Lima, Luciane Mota, Cardoso, Luciana Santos, Santos, Silvane Braga, Oliveira, Ricardo Riccio, Oliveira, Sergio Costa, Goes, Alfredo Miranda, Loukas, Alex, and Araujo, Maria (2017) Schistosoma antigens downregulate CXCL9 production by PBMC of HTLV-1-infected individuals. Acta Tropica, 167. pp. 157-162.

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Abstract

HTLV-1 is the causal agent of Adult T cell Leukemia/lymphoma (ATLL) and HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). The immune response to HTLV-1-infection is polarized to the Thl -type, and the presence of CXCL9/CXCL10 chemokines may lead to an increase in the recruitment of pro -inflammatory molecules in spinal cord tissue, contributing to the damage observed in the development of HAM/TSP. It has been observed that in chronic helminth-infections, such as schistosomiasis, there is a deviation toward the Th2/regulatory immune response.

Objective: To evaluate the ability of Schistosoma spp. proteins to decrease the in vitro CXCL9 and CXCL10 production by PBMC of HTLV-1-infected individuals.

Methods: The Schistosoma proteins rSm29, rSh-TSP-2 and PIII were added to PBMC cultures of HTLV-1infected individuals and the levels of chemokines in the supernatants were measured using a sandwich ELISA method.

Results: The addition of rSm29 to the cultures resulted in decreased production of CXCL9 in all the analyzed individuals and HAM/TSP group (18167 9727 pg/mL, p = 0.044; 20237 6023 pg/mL, p = 0.028, respectively) compared to the levels in unstimulated cultures (19745 +/- 9729 pg/mL; 25078 +/- 2392 pg/mL, respectively). The addition of rSh-TSP-2 decreased the production of CXCL9 in all studied individuals and carriers group (16136 +/- 9233 pg/mL, p = 0.031; 13977 +/- 8857 pg/mL, p = 0.026) vs unstimulated cultures (19745 +/- 9729 pg/mL; 18121 +/- 10508 pg/mL, respectively). Addition of Pill did not alter the results. There was no significant change in the levels of CXCL10 by the addition of the studied proteins.

Conclusion: The Schistosoma proteins used in this study were able to down modulate the production of CXCL9, a chemokine associated with the inflammatory process in HTLV-1-infection.

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