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1. Introduction
2. Resistance vs. tolerance to infection
3. Tolerance to infection: tissue damage control (1)
4. Tolerance to infection: tissue damage control (2)
5. Tolerance to infection: tissue damage control (3)
6. Tolerance to infection: tissue damage control (4)
7. Host tolerance to infection in mammals
8. Tolerance to Plasmodium infection
9. Molecular basis of damage control and tolerance
10. Tissue damage control: stress-responsive genes
11. The stress-responsive heme oxygenase-1 (HO-1)
12. Plasmodium infection and HO-1 gene expression
13. HO-1 expression provides tissue damage control
14. Tolerance to Plasmodium infection by HO-1 (1)
15. Tolerance to Plasmodium infection by HO-1 (2)
16. Were stress-responsive genes naturally selected?
17. Sickle cell anemia: a molecular disease
18. The molecular basis for sickle cell anemia
19. Sickle cell trait is protective against malaria
20. Plasmodium infection: cerebral malaria
21. Cerebral malaria: pathology (1)
22. Cerebral malaria: pathology (2)
23. CD8+ T cell-driven neuroinflammation
24. Hemolytic CD8+ T cell-driven neuroinflammation
25. Sickle cell anemia
26. Accumulation of free heme in the plasma
27. The sickle HbSAD mouse
28. Sickle HbSAD mice: lack of overt pathology
29. Sickle HbSAD mice: plasma free heme
30. Free heme suppresses cerebral malaria in mice
31. Free heme confers host tolerance to malaria
32. Sickle HbSAD mice survive cerebral malaria (1)
33. Sickle HbSAD mice survive cerebral malaria (2)
34. Sickle HbSAD mice survive cerebral malaria (3)
35. Sickle HbSAD mice induce HO-1 expression (1)
36. Expression HO-1 in sickle HbSAD mice
37. Nrf2 regulates the expression of HO-1
38. Sickle HbSAD mice develop tolerance via Nrf2 (1)
39. Sickle HbSAD mice develop tolerance via Nrf2 (2)
40. Sickle HbSAD mice induce HO-1 expression (2)
41. Decreased HO-1 expression in Hmox1+/- mice
42. Sickle HbSAD mice develop tolerance via HO-1 (1)
43. Sickle HbSAD mice develop tolerance via HO-1 (2)
44. Sickle HbSAD mice develop tolerance via HO-1 (3)
45. Sickle HbSAD mice develop tolerance via HO-1 (4)
46. HbSAD mice do not develop brain edema (1)
47. HbSAD mice do not develop brain edema (2)
48. The protective effect of sickle hemoglobin
49. HbSAD mice repress CD8+ T cell activation (1)
50. Effect of accumulation of low levels of free heme
51. HbSAD mice repress CD8+ T cell activation (2)
52. HbSAD mice repress CD8+ T cell activation (3)
53. A mechanism of sickle cell protection
54. Conclusions
55. Acknowledgements (1)
56. Acknowledgements (2)

Topics Covered

• Host defense strategies against pathogenic microorganisms and parasites
• Expression of stress-responsive genes provide tissue damage control, uncoupling different forms of stress associated with inflammation and immunity from tissue damage and disease
• Tissue damage control confers host tolerance to infection
• Heme oxygenase-1 is a stress-responsive gene that provides tissue damage control
• Heme oxygenase-1 confers host tolerance to Plasmodium infection
• Preservation of Heme oxygenase-1 system during human evolution

Links

Series:

• Cells of the Innate Immune System

Categories:

• Biochemistry
• Cell Biology
• Immunology
• Microbiology

Therapeutic Areas:

• Immunology & Inflammation

Talk Citation

Publication History

• Published on April 29, 2012

Financial Disclosures

• Dr. Miguel P. Soares has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.