scholarly journals Limited Role of CD4+Foxp3+Regulatory T Cells in the Control of Experimental Cerebral Malaria

2009 ◽  
Vol 183 (11) ◽  
pp. 7014-7022 ◽  
Author(s):  
Christiane Steeg ◽  
Guido Adler ◽  
Tim Sparwasser ◽  
Bernhard Fleischer ◽  
Thomas Jacobs
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cerebral Malaria ◽  
Experimental Cerebral Malaria ◽  
Limited Role

scholarly journals A Role for Natural Regulatory T Cells in the Pathogenesis of Experimental Cerebral Malaria

2007 ◽  
Vol 171 (2) ◽  
pp. 548-559 ◽  
Author(s):  
Fiona H. Amante ◽  
Amanda C. Stanley ◽  
Louise M. Randall ◽  
Yonghong Zhou ◽  
Ashraful Haque ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cerebral Malaria ◽  
Experimental Cerebral Malaria

scholarly journals Limited role of regulatory T cells during acute Theiler virus-induced encephalitis in resistant C57BL/6 mice

2014 ◽  
Vol 11 (1) ◽  
Author(s):  
Chittappen K Prajeeth ◽  
Andreas Beineke ◽  
Cut Dahlia Iskandar ◽  
Viktoria Gudi ◽  
Vanessa Herder ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Limited Role

scholarly journals Suppression of Plasmodium MIF-CD74 Signaling Protects Against Severe Malaria

2021 ◽  
Author(s):  
Alvaro Baeza Garcia ◽  
Edwin Siu ◽  
Xin Du ◽  
Lin Leng ◽  
Blandine Franke-Fayard ◽  
...  
Keyword(s):  
T Cells ◽  
Inflammatory Response ◽  
Cerebral Malaria ◽  
Macrophage Migration Inhibitory Factor ◽  
Molecular Mechanisms ◽  
Macrophage Migration ◽  
Erythrocytic Stage ◽  
Experimental Cerebral Malaria ◽  
Brain Microvessels

AbstractMalaria begins when mosquito-borne Plasmodium sporozoites invade hepatocytes and usurp host pathways to support the differentiation and multiplication of erythrocyte-infective merozoite progeny. The deadliest complication of infection, cerebral malaria, accounts for the majority of malarial fatalities. Although our understanding of the cellular and molecular mechanisms underlying the pathology remains incomplete, recent studies support the contribution of systemic and neuroinflammation as the cause of cerebral edema and blood-brain barrier (BBB) dysfunction. All Plasmodium species encode an orthologue of the innate cytokine, Macrophage Migration Inhibitory Factor (MIF), which functions in mammalian biology to regulate innate responses. Plasmodium MIF (PMIF) similarly signals through the host MIF receptor CD74, leading to an enhanced inflammatory response. We investigated the PMIF-CD74 interaction in the onset of experimental cerebral malaria (ECM) using CD74 deficient (Cd74−/−) mice, which were found to be protected from ECM. The protection was associated with the inability of brain microvessels from Cd74−/− hosts to present parasite antigen to sequestered Plasmodium-specific CD8+ T cells. Infection of mice with PMIF-deficient sporozoites (PbAmif-) also protected mice from ECM, highlighting the pivotal role of PMIF in the pre-erythrocytic stage of the infection. A novel pharmacologic PMIF-selective antagonist reduced PMIF/CD74 signaling and fully protected mice from ECM. These findings reveal a conserved mechanism for Plasmodium usurpation of host CD74 signaling and suggest a tractable approach for new pharmacologic intervention.

scholarly journals Suppression of CD4+Effector Responses by Naturally Occurring CD4+CD25+Foxp3+Regulatory T Cells Contributes to Experimental Cerebral Malaria

2015 ◽  
Vol 84 (1) ◽  
pp. 329-338 ◽  
Author(s):  
Anne-Laurence Blanc ◽  
Tarun Keswani ◽  
Olivier Gorgette ◽  
Antonio Bandeira ◽  
Bernard Malissen ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Cerebral Malaria ◽  
T Cell Response ◽  
Experimental Cerebral Malaria ◽  
Content Type ◽  
Naturally Occurring ◽  
Cell Enrichment

The role of naturally occurring CD4+CD25+Foxp3+regulatory T cells (nTreg) in the pathogenesis of cerebral malaria (CM), which involves both pathogenic T cell responses and parasite sequestration in the brain, is still unclear. To assess the contribution and dynamics of nTreg during the neuropathogenesis, we unbalanced the ratio between nTreg and naive CD4+T cells in an attenuated model ofPlasmodium bergheiANKA-induced experimental CM (ECM) by using a selective cell enrichment strategy. We found that nTreg adoptive transfer accelerated the onset and increased the severity of CM in syngeneic C57BL/6 (B6)P. bergheiANKA-infected mice without affecting the level of parasitemia. In contrast, naive CD4+T cell enrichment prevented CM and promoted parasite clearance. Furthermore, early during the infection nTreg expanded in the spleen but did not efficiently migrate to the site of neuroinflammation, suggesting that nTreg exert their pathogenic action early in the spleen by suppressing the protective naive CD4+T cell response toP. bergheiANKA infectionin vivoin both CM-susceptible (B6) and CM-resistant (B6-CD4−/−) mice. However, their sole transfer was not sufficient to restore CM susceptibility in two CM-resistant congenic strains tested. Altogether, these results demonstrate that nTreg are activated and functional duringP. bergheiANKA infection and that they contribute to the pathogenesis of CM. They further suggest that nTreg may represent an early target for the modulation of the immune response to malaria.

scholarly journals IL-33-Mediated Protection against Experimental Cerebral Malaria Is Linked to Induction of Type 2 Innate Lymphoid Cells, M2 Macrophages and Regulatory T Cells

2015 ◽  
Vol 11 (2) ◽  
pp. e1004607 ◽  
Author(s):  
Anne-Gaelle Besnard ◽  
Rodrigo Guabiraba ◽  
Wanda Niedbala ◽  
Jennifer Palomo ◽  
Flora Reverchon ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cerebral Malaria ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
M2 Macrophages ◽  
Experimental Cerebral Malaria

scholarly journals CD4+ Natural Regulatory T Cells Prevent Experimental Cerebral Malaria via CTLA-4 When Expanded In Vivo

2010 ◽  
Vol 6 (12) ◽  
pp. e1001221 ◽  
Author(s):  
Ashraful Haque ◽  
Shannon E. Best ◽  
Fiona H. Amante ◽  
Seri Mustafah ◽  
Laure Desbarrieres ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cerebral Malaria ◽  
Experimental Cerebral Malaria

scholarly journals Chemokine Receptor CCR2 Is Not Essential for the Development of Experimental Cerebral Malaria

2003 ◽  
Vol 71 (6) ◽  
pp. 3648-3651 ◽  
Author(s):  
Elodie Belnoue ◽  
Fabio T. M. Costa ◽  
Ana M. Vigário ◽  
Tatiana Voza ◽  
Françoise Gonnet ◽  
...  
Keyword(s):  
T Cells ◽  
Cerebral Malaria ◽  
Chemokine Receptor ◽  
Experimental Cerebral Malaria ◽  
T Cell Migration ◽  
Mice Brain ◽  
The Brain ◽  
Deficient Mice ◽  
Chemokine Receptor Ccr2

ABSTRACT Infection with Plasmodium berghei ANKA induces cerebral malaria in susceptible mice. Brain-sequestered CD8+ T cells are responsible for this pathology. We have evaluated the role of CCR2, a chemokine receptor expressed on CD8+ T cells. Infected CCR2-deficient mice were as susceptible to cerebral malaria as wild-type mice were, and CD8+ T-cell migration to the brain was not abolished.

scholarly journals On the Pathogenic Role of Brain-Sequestered αβ CD8+T Cells in Experimental Cerebral Malaria

2002 ◽  
Vol 169 (11) ◽  
pp. 6369-6375 ◽  
Author(s):  
Elodie Belnoue ◽  
Michèle Kayibanda ◽  
Ana M. Vigario ◽  
Jean-Christophe Deschemin ◽  
Nico van Rooijen ◽  
...  
Keyword(s):  
T Cells ◽  
Cerebral Malaria ◽  
Cd8 T Cells ◽  
Pathogenic Role ◽  
Experimental Cerebral Malaria

scholarly journals Depletion of CD4+ or CD8+ T-cells prevents Plasmodium berghei induced cerebral malaria in end-stage disease

Parasitology ◽  
1997 ◽  
Vol 114 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C. HERMSEN ◽  
T. VAN DE WIEL ◽  
E. MOMMERS ◽  
R. SAUERWEIN ◽  
W. ELING
Keyword(s):  
T Cells ◽  
Cerebral Malaria ◽  
Cd8 T Cells ◽  
Plasmodium Berghei ◽  
Experimental Cerebral Malaria ◽  
Chloroquine Treatment ◽  
Stage Disease ◽  
End Stage ◽  
Further Development

The role of T-cells in development of experimental cerebral malaria was analysed in C57B1/6J and C57B1/10 mice infected with Plasmodium berghei K173 or Plasmodium berghei ANKA by treatment with anti-CD4 or anti-CD8 mAbs. Mice were protected against cerebral malaria (CM) when anti-CD4 or anti-CD8 mAbs were injected before or during infection. Even in mice in end-stage disease, i.e. with a body temperature below 35·5 °C, treatment with anti-CD4 or anti-CD8 antibodies or the combination protected against CM, whereas chloroquine treatment was completely ineffective in inhibiting further development of the cerebral syndrome.

Sign in / Sign up

Export Citation Format

Share Document