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Autophagic induction modulates splenic plasmacytoid dendritic cell mediated immune response in cerebral malarial

Anirban Sengupta1, Tarun Keswani2, Samrat Sarkar1

  • 1Immunology Laboratory, Department of Zoology, University of Calcutta, 35, Ballygunge Circular Road, Kolkata, 700019, India.

Microbes and Infection
|June 12, 2019
PubMed

Insights

Inducing autophagic flux in plasmacytoid dendritic cells (pDC) with rapamycin improves malaria outcomes. This enhances pDC immune response, reduces parasite load, and balances inflammation for better host defense against Plasmodium infection.

Area of Science:

  • Immunology
  • Parasitology
  • Cell Biology

Background:

  • Splenic plasmacytoid dendritic cells (pDC) can harbor Plasmodium parasites, contributing to malaria.
  • Incomplete autophagy in pDC may lead to impaired antigen processing and weak immune responses.
  • Understanding pDC's role in malaria pathogenesis is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the effect of rapamycin-induced autophagic flux on pDC function during Plasmodium infection.
  • To determine if enhancing autophagic flux in pDC can improve host immune response and prognosis in malaria.

Main Methods:

  • Treatment of infected mice with rapamycin to induce autophagic flux in pDC.
  • Transfer of pDC from treated and untreated infected mice to naïve mice to assess malaria progression.
  • Analysis of pDC phagocytic potential, adhesion, antigen presentation, co-stimulatory molecule expression, and T cell responses.
  • Evaluation of cytokine profiles (IL10:TNFα ratio) and immune cell ratios (Treg:Th17, myeloid DC:pDC).

Main Results:

  • Rapamycin treatment enhanced pDC-centered immune responses, leading to reduced parasitemia in recipient mice.
  • Autophagic induction in pDC downregulated adhesion while maintaining phagocytic capacity, limiting parasite burden.
  • Rapamycin-treated pDC exhibited improved antigen presentation with higher expression of CD80, CD86, DEC205, and MHCI.
  • pDC influenced T cell differentiation, promoted CD28 expression on CD8+ T cells, suppressed FasL, and shifted the immune response from Th1 to a balanced Th2 profile.

Conclusions:

  • Induction of autophagic flux in splenic pDC via rapamycin is a promising strategy to combat malaria pathogenicity.
  • Enhancing pDC autophagy improves immune surveillance, antigen presentation, and modulates T cell responses for better malaria control.
  • Targeting pDC autophagy offers a potential therapeutic avenue for managing Plasmodium infections and reducing host damage.
Keywords:
AutophagyCerebral malariaPlasmodium bergheiTh1-Th2 immune responsemDC-pDC ratiopDC-antigen presentation

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