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Journal of Immunology Research
Volume 2017 (2017), Article ID 3062892, 6 pages
Research Article

In Vitro Immunomodulatory Activity of a Transition-State Analog Inhibitor of Human Purine Nucleoside Phosphorylase in Cutaneous Leishmaniasis

1Serviço de Imunologia do Complexo Hospitalar Universitário Professor Edgard Santos (Com-HUPES), Universidade Federal da Bahia, Salvador, BA, Brazil
2Centro de Pesquisas em Biologia Molecular e Funcional (CPBMF), Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, RS, Brazil
3Fundação Oswaldo Cruz (FIOCRUZ), Instituto Gonçalo Moniz (CPqGM), Salvador, BA, Brazil

Correspondence should be addressed to Edgar Marcelino de Carvalho; rb.abfu@onumi

Received 14 May 2017; Accepted 31 July 2017; Published 27 August 2017

Academic Editor: Nejat K. Egilmez

Copyright © 2017 Natália Barbosa Carvalho et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cutaneous leishmaniasis (CL) is the most common clinical form of American tegumentary leishmaniasis caused by Leishmania (Viannia) braziliensis. CL is associated with a strong Th1 immune response. This exacerbated inflammatory response is correlated with severity of disease and delays the healing time of the ulcer. The fourth-generation immucillin derivative (DI4G), a potent inhibitor of purine nucleoside phosphorylase, has been proposed as a promising agent in the treatment of diseases associated with T cell activation. Herein, we evaluated the in vitro immunomodulatory activity of DI4G in cells of patients presenting with CL. Peripheral blood mononuclear cells (PBMC) from CL patients were stimulated with soluble leishmania antigen (SLA), in the presence or absence of DI4G, and IFN-γ, TNF, CXCL9, and CXCL10 levels were determined by ELISA. Lymphocyte proliferation in the presence or absence of DI4G was also evaluated, using flow cytometry. DI4G was able to decrease () IFN-γ production but did not change the TNF, CXCL9, and CXCL10 levels. DI4G decreased () the lymphoproliferative response mediated by CD8+ T cells, but not that by CD4+ T cells. DI4G is able to attenuate the exaggerated immune response in CL, exhibiting immunomodulatory activity in IFN-γ production and in CD8+ T cell proliferation.