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Infect Immun, February 1998, p. 499-504, Vol. 66, No. 2
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Changes in Expression of Signal Transduction Proteins in T Lymphocytes of Patients with Leprosy

Arnold H. Zea,1,2,* Maria T. Ochoa,3,4 Paritosh Ghosh,5 Dan L. Longo,6 W. Gregory Alvord,7 Liliana Valderrama,3 Rafael Falabella,4 Linda K. Harvey,2 Nancy Saravia,3 Luis H. Moreno,4 and Augusto C. Ochoa1,2,*

Immunotherapy Program, Stanley S. Scott Cancer Center, Louisiana State University Medical Center, New Orleans, Louisiana 701121; National Cancer Institute-Frederick Cancer Research and Development Center/Science Applications International Corporation, Frederick, Maryland 217022; Fundacion CIDEIM, A.A. 5390,3 and Servicio de Dermatología, Hospital Universitario del Valle,4 Cali, Colombia; Department of Microbiology/Immunology, University of Miami, Miami, Florida 331365; National Institute on Aging, National Institutes of Health, Baltimore, Maryland 212246; and Data Management Services, Inc., Frederick Cancer Research and Development Center, Frederick, Maryland 217027

Received 2 June 1997/Returned for modification 5 August 1997/Accepted 3 November 1997

Advanced stages of mycobacterial diseases such as leprosy and tuberculosis are characterized by a loss of T-cell function. The basis of this T-cell dysfunction is not well understood. The present report demonstrates major alterations in the expression of signal transduction molecules in T cells of leprosy patients. These alterations were most frequently observed in lepromatous leprosy (LL) patients. Of 29 LL patients, 69% had decreased T-cell receptor zeta -chain expression, 48% had decreased p56lck tyrosine kinase, and 63% had a loss of nuclear transcription factor NF-kappa B p65. An electrophoretic mobility shift assay with the gamma interferon core promoter region revealed a loss of the Th1 DNA-binding pattern in LL patients. In contrast, tuberculoid leprosy patients had only minor signal transduction alterations. These novel findings might improve our understanding of the T-cell dysfunction observed in leprosy and other infectious diseases and consequently might lead to better immunologic evaluation of patients.

* Corresponding author. Mailing address for Arnold H. Zea: Neuroscience Center, 2020 Gravier St., Suite D, Louisiana State University Medical Center, New Orleans, LA 70112. Phone: (504) 599-0911. Fax: (504) 599-0864. E-mail: azea{at}lsumc.edu. Mailing address for Augusto C. Ochoa: 1542 Tulane Ave., Suite 604K, Louisiana State University Medical Center, New Orleans, LA 70112. Phone: (504) 568-4622. Fax: (504) 568-3694. E-mail: aochoa{at}lsumc.edu.




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