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By Frank J. Dixon and Henry G. Kunkel (Eds.)

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1914). 2. lmmunitaetsfursch. Exp. , No. I 21, 604. 38. Cochrane, C. , Miiller-Eberhard, H. , and Aikin, B. S. (1970). J. Immunol. 105, 55. 39. Colten, H. , and Bienenstock, J. (1974). Adv. Exp. Med. Biol. 45, 305. 40. Cooper, N. R. ( 1971). Prog. , Int! Congr. , Ist, 1971 p. 567. 41. Cooper, N. R. (1973). J . Exp. Med. 137,451. 42. Cooper, N. , and Ziccardi, R. J. (1976). In “Proteolysis and Physiological Regulation” (D. W. Ribbons and K. ) Miami Winter Symposia, Vol. 11, Academic Press, New York (in press).

Similar results were obtained by Graff et al. ( 9 3 ) who showed that C3, C5, C6, and C7 are required for zymosan- or restocetin-induced aggregation and release reactions of human platelets. The two terminal components were not needed for these noiicytolytic events. Solid evidence for a role of the alternative pathway in disease in the absence of classic pathway activation is difficult to obtain except in cases with genetic deficiencies of one of the early acting components. This difficrrlty may be explained by the fact that C3b generated through the classical pathway or through other tiyptic proteinases can activate and bind PA and that the resulting C3b,I3 complex if deposited onto a surface can activate and bind properdin ( 151,152).

Invest. 52, 634. 147. McLean, R. , and Michael, A. F. (1974). Prog. , Int. Congr. , 2nd, 1974 Vol. 5, p. 69. 148. McNall, E. G. (1957). Proc. Exp. Biol. Med. 94, 399. 149. Medicus, R. , and Miiller-Eberhard, H. J. (1976). J. lmmunol 116, 1741. 150. Medicus, R. , and Muller-Eberhard, H. J. (1976). Fed. ,Fed. Am. SOC. Exp. Biol. 35, 6’54. 151. Medicus, R. , and Miiller-Eberhard, H. J. (1976). 1. Erp. Med. (in press). 151a. Medicus, R. , and Muller-Eberhard, H. J. (1976). Scand. J. Immunol. (in press).

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