Tags

Type your tag names separated by a space and hit enter

Natural regulatory (CD4+CD25+FOXP+) T cells control the production of pro-inflammatory cytokines during Plasmodium chabaudi adami infection and do not contribute to immune evasion.
Int J Parasitol. 2008 Feb; 38(2):229-38.IJ

Abstract

Different functions have been attributed to natural regulatory CD4+CD25+FOXP+ (Treg) cells during malaria infection. Herein, we assessed the role for Treg cells during infections with lethal (DS) and non-lethal (DK) Plasmodium chabaudi adami parasites, comparing the levels of parasitemia, inflammation and anaemia. Independent of parasite virulence, the population of splenic Treg cells expanded during infection, and the absolute numbers of activated CD69+ Treg cells were higher in DS-infected mice. In vivo depletion of CD25+ T cells, which eliminated 80% of CD4+FOXP3+CD25+ T cells and 60-70% of CD4+FOXP3+ T cells, significantly decreased the number of CD69+ Treg cells in mice with lethal malaria. As a result, higher parasite burden and morbidity were measured in the latter, whereas the kinetics of infection with non-lethal parasites remained unaffected. In the absence of Treg cells, parasite-specific IFN-gamma responses by CD4+ T cells increased significantly, both in mice with lethal and non-lethal infections, whereas IL-2 production was only stimulated in mice with non-lethal malaria. Following the depletion of CD25+ T cells, the production of IL-10 by CD90(-) cells was also enhanced in infected mice. Interestingly, a potent induction of TNF-alpha and IFN-gamma production by CD4+ and CD90(-) lymphocytes was measured in DS-infected mice, which also suffered severe anaemia earlier than non-depleted infected controls. Taken together, our data suggest that the expansion and activation of natural Treg cells represent a counter-regulatory response to the overwhelming inflammation associated with lethal P.c. adami. This response to infection involves TH1 lymphocytes as well as cells from the innate immune system.

Authors+Show Affiliations

Department of Biological Sciences, Université du Québec à Montréal, Case postale 8888, Succursale centre-ville, Montréal, Que., Canada H3C 3P8.No 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

17868677

Citation

Cambos, M, et al. "Natural Regulatory (CD4+CD25+FOXP+) T Cells Control the Production of Pro-inflammatory Cytokines During Plasmodium Chabaudi Adami Infection and Do Not Contribute to Immune Evasion." International Journal for Parasitology, vol. 38, no. 2, 2008, pp. 229-38.
Cambos M, Bélanger B, Jacques A, et al. Natural regulatory (CD4+CD25+FOXP+) T cells control the production of pro-inflammatory cytokines during Plasmodium chabaudi adami infection and do not contribute to immune evasion. Int J Parasitol. 2008;38(2):229-38.
Cambos, M., Bélanger, B., Jacques, A., Roulet, A., & Scorza, T. (2008). Natural regulatory (CD4+CD25+FOXP+) T cells control the production of pro-inflammatory cytokines during Plasmodium chabaudi adami infection and do not contribute to immune evasion. International Journal for Parasitology, 38(2), 229-38.
Cambos M, et al. Natural Regulatory (CD4+CD25+FOXP+) T Cells Control the Production of Pro-inflammatory Cytokines During Plasmodium Chabaudi Adami Infection and Do Not Contribute to Immune Evasion. Int J Parasitol. 2008;38(2):229-38. PubMed PMID: 17868677.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Natural regulatory (CD4+CD25+FOXP+) T cells control the production of pro-inflammatory cytokines during Plasmodium chabaudi adami infection and do not contribute to immune evasion. AU - Cambos,M, AU - Bélanger,B, AU - Jacques,A, AU - Roulet,A, AU - Scorza,T, Y1 - 2007/07/26/ PY - 2007/04/07/received PY - 2007/07/09/revised PY - 2007/07/16/accepted PY - 2007/9/18/pubmed PY - 2008/6/27/medline PY - 2007/9/18/entrez SP - 229 EP - 38 JF - International journal for parasitology JO - Int. J. Parasitol. VL - 38 IS - 2 N2 - Different functions have been attributed to natural regulatory CD4+CD25+FOXP+ (Treg) cells during malaria infection. Herein, we assessed the role for Treg cells during infections with lethal (DS) and non-lethal (DK) Plasmodium chabaudi adami parasites, comparing the levels of parasitemia, inflammation and anaemia. Independent of parasite virulence, the population of splenic Treg cells expanded during infection, and the absolute numbers of activated CD69+ Treg cells were higher in DS-infected mice. In vivo depletion of CD25+ T cells, which eliminated 80% of CD4+FOXP3+CD25+ T cells and 60-70% of CD4+FOXP3+ T cells, significantly decreased the number of CD69+ Treg cells in mice with lethal malaria. As a result, higher parasite burden and morbidity were measured in the latter, whereas the kinetics of infection with non-lethal parasites remained unaffected. In the absence of Treg cells, parasite-specific IFN-gamma responses by CD4+ T cells increased significantly, both in mice with lethal and non-lethal infections, whereas IL-2 production was only stimulated in mice with non-lethal malaria. Following the depletion of CD25+ T cells, the production of IL-10 by CD90(-) cells was also enhanced in infected mice. Interestingly, a potent induction of TNF-alpha and IFN-gamma production by CD4+ and CD90(-) lymphocytes was measured in DS-infected mice, which also suffered severe anaemia earlier than non-depleted infected controls. Taken together, our data suggest that the expansion and activation of natural Treg cells represent a counter-regulatory response to the overwhelming inflammation associated with lethal P.c. adami. This response to infection involves TH1 lymphocytes as well as cells from the innate immune system. SN - 0020-7519 UR - https://www.unboundmedicine.com/medline/citation/17868677/Natural_regulatory__CD4+CD25+FOXP+__T_cells_control_the_production_of_pro_inflammatory_cytokines_during_Plasmodium_chabaudi_adami_infection_and_do_not_contribute_to_immune_evasion_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0020-7519(07)00250-0 DB - PRIME DP - Unbound Medicine ER -