# Immune Sensing of Candida albicans

**Authors:** Ebrima Bojang, Harlene Ghuman, Pizga Kumwenda, Rebecca A. Hall

PMC · DOI: 10.3390/jof7020119 · Journal of Fungi · 2021-02-06

## TL;DR

This review explains how the immune system detects and responds to Candida albicans, a fungus that causes various infections, and how these responses differ depending on the infection site.

## Contribution

The paper provides a comprehensive overview of immune receptor interactions and differential immune responses to Candida albicans in distinct infection types.

## Key findings

- Phagocytes use PAMP-PRR interactions to detect and respond to Candida albicans.
- C. albicans can alter its cell wall to evade immune detection and establish infections.
- Different immune cells, like neutrophils and dendritic cells, dominate responses in kidney and skin infections, respectively.

## Abstract

Candida albicans infections range from superficial to systemic and are one of the leading causes of fungus-associated nosocomial infections. The innate immune responses during these various infection types differ, suggesting that the host environment plays a key role in modulating the host–pathogen interaction. In addition, C. albicans is able to remodel its cell wall in response to environmental conditions to evade host clearance mechanisms and establish infection in niches, such as the oral and vaginal mucosa. Phagocytes play a key role in clearing C. albicans, which is primarily mediated by Pathogen Associated Molecular Pattern (PAMP)–Pattern Recognition Receptor (PRR) interactions. PRRs such as Dectin-1, DC-SIGN, and TLR2 and TLR4 interact with PAMPs such as β-glucans, N-mannan and O-mannan, respectively, to trigger the activation of innate immune cells. Innate immune cells exhibit distinct yet overlapping repertoires of PAMPs, resulting in the preferential recognition of particular Candida morphotypes by them. The role of phagocytes in the context of individual infection types also differs, with neutrophils playing a prominent role in kidney infections, and dendritic cells playing a prominent role in skin infections. In this review, we provide an overview of the key receptors involved in the detection of C. albicans and discuss the differential innate immune responses to C. albicans seen in different infection types such as vulvovaginal candidiasis (VVC) and oral candidiasis.

## Linked entities

- **Proteins:** CLEC7A (C-type lectin domain containing 7A), CD209 (CD209 molecule), TLR2 (toll like receptor 2), TLR4 (toll like receptor 4)
- **Diseases:** vulvovaginal candidiasis (MONDO:0006014), oral candidiasis (MONDO:0005886)
- **Species:** Candida albicans (taxon 5476)

## Full-text entities

- **Genes:** IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, Clec4e (C-type lectin domain family 4, member e) [NCBI Gene 56619] {aka Clecsf9, Mincle}, Cxcr1 (C-X-C motif chemokine receptor 1) [NCBI Gene 227288] {aka Il8ra}, CDH2 (cadherin 2) [NCBI Gene 1000] {aka ACOGS, ADHD8, ARVD14, CD325, CDHN, CDw325}, CD209 (CD209 molecule) [NCBI Gene 30835] {aka CDSIGN, CLEC4L, DC-SIGN, DC-SIGN1, hDC-SIGN}, Ccr1 (C-C motif chemokine receptor 1) [NCBI Gene 12768] {aka Cmkbr1, Mip-1a-R}
- **Diseases:** systemic disease (MESH:D034721), invasive fungal infections (MESH:D000072742), C. parapsilosis (OMIM:211750), Skin Infection (MESH:D007239), neutropenia (MESH:D009503), Candida infections (MESH:D002177), thrombosis (MESH:D013927), fungal (MESH:D009181), Vaginal Candidiasis (MESH:D014627), recurrent infections (MESH:D000084063), tissue damage (MESH:D017695), Oral Candidiasis (MESH:D002180), neutrophil dysfunction (MESH:C564942), inflammation (MESH:D007249), Thrombocytopenia (MESH:D013921), uncontrolled diabetes (MESH:D003920), nosocomial infections (MESH:D003428), infective endocarditis (MESH:D004696), invasive candidiasis (MESH:D058365), tooth decay (MESH:D003731), HIV (MESH:D015658), injury (MESH:D014947), superficial infections (MESH:D006259), systemic infection (MESH:D012141), athlete's foot and nail infections (MESH:D014008), nail infections (MESH:D009260), xerostomia (MESH:D014987), infected kidney (MESH:D007674), systemic candidiasis (MESH:C536777), nappy rash (MESH:D005076), neutropenic (MESH:D044504), NET (MESH:C536657), VVC (MESH:D002181), platelet aggregation (MESH:D001791), neutrophil extracellular (MESH:C535509), mouth and throat cancer (MESH:D009062), chronic granulomatous disease (MESH:D006105), Candidemia (MESH:D058387), sepsis (MESH:D018805)
- **Chemicals:** carbon (MESH:D002244), mannans (MESH:D008351), glucan (MESH:D005936), ROS (MESH:D017382), Phospholipomannans (MESH:C400188), beta-1,3-glucan (MESH:C033363), pentose phosphate (MESH:D010428), beta-glucan (MESH:D047071), gliotoxin (MESH:D005912), glucose (MESH:D005947), chitin (MESH:D002686), Heparan sulphate (MESH:D006497), superoxide (MESH:D013481), lactate (MESH:D019344), H+ (MESH:D006859), Ca2+ (-), NADPH (MESH:D009249), steroids (MESH:D013256)
- **Species:** Candida albicans (species) [taxon 5476], Aspergillus (genus) [taxon 5052], Lodderomyces parapsilosis (species) [taxon 5480], Mus musculus (house mouse, species) [taxon 10090], Human immunodeficiency virus 1 (no rank) [taxon 11676], Cryptococcus (genus) [taxon 79213], Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** R00966X
- **Cell lines:** CHO — Cricetulus griseus (Chinese hamster), Spontaneously immortalized cell line (CVCL_0213)

## Full text

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## Figures

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## References

144 references — full list in the complete paper: https://tomesphere.com/paper/PMC7914548/full.md

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Source: https://tomesphere.com/paper/PMC7914548