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The deposition of C3b on the cell surface initiates the alternative pathway (see Figure 4.2C). C3b is generated in the circulation in small amounts by the spontaneous cleavage of a reactive thiol group in C3; this “preformed” C3b can bind to proteins and carbohydrates expressed on cell surfaces, either of a pathogen or of a host (mammalian) cell. (If C3b does not bind to one of these surfaces, it is rapidly inactivated.)

Thus, in a sense, the alternative pathway is always “on,” and continual activation could damage cells of the host. However, as we describe in more detail subsequently, mammalian cells regulate the progression of the alternative pathway. Microbial cells lack such regulators and cannot prevent the development of subsequent steps in the alternative pathway.

Following the deposition of C3b, the serum protein factor B combines with C3b on the cell surface to form a complex, C3bB. Factor D then cleaves factor B in the cell surface‐associated C3bB complex, generating fragments Ba, which is released into the fluid phase, and Bb, which remains attached to C3b. C3bBb is the alternative pathway C3 convertase, which cleaves C3 into C3a and C3b.