Folia Microbiologica

, Volume 52, Issue 3, pp 297–312 | Cite as

Candidiasis — Do we need to fight or to tolerate theCandida fungus?

  • M. Raška
  • J. Běláková
  • M. Křupka
  • E. Weigl


Candidiases, infections caused by germination forms of theCandida fungus, represent a heterogeneous group of diseases from systemic infection, through mucocutaneous form, to vulvovaginal form. Although caused by one organism, each form is controlled by distinct host immune mechanisms. Phagocytosis by polymorphonuclears and macrophages is generally accepted as the host immune mechanism forCandida elimination. Phagocytes require proinflammatory cytokine stimulation which could be harmful and must be regulated during the course of infection by the activity of CD8+ and CD4+ T cells. In the vaginal tissue the phagocytes are inefficient and inflammation is generally an unwanted reaction because it could damage mucosal tissue and break the tolerance to common vagina antigens including the otherwise saprophytingCandida yeast. Recurrent form of vulvovaginal candidiasis is probably associated with breaking of such tolerance. Beside the phagocytosis, specific antibodies, complement, and mucosal epithelial cell compriseCandida eliminating immune mechanisms. They are regulated by CD4+ and CD8+ T cells which produce cytokines IL-12, IFN-γ, IL-10, TGF-β,etc. as the response to signals from dendritic cells specialized to sense actualCandida morphotypes. During the course ofCandida infection proinflammatory signals (if initially necessary) are replaced successively by antiinflammatory signals. This balance is absolutely distinct during each candidiasis form and it is crucial to describe and understand the basic principles before designing new therapeutic and/or preventive approaches.


Candida Albicans Candidiasis Killer Toxin Vaginal Candidiasis Vaginal Fluid 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


C3, C4

components of the complement cascade


chronic mucocutaneous candidiasis


oligodeoxynucleotide-containing nonmethylated cytosine-phosphate-guanosine motifs


receptors for components of the complement cascade


dendritic cell


antigen-binding domain of Ig


receptors for constant domain of Ig


granulocyte-macrophage colony-stimulating factor

H-2k, H-2d

mouse MHC phenotypes


human immunodeficiency virus


heat-shock protein 81 kDa






interferon γ


killer toxin ofPichia anomala

MAP kinase

mitogen-activated protein kinase


mannan-binding lectin


major histocompatibility complex


mannose receptor


oral epithelial cell


oropharyngeal candidiasis


pathogen-associated molecular pattern




pattern-recognition receptor


recurrent vulvovaginal candidiasis


secreted aspartyl proteinase


severe combined immune deficiency


T-cell-derived antigen-binding molecule


transforming growth factor β

TH1, TH2

helper T cell subsets


Toll-like receptor


regulatory T cells


vaginal epithelial cell


vulvovaginal candidiasis


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Copyright information

© Institute of Microbiology, Academy of Sciences of the Czech Republic 2007

Authors and Affiliations

  • M. Raška
    • 1
  • J. Běláková
    • 1
  • M. Křupka
    • 1
  • E. Weigl
    • 1
  1. 1.Department of Immunology, Medical FacultyPalacký UniversityOlomoucCzechia

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