Folia Microbiologica

, Volume 52, Issue 3, pp 297–312

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

Article

DOI: 10.1007/BF02931313

Cite this article as:
Raška, M., Běláková, J., Křupka, M. et al. Folia Microbiol (2007) 52: 297. doi:10.1007/BF02931313

Abstract

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.

Abbreviations

C3, C4

components of the complement cascade

CMC

chronic mucocutaneous candidiasis

CpG ODN

oligodeoxynucleotide-containing nonmethylated cytosine-phosphate-guanosine motifs

CR, CR3

receptors for components of the complement cascade

DC

dendritic cell

Fab

antigen-binding domain of Ig

FcγR

receptors for constant domain of Ig

GM-CSF

granulocyte-macrophage colony-stimulating factor

H-2k, H-2d

mouse MHC phenotypes

HIV

human immunodeficiency virus

Hsp90

heat-shock protein 81 kDa

Ig

immunoglobulin

IL

interleukin

IFN-γ

interferon γ

KT

killer toxin ofPichia anomala

MAP kinase

mitogen-activated protein kinase

MBL

mannan-binding lectin

MHC

major histocompatibility complex

MR

mannose receptor

OEC

oral epithelial cell

OPC

oropharyngeal candidiasis

PAMP

pathogen-associated molecular pattern

PMN

polymorphonuclear

PRR

pattern-recognition receptor

RVVC

recurrent vulvovaginal candidiasis

SAP

secreted aspartyl proteinase

SCID

severe combined immune deficiency

TABM

T-cell-derived antigen-binding molecule

TGF-β

transforming growth factor β

TH1, TH2

helper T cell subsets

TLR

Toll-like receptor

Treg

regulatory T cells

VEC

vaginal epithelial cell

VVC

vulvovaginal candidiasis

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