By Henry G. Kunkel and Frank J. Dixon (Eds.)
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Additional info for Advances in Immunology, Vol. 29
A kinetic analysis of the measured events is shown in Fig. 12. Pathway 36 HANS J. MULLER-EBERHARD AND ROBERT D. SCHREIBER / Lvsis Properdin Uptake 0 2 4 I 6 Time (hours) FIG. 12. Injury and death of Raji cells caused by the purified cytolytic alternative pathway. , 1980). activation was relatively rapid as evidenced by the fact that properdin uptake was maximal at 1 hour (8000 molecules per cell). Membrane attack complex formation was maximal at 4 hours as indicated by C9 uptake (90,000 molecules per cell).
It is the latter reaction that determines whether the pathway is propagated or abrogated. , 1980). A. Although not known with certainty, the initial enzyme appears to be the 20 HANS J. MULLER-EBERHARD AND ROBERT D. , 1978). The first molecule of C3b produced by this hypothetical enzyme will then set in motion the positive feedback reaction. That no extraneous enzyme is involved is indicated by the total dependence of C 3 activation on factor B and factor D (Table VI). Because factor D occurs in serum or plasma in active form (Lesavre and Muller-Eberhard, 1978)always ready to act on its substrate, provided it is suitably presented, there is probably a continuous low grade formation of C3,Bb.
It appears likely that antibody and properdin, which increase the rate of C 3 uptake by the virus-infected cells, also increase the rate of MAC accumulation on the cells. Thus, as in the case of Raji cells (see above), fast accumulation of MAC on a nucleated target cell may facilitate lysis. XI. Inactivation of Viruses An impressive literature is developing describing the classical pathway’s capacity to inactivate viruses with or without antiviral antibody (Cooper, 1979). In contrast, little is known about the role of the alternative pathway in virus neutralization.
Advances in Immunology, Vol. 29 by Henry G. Kunkel and Frank J. Dixon (Eds.)