Abstract
The complement system is a fundamental part of the innate immune system, playing a crucial role in host defense against various pathogens, such as bacteria, viruses, and fungi. Activation of complement results in production of several molecules mediating chemotaxis, opsonization, and mast cell degranulation, which can contribute to the elimination of pathogenic organisms and inflammation. Furthermore, the complement system also has regulating properties in inflammatory and immune responses. Complement activity in diseases is rather complex and may involve both aberrant expression of complement and genetic deficiencies of complement components or regulators. The skin represents an active immune organ with complex interactions between cellular components and various mediators. Complement involvement has been associated with several skin diseases, such as psoriasis, lupus erythematosus, cutaneous vasculitis, urticaria, and bullous dermatoses. Several triggers including auto-antibodies and micro-organisms can activate complement, while on the other hand complement deficiencies can contribute to impaired immune complex clearance, leading to disease. This review provides an overview of the role of complement in inflammatory skin diseases and discusses complement factors as potential new targets for therapeutic intervention.
Highlights
The Complement SystemThe complement system consists of a network of more than 50 different plasma and membraneassociated proteins
psoriatic leukotactic factor (PLF)/C5a did not induce proliferation or influenced the viability of cultured human epidermal cells [32]. These results suggest that PLF/C5a requires specific circumstances necessary to exert its effect on skin, most probably the presence of neutrophils from the circulation
Besides the protective role of complement, improper regulated activation of complement can lead to extensive tissue damage
Summary
A. van Doorn 3, Robert Rissmann 4, Errol P. Reviewed by: Zoltan Prohaszka, Semmelweis University, Hungary Arvind Sahu, National Centre for Cell Science, India. Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal
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