Memory T cells protect against Plasmodium vivax infection

Jangpatarapongsa, Kulachart; Sirichaisinthop, Jeeraphat; Sattabongkot, Jetsumon; Montgomery, Scott; Udomsangpetch, Rachanee

doi:10.1016/j.micinf.2005.09.003

Cited by 24 publications

(29 citation statements)

References 19 publications

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“…Similar findings have been reported in both P. vivax and P. falciparum infections [21–24]. Even though there is evidence that CD8 Treg produce IL-10 to suppress T cell responses [25], our result showed a significant correlation between elevated levels of Tr1 and FOXP3 + Treg, a result further corroborating our earlier finding of increased levels of total CD4 + T cells during acute P. vivax infections [2]. In parallel, we also found a concurrent increase levels of Treg and expression of IL-10 when PBMC from naive controls were stimulated with P. vivax antigens in vitro .…”

Section: Discussionsupporting

confidence: 92%

“…There are evidence indicates that Treg can suppress T-cell responses through the production of IL-10 and TGF-β [17, 18], whereas they may suppress B-cell maturation and differentiation directly [19, 20] or indirectly through the down-regulation of IL-2 or IL-4 production in responder lymphocytes. This may account for low parasite-specific antibody levels seen in P. vivax patients [2]. …”

Section: Discussionmentioning

confidence: 99%

“…Our recent study has shown that anti- P. vivax antibody levels were very low in immune individuals living in endemic area and in patients with acute P. vivax malaria. For the cell-mediated arm, an acute P. vivax infection was associated with the activation of memory T cells belonging to either a cytotoxic or helper phenotype [2]. Additionally, previous evidence [3, 4] shows that immunization with pre-erythocytic antigens can induce IFN-γ release.…”

Section: Introductionmentioning

confidence: 99%

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Plasmodium vivax parasites alter the balance of myeloid and plasmacytoid dendritic cells and the induction of regulatory T cells

et al. 2008

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Immunity induced by Plasmodium vivax infections leads to memory T-cell recruitment and activation during subsequent infections. Here, we investigated the role of regulatory T cells (Treg) in coordination with the host immune response during P. vivax infection. Our results showed a significant increase in the percentage of FOXP31 Treg, IL-10-secreting Type I Treg (Tr1) and IL-10 levels in patients with acute P. vivax infection as compared with those found in either naïve or immune controls. The concurrent increase in the Treg population could also be reproduced in vitro using peripheral blood mononuclear cells from naïve controls stimulated with crude antigens extracted from P. vivax-infected red blood cells. Acute P. vivax infections were associated with a significant decrease in the numbers of DC, indicating a general immunosuppression during P. vivax infections. However, unlike P. falciparum infections, we found that the ratio of myeloid DC (MDC) to plasmacytoid DC (PDC) was significantly lower in acute P. vivax patients than that of naïve and immune controls. Moreover, the reduction in PDC may be partly responsible for the poor antibody responses during P. vivax infections. Taken together, these results suggest that P. vivax parasites interact with DC, which alters the MDC/PDC ratio that potentially leads to Treg activation and IL-10 release.Key words: Dendritic cell . IL-10 . Malaria . Plasmodium vivax . Regulatory T cell Eur. J. Immunol. 2008. 38: 2697-2705 DOI 10.1002 Immunity to infection 2697 IntroductionMalaria is a common tropical disease causing deaths among Plasmodium falciparum-infected children mainly in Sub-Saharan Africa [1]. P. falciparum causes malignant tertian malaria that accounts for most malaria-associated deaths, whereas P. vivax causes relapsing fever and the infection rarely becomes fatal. Although a better understanding of immunity is needed for the design of effective vaccines, immune regulation in the host during malaria infection is not fully understood, and few studies have been conducted in patients with P. vivax infections. Our recent study has shown that anti-P. vivax antibody levels were very low in immune individuals living in endemic area and in patients with acute P. vivax malaria. For the cell-mediated arm, an acute P. vivax infection was associated with the activation of memory T cells belonging to either a cytotoxic or helper phenotype [2]. Additionally, previous evidence [3,4] shows that immunization with pre-erythrocytic antigens can induce IFN-g release. This suggests that P. vivax can activate the immune system via the Th1 pathway. However, a possible suppressing mechanism arises from the activation of regulatory T cells (Treg) as has been shown in a murine malaria study [5]. Treg constitutively express CD25, which is the IL-2/a chain receptor [6]. Co-presentation of CD25 with forkhead box protein P3 (FOXP3) dictates the immune-suppressive role of Treg via the release of . Treg have been shown to alter the balance between myeloid dendritic cells (MDC) and plasmacytoi...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Plasmodium vivax parasites alter the balance of myeloid and plasmacytoid dendritic cells and the induction of regulatory T cells

et al. 2008

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“…Those authors interpreted the reduction in the lymphocyte subpopulations in the peripheral blood as a suppressant effect in the response to the P. vivax [55, 56, 63–65]. According to them, such reduction could be due to the high apoptosis levels or to the relocation of the cells in the liver and in other lymphoid compartments [55, 64, 66–68]. In the present study, the major changes, occurred in T-lymphocyte subsets, were observed in the group with recurrent malaria; however, further investigations must be performed to elucidate it, as the phenomenon is more accentuated in this group.…”

Section: Discussionmentioning

confidence: 99%

Immune response pattern in recurrent Plasmodium vivax malaria

Chaves

Costa

Pereira

et al. 2016

Malar J

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BackgroundPlasmodium vivax is the causative agent of human malaria of large geographic distribution, with 35 million cases annually. In Brazil, it is the most prevalent species, being responsible by around 70 % of the malaria cases.MethodsA cross-sectional study was performed in Manaus (Amazonas, Brazil), including 36 adult patients with primary malaria, 19 with recurrent malaria, and 20 endemic controls. The ex vivo phenotypic features of circulating leukocyte subsets (CD4+ T-cells, CD8+ T-cells, NK, NKT, B, B1 and Treg cells) as well as the plasmatic cytokine profile (IL-2, IL-4, IL-6, IL-10, TNF and IFN-γ) were assessed, aiming at establishing patterns of immune response characteristic of primary malaria vs recurrent malaria as compared to endemic controls.ResultsThe proportion of subjects with high levels of WBC was reduced in malaria patients as compared to the endemic control. Monocytes were diminished particularly in patients with primary malaria. The proportion of subjects with high levels of all lymphocyte subsets was decreased in all malaria groups, regardless their clinical status. Decreased proportion of subjects with high levels of CD4+ and CD8+ T-cells was found especially in the group of patients with recurrent malaria. Data analysis indicated significant increase in the proportion of the subjects with high plasmatic cytokine levels in both malaria groups, characterizing a typical cytokine storm. Recurrent malaria patients displayed the highest plasmatic IL-10 levels, that correlated directly with the CD4+/CD8+ T-cells ratio and the number of malaria episodes.ConclusionThe findings confirm that the infection by the P. vivax causes a decrease in peripheral blood lymphocyte subsets, which is intensified in the cases of “recurrent malaria”. The unbalanced CD4+/CD8+ T-cells ratio, as well as increased IL-10 levels were correlated with the number of recurrent malaria episodes. These results suggest that the gradual remodelling of the immune response is dependent on the repeated exposure to the parasite, which involves a strict control of the immune response mediated by the CD4+/CD8+ T-cell unbalance and exacerbated IL-10 secretion.Electronic supplementary materialThe online version of this article (doi:10.1186/s12936-016-1501-5) contains supplementary material, which is available to authorized users.

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“…Entretanto, estudos de fenotipagem celular em episódios agudos de malária vivax usando extrato de P. vivax mostraram alta proporção de linfócitos T CD4 com fenótipo de células de memória (CD4+CD45RO+), sugerindo que as células T de memória não foram suprimidas por este parasita (Jangpatarapongsa et al, 2006).…”

Section: Resultsunclassified

Fatores de risco, distribuição espacial e perspectivas de controle da malária: estudo longitudinal em uma comunidade rural da Amazônia (Granada, Acre).

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Memory T cells protect against Plasmodium vivax infection

Cited by 24 publications

References 19 publications

Plasmodium vivax parasites alter the balance of myeloid and plasmacytoid dendritic cells and the induction of regulatory T cells

Plasmodium vivax parasites alter the balance of myeloid and plasmacytoid dendritic cells and the induction of regulatory T cells

Immune response pattern in recurrent Plasmodium vivax malaria

Fatores de risco, distribuição espacial e perspectivas de controle da malária: estudo longitudinal em uma comunidade rural da Amazônia (Granada, Acre).

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