A Plausible Role for Collectins in Skin Immune Homeostasis

Abstract

The skin is a complex organ that faces the external environment and participates in the innate immune system. Skin immune homeostasis is necessary to defend against external microorganisms and to recover from stress to the skin. This homeostasis depends on interactions among a variety of cells, cytokines, and the complement system. Collectins belong to the lectin pathway of the complement system, and have various roles in innate immune responses. Mannose-binding lectin (MBL), collectin kidney 1, and liver (CL-K1, CL-L1) activate the lectin pathway, while all have multiple functions, including recognition of pathogens, opsonization of phagocytosis, and modulation of cytokine-mediated inflammatory responses. Certain collectins are localized in the skin, and their expressions change during skin diseases. In this review, we summarize important advances in our understanding of how MBL, surfactant proteins A and D, CL-L1, and CL-K1 function in skin immune homeostasis. Based on the potential roles of collectins in skin diseases, we suggest therapeutic strategies for skin diseases through the targeting of collectins and relevant regulators.

Mannan‐binding lectin exacerbates the severity of psoriasis by promoting plasmacytoid dendritic cell differentiation via the signal transducer and activator of transcription 3–interferon regulatory factor 8 axis

“…However, it seems that MBL has dual effects in the regulation of skin inflammation. On the one hand, decreased MBL levels resulting from variant MBL2 polymorphisms are responsible for the progression of dermatomyositis and oral lichen planus, which might be attributed to the impaired clearance of apoptotic cells in the skin 17,19,20,25 . On the other hand, MBL exacerbated cutaneous burn injury and ischemia/reperfusion injury by facilitating inflammatory responses 34,35 .…”

“…[29][30][31] In this study, the MBL level was significantly increased and showed a positive Mannan-binding lectin is a recognition molecule of the lectin complement pathway, and involved in microbial infection, the inflammatory response, and autoimmune diseases. 20 It is worth focusing on the diverse roles of MBL in the occurrence of skin diseases.…”

“…On the one hand, decreased MBL levels resulting from variant MBL2 polymorphisms are responsible for the progression of dermatomyositis and oral lichen planus, which might be attributed to the impaired clearance of apoptotic cells in the skin. 17,19,20,25 On the other hand, MBL exacerbated cutaneous burn injury and ischemia/reperfusion injury by facilitating inflammatory responses. 34,35 In addition, elevated circulating MBL levels were considered to be related to the main clinical features in Behçet's disease.…”

“…It has been studied that the MBL2 polymorphism is relevant to several skin diseases, such as dermatomyositis, lichen planus, and Behçet’s disease 17–19 . MBL is synthesized predominantly in the liver and circulates into blood but is also deposited on the lesional skin of systemic lupus erythematosus (SLE) and pemphigus 20–22 . Further evidence indicates that plasma MBL levels have relation with the disease activity of SLE and could represent a biomarker of this disease 23,24 .…”

“…[17][18][19] MBL is synthesized predominantly in the liver and circulates into blood but is also deposited on the lesional skin of systemic lupus erythematosus (SLE) and pemphigus. [20][21][22] Further evidence indicates that plasma MBL levels have relation with the disease activity of SLE and could represent a biomarker of this disease. 23,24 The above studies indicate the effect of MBL in the pathogenesis of autoimmune skin diseases.…”