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Infection and Immunity, April 2000, p. 1760-1764, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Comparison of the Immune Profile of Nonhealing Cutaneous Leishmaniasis Patients with Those with Active Lesions and Those Who Have Recovered from Infection

Soheila Ajdary,1 Mohammad H. Alimohammadian,1 Mohammad B. Eslami,2 Kaare Kemp,3 and Arsalan Kharazmi3,*

Department of Immunology, Pasteur Institute,1 and Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences,2 Tehran, Iran, and Center for Medical Parasitology, Department of Clinical Microbiology, University Hospital (Rigshospitalet), Copenhagen, Denmark3

Received 12 July 1999/Returned for modification 25 August 1999/Accepted 21 December 1999

Th1-type cellular immune responses play a critical role in protection against infection with Leishmania parasites, whereas activation of Th2-type cells results in progressive disease. Cutaneous leishmaniasis caused by Leishmania major is often a self-healing disease; however, persistent nonhealing forms are also known. In the present study, we have described cell-mediated immune responses in nonhealing patients by measuring T-cell proliferation, cytokine production, and phenotypic characterization of these cells. The responses were compared with those of patients with active lesions, patients who had recovered from infection, and healthy controls. Peripheral blood mononuclear cells from patients with active lesions and recovered donors proliferated vigorously and produced Th1-type cytokine when stimulated with L. major antigens, whereas in nonhealing patients the proliferative responses were significantly lower and showed a Th2-type response to Leishmania antigens. Interleukin-10 (IL-10) production was not a feature of L. major stimulation. Flow cytometric analysis revealed that L. major antigen induced proliferation of the CD4-positive population and that these cells were the major source of gamma interferon and IL-4. These results show a distinct dichotomy in the cytokine response to L. major infection.

* Corresponding author. Mailing address: Department of Clinical Microbiology, Rigshospitalet, Afsnit 7806, Tagensvej 20, DK-2200 Copenhagen N, Denmark. Phone: (45) 35457734. Fax: (45) 35456831. E-mail: kharazmi{at}inet.uni2.dk.

Infection and Immunity, April 2000, p. 1760-1764, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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