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Human Heat Labile Opsonins: Evidence for Their Mediation via the Alternate Pathway of Complement Activation¹

From the Department of Internal Medicine, Rheumatic Diseases Unit, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Abstract

The possible participation of the alternate pathway of C3 activation in the activation of human heat labile opsonins by bacteria has been investigated. It was shown that: a) opsonization took place normally in human sera completely lacking C1q; b) complete absorption of immunoglobulins and C1q from agammaglobulinemic sera failed to abolish opsonic capacity; c) heat labile opsonic capacity for Escherichia coli was markedly reduced by heating normal serum at 50°C for 30 min, conditions which inactivate a component of the alternate pathway of complement activation and d) addition to such heated serum of purified C3 proactivator, a constituent of the alternate pathway, resulted in restoration of a significant fraction of the opsonic activity. These results indicate that heat labile opsonization is mediated via an alternate pathway of C3 activation.

Footnotes

¹ This investigation was supported by United States Public Health Service Research Grant AM-09989 and Training Grant AM-05154.

² Post-doctoral Fellow, The Arthritis Foundation.