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Printable Handouts
Navigable Slide Index
- Introduction
- The toll of infectious diseases
- The golden age of microbiology
- How do we kill bacteria?
- Innate immunity
- Ilya Metchnikov
- Toll is important for host defense
- The Toll-like receptor signal pathway
- TLRs as pattern recognition receptors
- Adaptive immunity
- Innate versus specific immunity
- The host defense to an infection
- Th1/Th2 hypothesis and EAE
- IL-12R vs. IL-23R
- A new T-helper subset
- IL-1 and IL-23 drive differentiation of human TH17
- IL-1 and PGE2 drive differentiation of human TH17
- A new T-helper subset
- IL-17 family members
- The roles of IL-17A and IL-17F
- The roles of IL-17E
- IL-22 induces production of defensins
- Th17 responses in inflammation
- Are Th17 responses important in humans?
- Hyper IgE syndrome (1)
- IFN gamma defect in HIES
- Th17 populations in HIES
- Genetic cause: STAT3 mutations
- Hyper IgE syndrome (2)
- Autosomal dominant CMC
- Chronic mucocutaneous candidiasis (1)
- Chronic mucocutaneous candidiasis (2)
- Chronic mucocutaneous candidiasis (3)
- Chronic mucocutaneous candidiasis (4)
- STAT1 mutation in the CC domain
- Summary
- Cunclusions
- Acknowledgements
Topics Covered
- Resistance to infection
- Involvement of innate and adaptive immune responses
- Innate immunity modulates Th-responses
- Th17 are crucial for mucosal host defense
- Deficiencies in Th17 in patients lead to mucosal fungal and bacterial infections
Links
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Talk Citation
Netea, M. (2012, April 3). Th17 cells and innate immunity [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 15, 2025, from https://doi.org/10.69645/RVCO9832.Export Citation (RIS)
Publication History
- Published on April 3, 2012
Financial Disclosures
- Prof. Mihai Netea has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.