Immune Study Notes Lecture 6.docx

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Department
Microbiology and Immunology
Course Code
Microbiology and Immunology 3300B
Professor
Prof

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Immune Study Notes Lecture 6 1. What is inflammation? Body sends fluid, plasma proteins and immune cells to the site of tissue damage – can be acute or chronic, local or systemic effects and could be a part of the innate immune system. 2. What are the cardinal signs of inflammation? Calor – heat Dolor – pain Rubor – redness Tumor – swelling 3. What are the blood vessels associated with inflammatory sites? Post-capillary venules that come after capillaries; slow movement of RBC. They are lined with endothelial cells. 4. What happens when there is tissue damage? PAMPs or DAMPs will be present in the tissues; macrophages will recognize and emit chemokines or cytokines – this causes a change in the endothelium = sticky; immune cells roll a long and will go through the cells to the tissue where they will undergo chemotaxis to the area of damage. 5. What happens when chemokines get into the blood stream? Can go to the brain = fever, can go to liver = acute phase response, can go to the bone marrow to cause an increase in hematopoeisis or macrophages can be APC within the lymphnodes. 6. What is the first step when damage occurs? Detection: there are two ways to detect damage; the first is through different receptors. Mitochondria produce formyl peptides that bind fMLP receptors, and also have CpG DNA that binds TLR 9. There are metabolites produced by pathogens in the IC areas such as heat shock protein and HMG, as well as metabolites such as uric acid and ATP. Seocnd way is through immune cell binding – certain receptors such as mannose, lipids, complement, scavenger and dectin. 7. What is the second step? Activation of resident immune cells: macrophages take up the antigens and produce chemokines or cytokines – after this occurs there are multiple different effects. Cause cell differentiation and proliferation (monocytes into macrophages), dolor (pain), local affects anti pathogen response (stop transition or translation), activation of vascular endothelial and increased permeability. 8. How does activation of the endothelium occur? Through integrrins/ICAMs/Selectins and chemokines – ICAMs are high affinity adhesion molecules – stick leukocytes to endothelial cells on the luminal side. 9. What is the next step? Leukocyte recruitment: P-selectin binds sialyl lewis on the leukocyte – causes rolling (slow movement). Chemokines activate GPCR which eventually activates a cluster of integrins – once this happens ICAM molecules are present and they cause a strong bond; leading edge goes through the endothelial cells and goes to the site of infection. 10.What is the next step? Chemotaxis: specificity – gets them to the site of infection 11.Next? Killing through phagocytosis 12.Next? Systemic r
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