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UNC93B1 interacts with the calcium sensor STIM1 for efficient antigen cross-presentation in dendritic cells

Sophia Maschalidi1,2, Paula Nunes-Hasler3, Clarissa R Nascimento2,4,5

  • 1INSERM UMR1163, Laboratory of Normal and Pathological Homeostasis of the Immune System, Imagine Institute, 75015, Paris, France.

Nature Communications
|November 22, 2017
PubMed

Insights

Dendritic cells (DCs) require UNC93B1 and STIM1 for effective antigen cross-presentation. This interaction regulates calcium flux, crucial for stimulating CD8+ T cell responses against tumors.

Area of Science:

  • Immunology
  • Cell Biology
  • Calcium Signaling

Background:

  • Dendritic cells (DCs) are crucial for initiating adaptive immunity by presenting antigens to T cells.
  • The major histocompatibility complex class I (MHC-I) pathway in DCs enables presentation of exogenous antigens to CD8+ T cells.
  • Defects in Unc93b1 impair endosomal functions and antigen cross-presentation, impacting anti-tumor immunity.

Purpose of the Study:

  • To investigate the molecular mechanism linking UNC93B1 and STIM1 in dendritic cells.
  • To determine the role of the UNC93B1-STIM1 interaction in antigen cross-presentation and calcium signaling.
  • To elucidate the impact of this interaction on anti-tumor immune responses.

Main Methods:

  • Investigated the interaction between UNC93B1 and STIMIM1 in the endoplasmic reticulum.
  • Utilized a constitutively active STIM1 mutant to assess its impact on antigen processing in 3d-mutated DCs.
  • Performed STIM1 ablation in mouse and human cells to evaluate effects on cross-presentation.

Main Results:

  • UNC93B1 directly interacts with the calcium sensor STIM1 in the endoplasmic reticulum.
  • Restoration of STIM1 function, independent of UNC93B1 binding, rescued antigen degradation and cross-presentation in 3d-mutated DCs.
  • STIM1 deficiency significantly reduced antigen cross-presentation in both mouse and human cells.

Conclusions:

  • The UNC93B1-STIM1 cooperation is essential for regulating calcium flux in dendritic cells.
  • This interaction is critical for efficient antigen cross-presentation, a key process for initiating CD8+ T cell responses.
  • Targeting the UNC93B1-STIM1 pathway may offer therapeutic strategies for enhancing anti-tumor immunity.

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