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Terminal mannose residues expressed by Gram‐positive (Staphylococcus aureus) and Gram‐negative bacteria (Klebsiella, Escherichia coli, and Haemophilus influenzae type b), fungi (Candida and Aspergillus fumigatus), and yeast particles activate the lectin pathway by binding MBL. Many microbes, including the pathogen Streptococcus pneumoniae, express acetylated or neutral carbohydrate structures as part of extended polysaccharides, such as 1,3‐β‐D‐glucan; these are all bound by ficolin. Because the lectin pathway is activated by the molecular patterns expressed by pathogens (PAMPs, see Chapter 3) in the absence of antibody, it is part of the innate immune defenses and is involved in the rapid response to pathogens.

The terminal carbohydrate structures that activate the lectin pathway are generally not expressed on the surface of mammalian cells, so the lectin pathway of complement activation may be thought of as yet another way that the body discriminates between self and nonself. We referred to this critical concept earlier in the book, applicable in both innate immunity (pattern recognition receptors for pathogens expressed on cells of the innate immune system) and adaptive immunity (T and B cells respond to nonself antigens but do not respond to self‐antigens).

Figure 4.2. Early steps in activation of classical, lectin, and alternative complement pathways leading to formation of C3 convertase: C4aC2b in both classical and lectin pathways, and C3bBb in alternative pathway.