Plasmodium yoelii 17XL infection modified maturation and function of dendritic cells by skewing Tregs and amplificating Th17

Abstract

Background: Emerging data has suggested that Tregs, Th17, Th1 and Th2 are correlated with early immune mechanisms by controlling Plasmodium infection. Plasmodium infection appeared to impair the antigen presentation and maturation of DCs, leading to attenuation of specific cellular immune response ultimately. Hence, in this study, we aim to evaluate the relevance between DCs and Tregs/Th17 populations in the process and outcomes of infection with Plasmodium yoelii 17XL (P.y17XL). Methods: DCs detection/analysis dynamically was performed by Tregs depletion or Th17 neutralization in P.y17XL infected BALB/c mice via flow cytometry. Then the levels of cytokines production were detected using enzymelinked mmunosorbent assay (ELISA). Results: Our results indicated that Tregs depletion or Th17 neutralization in BALB/c mice infected with P.y17XL significantly up-regulated the percentages of mDC and pDC, increased the expressions of major histocompatibility complex (MHC) class II, CD80, CD86 on DCs and the levels of IL-10/IL-12 secreted by DCs, indicating that abnormal amplification of Tregs or Th17 may damage the maturation and function of DCs during the early stage of malaria infection. Interestingly, we also found that the abnormal amplification of Th17, as well as Tregs, could inhibit the maturation of DCs. Conclusions: Tregs skewing or Th17 amplification during the early stage of malaria infection may inhibit the maturation and function of DCs by modifying the subsets of DCs, expressions of surface molecules on DCs and secretion mode of cytokines.

Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection

“…Spleen cells from BALB/c mice were prepared at different time points after infections. To assess DCs, 1 × 10 6 cells were stained with FITC-conjugated CD11c monoclonal antibody (mAb) (clone HL-3) and PE-conjugated anti-CD11b (clone M1/70), PerCP-conjugated-CD45R/B220 (clone RA3-6B2), APC-conjugated anti-MHCII (clone M5/114.15.2; eBioscience, Thermo Fisher Scientific, Waltham, MA, USA) and PerCP-conjugated anti-CD80 (clone 16-10A1) [ 37 ].…”

“…To assess Tregs, FITC-conjugated anti-CD4 (clone GK1.5) and PE-conjugated anti-CD25 antibodies (clone PC61) were added to 1 × 10 6 spleen cells, which were resuspended in 100 μl of phosphate buffered saline (PBS) supplemented with 1% FCS for surface staining. The cells were then fixed and permeabilized, and intracytoplasmic staining was performed using APC-conjugated anti-Foxp3 (clone FJK16s; eBioscience) antibody [ 37 ]. The cells were then washed twice with PBS containing 1% FCS and suspended in 300 μl of PBS.…”

“…For the quantification of cytokines, splenocytes were harvested from mice at the indicated time points (day 0, 3 and 5) [ 37 ]. Spleen cells were adjusted to a final concentration of 10 7 cells/ml in RPMI-1640 supplemented with 10% heat-inactivated FCS.…”

Cytokine response in asymptomatic and symptomatic Plasmodium falciparum infections in children in a rural area of south-eastern Gabon

“…Indeed, protection mediated by pro-inflammatory response may be linked to the Th1 and Th17 cytokines responses that are associated with early immune mechanisms which control Plasmodium infection [32][33][34]. The intensity of Tregs and Th17 activation has also been shown to play an important role in regulating the maturation and function of dendritic cells in the early stages of Plasmodium infection, which is a key factor in the outcome of malaria infection [35].…”