The iC3b receptor of Candida albicans and its roles in pathogenesis

Margaret K Hostetter1

  • 1Department of Pediatrics, Yale School of Medicine, 333 Cedar Street, LMP 4085, P.O. Box 208064, New Haven, CT 06520-8064, USA. margaret.hostetter@yale.edu

Vaccine
|April 24, 2009
PubMed

Insights

Candida albicans possesses a cell wall receptor for iC3b, similar to integrins. This receptor, encoded by the INT1 gene, is crucial for fungal adhesion, hyphal growth, and virulence in mice.

Area of Science:

  • Mycology
  • Immunology
  • Molecular Biology

Background:

  • Candida albicans is an opportunistic fungal pathogen.
  • Understanding fungal cell wall components is vital for developing anti-fungal strategies.
  • Integrins play roles in cellular adhesion and immune responses.

Purpose of the Study:

  • To define a receptor for iC3b on Candida albicans.
  • To investigate the function of the INT1 gene and its encoded protein (Int1).
  • To explore the role of Int1 in fungal adhesion, morphogenesis, and virulence.

Main Methods:

  • Biochemical and immunologic studies were performed.
  • The INT1 gene and its encoded protein were analyzed.
  • In vitro and in vivo models, including a murine model, were used.

Main Results:

  • A receptor for iC3b was identified on the Candida albicans cell wall, exhibiting similarities to integrins CD11b and CD11c.
  • The INT1 gene encodes a 1659-amino acid protein (Int1) essential for epithelial cell adhesion.
  • Int1 is critical for hyphal morphogenesis and virulence in a murine model.
  • A peptide (Pep263) derived from the Int1 amino terminus exhibits superantigen-like activities.

Conclusions:

  • Candida albicans utilizes a cell wall receptor for iC3b, functionally related to integrins.
  • The Int1 protein is a key factor in fungal adhesion, hyphal development, and pathogenicity.
  • The discovery of Pep263 suggests novel mechanisms of immune modulation by Candida albicans.

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