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The Journal of Immunology, 1971, 106, 888 -899
Copyright © 1971 by The American Association of Immunologists, Inc.

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Studies of Immune Mechanisms in Leprosy

III. The Role of Cellular and Humoral Factors in Impairment of the in Vitro Immune Response1

Ward E. Bullock, Jr.2 and Paul Fasal

Division of Immunology and Infectious Disease, Department of Medicine, University of Rochester School of Medicine, Rochester, New York, and the Leprosy Service, United States Public Health Service Hospital, San Francisco, California

Abstract

Phytohemagglutinin (PHA)- and antigen-induced DNA synthesis was measured in leukocyte cultures from 16 patients with lepromatous leprosy, 12 with tuberculoid leprosy, and 20 normal persons. In cultures containing 20% autologous plasma, the responses of lepromatous leukocytes to PHA, purified protein derivative (PPD), streptolysin O (SLO) and antigens of Mycobacterium leprae were significantly below those of the control group. Simultaneous culture of lepromatous leukocytes washed and suspended in normal homologous plasma (20%) resulted in significantly increased SLO-induced DNA synthesis and a modest increase in response to PPD. The response to PHA and antigens of M. leprae remained unchanged. Except for PPD, the responses of tuberculoid leukocytes in autologous or homologous plasma were not significantly lower than normal. Nine of 14 lepromatous plasmas were found to contain a factor that depressed the response of normal leukocytes to PPD and SLO but not to PHA. The depressor factor is non-dialyzable, stable after prolonged storage at -20°C, and resistant to heating at 56°C; its activity is lost at relatively low dilutions. It is concluded that the in vitro demonstration of impaired cellular immune function in patients with leprosy may reflect a primary cellular defect, the depressive effect of a humoral factor, or both, to varying degrees.

Footnotes

1 Presented in part at the national meeting of the American Federation for Clinical Research, May 5, 1968, Atlantic City, New Jersey, and the Ninth International Leprosy Congress, London, England, September 18, 1968. This work was supported by United States Public Health Service Research Grant AI-07964 and a Buswell Fellowship in Medicine.

2 Present address: Division of Infectious Disease, Department of Medicine, University of Kentucky School of Medicine, Lexington, Kentucky 40506. Reprint requests should be sent to this address.




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