Regulatory T-Cell Dynamics in Cutaneous and Mucocutaneous Leishmaniasis due to Leishmania braziliensis

Nicolas Barros Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;

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Nestor Vasquez Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;

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Fernando Woll Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;

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Cesar Sanchez Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;

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Braulio Valencia Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;

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Alejandro Llanos-Cuentas Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;

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A. Clinton White Jr. Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;
Division of Infectious Disease, Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas

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Martin Montes Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Lima, Peru;
Division of Infectious Disease, Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas

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To evaluate the dynamics of regulatory T cells (Tregs) during tegumentary leishmaniasis, we assessed peripheral blood and biopsies from 54 patients. Patients with cutaneous leishmaniasis (CL) had a decreased proportion of Tregs in the peripheral blood, but the proportion was higher in the biopsies of lesions. During treatment of CL, circulating Tregs increased reaching normal proportions, whereas antigen-specific interferon-γ responses diminished. By contrast, circulating Tregs from mucosal leishmaniasis patients failed to normalize during treatment. C-C chemokine receptor type 5 was expressed on a large proportion of Tregs at the site of infection. These results demonstrate increased Tregs at the site of infection, possibly homing from the peripheral circulation.

Author Notes

Address correspondence to A. Clinton White Jr., Division of Infectious Disease, Department of Internal Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0435. E-mail: acwhite@utmb.edu

Financial support: The experiments reported in this article have been supported by funds from the National Institute of Health (NIH) grant (1RO1 A1075575-01A1), and a Fogarty Training grant (D43TW006569).

Authors’ addresses: Nicolas Barros and Fernando Woll, University of Texas Southwestern, Dallas, TX, E-mails: nicolas_barros@hotmail.com and fernando.woll@upch.pe. Nestor Vasquez, Braulio Valencia, and Martin Montes, Instituto de Medicina Tropical Alexander von Humboldt, Universidad Peruana Cayetano Heredia, Lima, Peru, E-mails: nvasquez.92@gmail.com, braulio.valencia@upch.pe, and martinmd@mac.com. Cesar Sanchez, Instituto Nacional de Salud, Lima, Peru, E-mail: cesarsanz4@yahoo.com. Alejandro Llanos-Cuentas, Malaria and Leishmaniasis Division, Instituto de Medicina Tropical Alexander von Humboldt, Lima, Peru, E-mail: alejandro.llanos.c@upch.pe. A. Clinton White Jr., Department of Internal Medicine, UTMB, Galveston, TX, E-mail: acwhite@utmb.edu.

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