Читать книгу Immunology - Richard Coico - Страница 106

1 E. All these functions are mediated by complement components that are generated later in the complement activation sequence than C3. Thus, all these functions are disrupted in the absence of C3.

2 D. Complement is required for lysis of bacteria by IgM or IgG (classical pathway). Complement is not required for lysis of erythrocytes by lecithinase or for phagocytosis. However, opsonins such as C3b that are generated during complement activation can enhance phagocytosis. Although some tumor cells can initiate the alternative pathway of complement activation, complement plays no role in NK‐mediated lysis of these cells.

3 A. Inherited homozygous deficiency of one of the early proteins of the classical complement pathway (C1, C4, or C2) is strongly associated with the development of SLE‐like symptoms. These deficiencies probably result in abnormal processing of immune complexes in the absence of a functional classical pathway of complement fixation. In these conditions, serum levels of C3 and C4 decrease due to the large number of immune complexes that bind to them. Deficiencies in the late components are associated with recurrent infections with pyogenic organisms.

4 D. C5a is an anaphylatoxin, which induces degranulation of mast cells, resulting in the release of histamine, causing vasodilation and contraction of smooth muscles. C5a is also chemotactic, attracting leukocytes to the area of its release where an antigen is reacting with antibodies and activates the complement system; this is a part of the inflammatory response to an infection. C5b deposits on membranes and initiates the formation of the terminal membrane attack complex. Neither C5a nor C5b promotes the attachment of lymphocytes to macrophages.

5 D. The alternative pathway of complement activation connects with the classical pathway at the activation of C3. Thus, it does not require C1, C4, or C2. Properdin is essential for the activation through the alternative pathway, since it stabilizes the complex formed between C3b and activated serum factor B, C3bBb, which acts as a C3 convertase, and activates C3. During activation of the alternative pathway both C3a and C5a are generated; both are anaphylatoxins and cause degranulation of mast cells. Factor H is a key regulator of the alternative pathway.

6 A. DAF is a cell surface regulator of complement activation that destabilizes the C3 convertases of the alternate and classical pathways (C3bBb and C4b2a, respectively). Like other regulators of complement activation—including CR1, factor H, and C4bBP—these proteins accelerate decay (dissociation) of the C3 convertase, releasing the component with enzymatic activity (Bb or C2a) from the component bound to the cell membrane (C3b or C4b).

7 E. Each of these pathogens and particles of microbial origin can initiate the alternative pathway of complement activation. Teichoic acid from the cell walls of Gram‐positive organisms, as well as parasites such as trypanosomes, can also activate complement via this pathway.