Abstract
The innate immune system is the first line of host defense against infection and is comprised of humoral and cellular mechanisms that recognize potential pathogens within minutes or hours of entry. The effector components of innate immunity include epithelial barriers, phagocytes, and natural killer cells, as well as cytokines and the complement system. Complement plays an important role in the immediate response against microorganisms, including Streptococcus sp. The lectin pathway is one of three pathways by which the complement system can be activated. This pathway is initiated by the binding of mannose-binding lectin (MBL), collectin 11 (CL-K1), and ficolins (Ficolin-1, Ficolin-2, and Ficolin-3) to microbial surface oligosaccharides and acetylated residues, respectively. Upon binding to target molecules, MBL, CL-K1, and ficolins form complexes with MBL-associated serine proteases 1 and 2 (MASP-1 and MASP-2), which cleave C4 and C2 forming the C3 convertase (C4b2a). Subsequent activation of complement cascade leads to opsonization, phagocytosis, and lysis of target microorganisms through the formation of the membrane-attack complex. In addition, activation of complement may induce several inflammatory effects, such as expression of adhesion molecules, chemotaxis and activation of leukocytes, release of reactive oxygen species, and secretion of cytokines and chemokines. In this chapter, we review the general aspects of the structure, function, and genetic polymorphism of lectin-pathway components and discuss most recent understanding on the role of the lectin pathway in the predisposition and clinical progression of Rheumatic Fever.
Highlights
COMPLEMENT SYSTEM: AN OVERVIEW The high complexity of the human immune system provides effective defense against an impressive number of pathogens and protection to undesirable response against self-components
All three pathways are initiated by multiple stimuli independently from each other and subsequently the proteolytic cascades converge toward the activation of the major component C3, which results in the assembly of the membrane-attack complex (MAC) (Figure 2) [5]
It is initiated by the binding of pattern-recognition plasma molecules such as mannose-binding lectin (MBL), collectin 11 (CL-K1), or ficolins to carbohydrates or acetylated residues present on microorganisms or to aberrant glycocalyx patterns on apoptotic, necrotic, or malignant cells [7]
Summary
COMPLEMENT SYSTEM: AN OVERVIEW The high complexity of the human immune system provides effective defense against an impressive number of pathogens and protection to undesirable response against self-components. LECTIN PATHWAY OF COMPLEMENT ACTIVATION The lectin pathway is initiated when pattern-recognition molecules (MBL, CL-K1, and ficolins) bind to the so-called pathogenassociated molecular patterns (PAMPs) (D-mannose, N-acetyl-Dglucosamine, or acetyl groups), on the surface of pathogens or to apoptotic or necrotic cells [9]. MBL induces several biological effects such as complement activation by the lectin pathway, opsonophagocytosis, modulation of inflammation, and recognition of altered self-structures [32].
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