative stress damage, and induction of angiogenesis, but the specific mechanism remains ambiguous. Therefore, in this review, we discuss the possible role of macrophage polarization in the pathological processes of vascular skin diseases. In addition, it is proposed that regulation of macrophage polarization may become a potential strategy for controlling these disorders.
Highlights
Macrophages are a group of innate immune cells coming from peripheral blood monocytes
In the process of M1 macrophage polarization, two well-known signals, namely, IFN-γ and LPS, are mainly involved [16,17,18]. After binding to their corresponding receptors (IFNGR and TLR4), IFN-γ and LPS recruit the adaptors of Janus kinase 1/2 (JAK1/2), Toll-like receptor (TLR) domaincontaining adapter protein [interferon-β (TRIF) and myeloid differentiation factor 88 (MyD88)], further activating the downstream factors of interferon regulatory factor 3 (IRF3), IL-1 receptor-associated kinase 4 (IRAK-4), TNF receptorassociated factor 6 (TRAF-6), and inhibitor of nuclear factor kappa B kinase (IKK-β), resulting in the activation of signal transducer and activator of transcription 1 (STAT1) and nuclear factor kappa B (NF-κB) [19,20,21]
The effect of macrophage in different vascular dermatosis is variable owing to their M1/M2 phenotypes
Summary
Macrophages are a group of innate immune cells coming from peripheral blood monocytes Owing to their multifunctional activities, macrophages potently work in homeostasis maintenance, inflammation, angiogenesis, wound healing, etc. Macrophage polarization often occurs in an inflammatory process and many studies about inflammatory disorders or inflammation-related vascular diseases always focus on these two polarized macrophages [8,9,10]. It is found macrophage polarization heavily functions in some immune-mediated inflammatory vascular dermatoses, like Behcet’s disease (BD), psoriasis, and systemic lupus erythematosus (SLE) [11,12,13]. Macrophage polarization imbalance would be a major contributor to these dermatoses, and thereby, regulation of macrophage polarization may be a potential target for vascular skin disease treatment
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