Phenotypic profiling of CD8+ T cells during Plasmodium vivax blood-stage infection

Hojo-Souza, Natália Satchiko; Pereira, Dhélio Batista; Passos, Lívia Silva Araújo; Gazzinelli-Guimarães, Pedro Henrique; Cardoso, Mariana Santos; Tada, Mauro Shugiro; Zaniní, Graziela Maria; Bartholomeu, Daniella Castanheira; Fujiwara, Ricardo Toshio; Bueno, Lilian Lacerda

doi:10.1186/s12879-015-0762-x

Cited by 15 publications

(10 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The reduction among those subpopulations was also evident in other studies carried out with P. vivax naturally infected individuals [55, 59, 63, 64]. 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].…”

Section: Discussionsupporting

confidence: 76%

Immune response pattern in recurrent Plasmodium vivax malaria

Chaves

Costa

Pereira

et al. 2016

Malar J

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 76%

Immune response pattern in recurrent Plasmodium vivax malaria

Chaves

Costa

Pereira

et al. 2016

Malar J

View full text Add to dashboard Cite

show abstract

“…In the present study, vivax malaria patients have shown significant low RANTES/CCL5 levels, but just weakly associated with IL-6, IL-12p40, IFN-γ or MCP-1/CCL2. The lower levels of RANTES/CCL5 could be explained by the CD8 + T cells reduction [43–45] and thrombocytopaenia [8, 10, 11, 44–46] observed during vivax malaria. A study carried out with children infected with P. falciparum observed an association between thrombocytopaenia and lower RANTES plasma levels [47].…”

Section: Discussionmentioning

confidence: 99%

On the cytokine/chemokine network during Plasmodium vivax malaria: new insights to understand the disease

Hojo-Souza

Pereira

Souza

et al. 2017

Malar J

Self Cite

View full text Add to dashboard Cite

BackgroundThe clinical outcome of malaria depends on the delicate balance between pro-inflammatory and immunomodulatory cytokine responses triggered during infection. Despite the numerous reports on characterization of plasma levels of cytokines/chemokines, there is no consensus on the profile of these mediators during blood stage malaria. The identification of acute phase biomarkers might contribute to a better understanding of the disease, allowing the use of more effective therapeutic approaches to prevent the progression towards severe disease. In the present study, the plasma levels of cytokines and chemokines and their association with parasitaemia and number of previous malaria episodes were evaluated in Plasmodium vivax-infected patients during acute and convalescence phase, as well as in healthy donors.MethodsSamples of plasma were obtained from peripheral blood samples from four different groups: P. vivax-infected, P. vivax-treated, endemic control and malaria-naïve control. The cytokine (IL-6, IL-10, IL-17, IL-27, TGF-β, IFN-γ and TNF) and chemokine (MCP-1/CCL2, IP-10/CXCL10 and RANTES/CCL5) plasma levels were measured by CBA or ELISA. The network analysis was performed using Spearman correlation coefficient.Results Plasmodium vivax infection induced a pro-inflammatory response driven by IL-6 and IL-17 associated with an immunomodulatory profile mediated by IL-10 and TGF-β. In addition, a reduction was observed of IFN-γ plasma levels in P. vivax group. A lower level of IL-27 was observed in endemic control group in comparison to malaria-naïve control group. No significant results were found for IL-12p40 and TNF. It was also observed that P. vivax infection promoted higher levels of MCP-1/CCL2 and IP-10/CXCL10 and lower levels of RANTES/CCL5. The plasma level of IL-10 was elevated in patients with high parasitaemia and with more than five previous malaria episodes. Furthermore, association profile between cytokine and chemokine levels were observed by correlation network analysis indicating signature patterns associated with different parasitaemia levels.ConclusionsThe P. vivax infection triggers a balanced immune response mediated by IL-6 and MCP-1/CCL2, which is modulated by IL-10. In addition, the results indicated that IL-10 plasma levels are influenced by parasitaemia and number of previous malaria episodes.

show abstract

“…The primary antibodies for IL-33 (sc-130625), HBx (sc-57760) and GAPDH (sc-32233), in addition to the goat anti-mouse IgG horseradish peroxidase-conjugated secondary antibody (sc-2302) were all purchased from Santa Cruz Biotechnology, Inc. 28; PBMCs were isolated. Subsequently, the proportional changes of naïve T cells (TN; CD45RA+CCR7+), central memory T cells (TCM; CD45RA-CCR7+) and effector memory T cells (TEM; CD45RA-CCR7-) were assessed (29,30). As presented in Fig.…”

Section: Reverse Transcription-quantitative Polymerase Chain Reactionmentioning

confidence: 99%

Interleukin-33-induced immune tolerance is associated with the imbalance of memory and naïve T-lymphocyte subsets

Shi

Tang

Sun

et al. 2016

Molecular Medicine Reports

View full text Add to dashboard Cite

The current study aimed to investigate the distribution of memory and naïve T cell (TN) subsets in hepatitis B virus (HBV)‑infected patients at different immune stages and investigate the effect of interleukin 33 (IL‑33) on the regulation of the T‑cell subsets. The distributions of memory and naïve T cells were detected by flow cytometry. ELISA was conducted to assess the levels of IL‑4, IL‑5, IL‑10, IL‑12, interferon γ and tumor necrosis factor α. The expression levels of IL‑33 and HBV x protein (HBx) were measured by reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. By detecting TNs, central memory T cells (TCM) and effector memory T cells (TEM), it was identified that the proportions of TCM and TEM in CD4+ T cells were increased in patients with HBV. The trend observed for levels of CD8+ TCM and TEM was similar to that of CD4+ T cells in the immune tolerance and immune activation groups, however CD8+ TCM and TEM were significantly reduced in patients who underwent treatment. The CD8+ TEM cells appeared to be more sensitive to HBV activation and drug therapy. In addition, IL‑33 stimulation was observed to induce imbalances of CD8+ TN and CD8+ TEM, and while the imbalances were directly regulated by HBx, IL‑33 was not a key factor for the expression of HBx. CD8+ TEM cells may be a sensitive marker to assess the immune state of patients with HBV and the effect of clinical therapy. Treatment targeting IL‑33 may be a potential method to reverse HBV‑induced immune tolerance.

show abstract

Phenotypic profiling of CD8+ T cells during Plasmodium vivax blood-stage infection

Cited by 15 publications

References 23 publications

Immune response pattern in recurrent Plasmodium vivax malaria

Immune response pattern in recurrent Plasmodium vivax malaria

On the cytokine/chemokine network during Plasmodium vivax malaria: new insights to understand the disease

Interleukin-33-induced immune tolerance is associated with the imbalance of memory and naïve T-lymphocyte subsets

Contact Info

Product

Resources

About