Deficiency of the Chemotactic Factor Inactivator in Human Sera with α<sub>1</sub>-Antitrypsin Deficiency

Peter A. Ward; Richard C. Talamo

doi:10.1172/JCI107209

^{Department of Pathology, The University of Connecticut Health Center, Farmington, Connecticut 06032}

^{Immunology Unit, Children's Service, Massachusetts General Hospital, Boston, Massachusetts 02114}

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^{Department of Pathology, The University of Connecticut Health Center, Farmington, Connecticut 06032}

^{Immunology Unit, Children's Service, Massachusetts General Hospital, Boston, Massachusetts 02114}

Find articles by Talamo, R. in: JCI | PubMed | Google Scholar

Published in Volume 52, Issue 2 on February 1, 1973
J Clin Invest. 1973;52(2):516–519. https://doi.org/10.1172/JCI107209.
© 1973 The American Society for Clinical Investigation

Published February 1, 1973 - Version history

As revealed by appropriate fractionation procedures, human serum deficient in α₁-antitrypsin (α₁-AT) is also deficient in the naturally occurring chemotactic factor inactivator. These serum donors had severe pulmonary emphysema. Serum from patients with clinically similar pulmonary disease, but with presence of α₁-AT in the serum, showed no such deficiency of the chemotactic factor inactivator. When normal human serum and α₁-AT-deficient human sera are chemotactically activated by incubation with immune precipitates, substantially more chemotactic activity is generated in α₁-AT-deficient serum. These data indicate that in α₁-AT-deficient serum there is an imbalance in the generation and control of chemotactic factors. It is suggested that the theory regarding development of pulmonary emphysema in patients lacking the α₁-antitrypsin in their serum should be modified to take into account a deficiency of the chemotactic factor inactivator.

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