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Infect Immun, March 1998, p. 1233-1236, Vol. 66, No. 3
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Transforming Growth Factor beta  and Immunosuppression in Experimental Visceral Leishmaniasis

Virmondes Rodrigues Jr.,1,* João Santana da Silva,2 and Antonio Campos-Neto3,4,*

Immunology Laboratory, Medical School of Triângulo Mineiro, Uberaba,1 MG, Department of Immunology, Medical School of Ribeirão Preto, Ribeirão Preto,2 SP, and Medical School of Itajubá,3 MG, Brazil, and Infectious Disease Research Institute, Seattle, Washington 981044

Received 26 September 1997/Returned for modification 13 November 1997/Accepted 3 December 1997

Hamsters infected with Leishmania donovani develop a disease similar to human kala-azar. They present hypergammaglobulinemia, and their T cells do not respond to parasite antigens. This unresponsiveness has been primarily ascribed to defects in antigen-presenting cells (APCs), because these cells are unable to stimulate proliferation of parasite-specific T cells from immunized animals. In this study, we show that APCs (adherent spleen cells) from L. donovani-infected hamsters produce high levels of the inhibitory cytokine transforming growth factor beta  (TGF-beta ). Immunohistochemical studies with an anti-TGF-beta monoclonal antibody (MAb) showed that this cytokine is abundantly produced in vivo by the spleen cells of infected animals. In addition, high levels of TGF-beta are produced in vitro by infected hamster cells, either spontaneously or after stimulation with parasite antigen or lipopolysaccharide. Furthermore, in vivo-infected adherent cells obtained from spleens of L. donovani-infected hamsters caused profound inhibition of the in vitro antigen-induced proliferative response of lymph node cells from hamsters immunized with leishmanial antigens. Moreover, this inhibition was totally abrogated by the anti-TGF-beta MAb. These results suggest that the immunosuppression observed in visceral leishmaniasis is, at least in part, due to the abundant production of TGF-beta during the course of the infection.

* Corresponding author. Mailing address for Antonio Campos-Neto: Infectious Disease Research Institute, 1124 Columbia St., Seattle, WA 98104-2015. Phone: (206) 667-5799. Fax: (206) 667-5715. E-mail: acampos{at}corixa.com. Mailing address for Virmondes Rodrigues, Faculdade de Medicina do Triângulo Mineiro, Laboratório de Immunologia, Rua Frei Paulino 30, Uberaba, MG 38025-180, Brazil. Phone: 55 34 312-7722. Fax: 55 34 312-6640. E-mail: vrodrigues{at}mednet.com.br.




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