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Anti-IL-2 treatment impairs the expansion of T(reg) cell population during acute malaria and enhances the Th1 cell response at the chronic disease.
PLoS One 2012; 7(1):e29894Plos

Abstract

Plasmodium chabaudi infection induces a rapid and intense splenic CD4(+) T cell response that contributes to both disease pathogenesis and the control of acute parasitemia. The subsequent development of clinical immunity to disease occurs concomitantly with the persistence of low levels of chronic parasitemia. The suppressive activity of regulatory T (T(reg)) cells has been implicated in both development of clinical immunity and parasite persistence. To evaluate whether IL-2 is required to induce and to sustain the suppressive activity of T(reg) cells in malaria, we examined in detail the effects of anti-IL-2 treatment with JES6-1 monoclonal antibody (mAb) on the splenic CD4(+) T cell response during acute and chronic P. chabaudi AS infection in C57BL/6 mice. JES6-1 treatment on days 0, 2 and 4 of infection partially inhibits the expansion of the CD4(+)CD25(+)Foxp3(+) cell population during acute malaria. Despite the concomitant secretion of IL-2 and expression of high affinity IL-2 receptor by large CD4(+) T cells, JES6-1 treatment does not impair effector CD4(+) T cell activation and IFN-γ production. However, at the chronic phase of the disease, an enhancement of cellular and humoral responses occurs in JES6-1-treated mice, with increased production of TNF-α and parasite-specific IgG2a antibodies. Furthermore, JES6-1 mAb completely blocked the in vitro proliferation of CD4(+) T cells from non-treated chronic mice, while it further increased the response of CD4(+) T cells from JES6-1-treated chronic mice. We conclude that JES6-1 treatment impairs the expansion of T(reg) cell population during early P. chabaudi malaria and enhances the Th1 cell response in the late phase of the disease.

Authors+Show Affiliations

Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, São Paulo, Brasil. cazago@usp.brNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22272258

Citation

Zago, Cláudia A., et al. "Anti-IL-2 Treatment Impairs the Expansion of T(reg) Cell Population During Acute Malaria and Enhances the Th1 Cell Response at the Chronic Disease." PloS One, vol. 7, no. 1, 2012, pp. e29894.
Zago CA, Bortoluci KR, Sardinha LR, et al. Anti-IL-2 treatment impairs the expansion of T(reg) cell population during acute malaria and enhances the Th1 cell response at the chronic disease. PLoS ONE. 2012;7(1):e29894.
Zago, C. A., Bortoluci, K. R., Sardinha, L. R., Pretel, F. D., Castillo-Méndez, S. I., Freitas do Rosário, A. P., ... D'Império Lima, M. R. (2012). Anti-IL-2 treatment impairs the expansion of T(reg) cell population during acute malaria and enhances the Th1 cell response at the chronic disease. PloS One, 7(1), pp. e29894. doi:10.1371/journal.pone.0029894.
Zago CA, et al. Anti-IL-2 Treatment Impairs the Expansion of T(reg) Cell Population During Acute Malaria and Enhances the Th1 Cell Response at the Chronic Disease. PLoS ONE. 2012;7(1):e29894. PubMed PMID: 22272258.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anti-IL-2 treatment impairs the expansion of T(reg) cell population during acute malaria and enhances the Th1 cell response at the chronic disease. AU - Zago,Cláudia A, AU - Bortoluci,Karina R, AU - Sardinha,Luiz R, AU - Pretel,Fernando D, AU - Castillo-Méndez,Sheyla I, AU - Freitas do Rosário,Ana Paula, AU - Hiyane,Meire I, AU - Muxel,Sandra M, AU - Rodriguez-Málaga,Sérgio M, AU - Abrahamsohn,Ises A, AU - Álvarez,José M, AU - D'Império Lima,Maria Regina, Y1 - 2012/01/17/ PY - 2011/07/15/received PY - 2011/12/07/accepted PY - 2012/1/25/entrez PY - 2012/1/25/pubmed PY - 2012/6/12/medline SP - e29894 EP - e29894 JF - PloS one JO - PLoS ONE VL - 7 IS - 1 N2 - Plasmodium chabaudi infection induces a rapid and intense splenic CD4(+) T cell response that contributes to both disease pathogenesis and the control of acute parasitemia. The subsequent development of clinical immunity to disease occurs concomitantly with the persistence of low levels of chronic parasitemia. The suppressive activity of regulatory T (T(reg)) cells has been implicated in both development of clinical immunity and parasite persistence. To evaluate whether IL-2 is required to induce and to sustain the suppressive activity of T(reg) cells in malaria, we examined in detail the effects of anti-IL-2 treatment with JES6-1 monoclonal antibody (mAb) on the splenic CD4(+) T cell response during acute and chronic P. chabaudi AS infection in C57BL/6 mice. JES6-1 treatment on days 0, 2 and 4 of infection partially inhibits the expansion of the CD4(+)CD25(+)Foxp3(+) cell population during acute malaria. Despite the concomitant secretion of IL-2 and expression of high affinity IL-2 receptor by large CD4(+) T cells, JES6-1 treatment does not impair effector CD4(+) T cell activation and IFN-γ production. However, at the chronic phase of the disease, an enhancement of cellular and humoral responses occurs in JES6-1-treated mice, with increased production of TNF-α and parasite-specific IgG2a antibodies. Furthermore, JES6-1 mAb completely blocked the in vitro proliferation of CD4(+) T cells from non-treated chronic mice, while it further increased the response of CD4(+) T cells from JES6-1-treated chronic mice. We conclude that JES6-1 treatment impairs the expansion of T(reg) cell population during early P. chabaudi malaria and enhances the Th1 cell response in the late phase of the disease. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/22272258/Anti_IL_2_treatment_impairs_the_expansion_of_T_reg__cell_population_during_acute_malaria_and_enhances_the_Th1_cell_response_at_the_chronic_disease_ L2 - http://dx.plos.org/10.1371/journal.pone.0029894 DB - PRIME DP - Unbound Medicine ER -