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Mycobacterium indicus pranii induces dendritic cell activation, survival, and Th1/Th17 polarization potential in a

Pawan Kumar1, Vini John1, Soumitra Marathe1

  • 1*National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India.

Journal of Leukocyte Biology
|January 17, 2015
PubMed

Insights

Mycobacterium immunomodulatory precursor (MIP) activates dendritic cells (DCs), enhancing immune responses against tuberculosis and tumors. MIP promotes DC survival and Th1/Th17 polarization via Toll-like receptors (TLRs).

Area of Science:

  • Immunology
  • Microbiology

Background:

  • Mycobacterium immunomodulatory precursor (MIP) is a nonpathogenic soil bacterium.
  • MIP exhibits immunomodulatory properties and protects against experimental tuberculosis (TB) and tumors.
  • Dendritic cells (DCs) are crucial for initiating anti-TB and anti-tumor immune responses.

Purpose of the Study:

  • To investigate the effect of MIP on dendritic cell (DC) behavior and activation mechanisms.
  • To elucidate the role of Toll-like receptors (TLRs) in MIP-induced DC activation.

Main Methods:

  • Stimulation of DCs with MIP (MIP(L) and MIP(K) variants).
  • Measurement of cytokine secretion (IL-6, IL-12p40, IL-10, TNF-α) and costimulatory molecule expression (CD40, CD80, CD86).
  • Assessment of DC apoptosis and survival using PI and Annexin V staining.
  • Analysis of anti-apoptotic protein expression (Bcl-2, Bcl-xl).
  • Co-culture of DCs with naive T cells to evaluate T cell polarization.
  • Experiments using MyD88(-/-) DCs and specific TLR knockout DCs (TLR2, TLR9).

Main Results:

  • MIP significantly increased IL-6, IL-12p40, IL-10, and TNF-α secretion by DCs.
  • MIP upregulated CD40, CD80, and CD86 expression on DCs.
  • MIP enhanced DC survival by inhibiting apoptosis, evidenced by increased Bcl-2 and Bcl-xl.
  • MIP-stimulated DCs promoted Th1/Th17 polarization in naive T cells.
  • MIP-induced DC activation was dependent on MyD88 and involved TLR2 and TLR9, with variations between MIP(L) and MIP(K).

Conclusions:

  • MIP effectively activates DCs, enhancing their function in immune responses.
  • MIP promotes DC survival and Th1/Th17 polarization, crucial for anti-TB and anti-tumor immunity.
  • TLRs, particularly TLR2 and TLR9, are critical mediators of MIP-induced DC activation.
Keywords:
T cell polarizationapoptosiscostimulatory moleculescytokinespattern recognition receptors

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