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Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
Published on: February 18, 2015
[Innate receptors and IL-17 in the immune response against human pathogenic fungi]
Abstract:
In recent years, the rise of human fungal infections has been associated to lack of early diagnosis, uneffective antifungal therapies and vaccines. Disturbance in immune homeostasis, which can be caused by medical interventions and immunosuppression nduced by disease, are well known as risk factors for these pathologies. Cells of the innate immune system are equipped with surface and cytoplasmic receptors for recognition of microorganisms called pattern recognition receptors (PRRs). PRRs recognize specific pathogen-associated molecular patterns (PAMPs) that are crucial for the activation and killing of pathogenic fungi by immune system. This review will outline the PRRs and cells required for effective antifungal immunity, with a special focus on the major antifungal cytokine IL-17. Finally, naturally occurring human mutations involved in the increased susceptibility to fungal infections are also discussed.
Insights
Human fungal infections are rising due to diagnostic and treatment challenges. Understanding pattern recognition receptors (PRRs) and Interleukin-17 (IL-17) is key to boosting antifungal immunity and addressing susceptibility.
Area of Science:
- Immunology
- Mycology
- Infectious Diseases
Background:
- Rising incidence of human fungal infections linked to diagnostic delays, ineffective treatments, and vaccines.
- Immune system disturbances, including immunosuppression, are significant risk factors for fungal pathologies.
- Innate immune cells utilize pattern recognition receptors (PRRs) to detect fungal pathogen-associated molecular patterns (PAMPs).
Purpose of the Study:
- To review pattern recognition receptors (PRRs) and cellular components crucial for antifungal immunity.
- To highlight the role of the antifungal cytokine Interleukin-17 (IL-17) in host defense against fungi.
- To discuss human genetic mutations that increase susceptibility to fungal infections.
Main Methods:
- Literature review focusing on innate immunity, PRRs, PAMPs, and cytokine signaling in fungal infections.
- Analysis of studies investigating cellular and molecular mechanisms of antifungal defense.
- Examination of research on genetic factors influencing susceptibility to human mycoses.
Main Results:
- PRRs and specific immune cells are essential for recognizing and eliminating pathogenic fungi.
- Interleukin-17 (IL-17) plays a pivotal role as a major antifungal cytokine.
- Naturally occurring human mutations can lead to increased susceptibility to fungal diseases.
Conclusions:
- Effective antifungal immunity relies on the coordinated action of PRRs, immune cells, and key cytokines like IL-17.
- Understanding these pathways is critical for developing improved diagnostics and therapies for fungal infections.
- Genetic predisposition significantly impacts an individual's risk of developing severe fungal diseases.
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