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The NF-κB regulator Bcl-3 modulates inflammation during contact hypersensitivity reactions in radioresistant cells

Ilaria Tassi1, Nimisha Rikhi1, Estefania Claudio1

  • 1Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

European Journal of Immunology
|January 24, 2015
PubMed

Insights

Bcl-3 deficiency exacerbates contact hypersensitivity by increasing inflammatory chemokines and immune cell recruitment. Bcl-3 limits inflammation in radioresistant cells, including keratinocytes, during later stages of the response.

Area of Science:

  • Immunology
  • Molecular Biology
  • Dermatology

Background:

  • Bcl-3, an atypical IκB family member, acts as a nuclear cofactor for NF-κB transcription factors.
  • Its role in inflammation is context-dependent, with potential roles in tumorigenesis and host defense.
  • Cell-specific functions of Bcl-3, particularly in skin immunity, remain largely uncharacterized.

Purpose of the Study:

  • To investigate the role of Bcl-3 in the contact hypersensitivity (CHS) mouse model.
  • To elucidate the cell-specific functions of Bcl-3 in mediating inflammatory responses in the skin.

Main Methods:

  • Utilized a contact hypersensitivity (CHS) mouse model induced by oxazolone.
  • Generated and analyzed Bcl-3-deficient mice and performed bone marrow (BM) chimera experiments.
  • Conducted specific ablation of Bcl-3 in keratinocytes to assess its function in radioresistant cells.

Main Results:

  • Bcl-3-deficient mice showed exacerbated and prolonged CHS responses.
  • Increased inflammation correlated with elevated CXCL2, CXCL9, and CXCL10 chemokine production and neutrophil/CD8(+) T cell recruitment.
  • Bcl-3's anti-inflammatory effect in CHS was dependent on its activity in radioresistant cells, including keratinocytes, which limited CD8(+) T cell infiltration.

Conclusions:

  • Bcl-3 acts as a critical regulator in the later stages of the contact hypersensitivity response.
  • Bcl-3 limits inflammation by modulating chemokine production and immune cell recruitment in radioresistant cells, notably keratinocytes.
  • These findings highlight Bcl-3's importance in controlling skin inflammatory conditions.

Keywords:
Bcl-3ChemokinesContact hypersensitivityKeratinocytesNF-κB

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