BIOL3003 MID SEM EXAM QUESTIONS AND ANSWERS
WITH COMPLETE SOLUTIONS VERIFIED
Immune Cell Recruitment
Rolling adhesion -> Firm Adhesion (ICAM-1 - LFA-1) -> Diapedesis (immune cell
squeezes through endothelium) -> Migration (along chemokine gradient to infection site)
Complement System
1. Classical: Ag:Ab complex activates = recruits inflammatory cells
2. MB-Lectin: lectin - sugars on pathogen activates = opsonisation with C3b
3. Alternative: hydrolysis of C3 lets complex bind pathogen = activates = killing by MAC
(contains C9, degrades membrane)
Function of Reactive O2 and N2 Species
1. inactivate key enzymes
2. destroy protein structure
3. lipid and DNA oxidation = cytotoxicity
4. solubilise proteases
Macrophage Pathways
Immediate = reactive O2 species, proteases, acidification
Delayed = NO production, anti-microbial peptides, nutrient depletion, macrophage death
Neutrophil and MAST cell responses
, NETs = contain chromatin and anti-microbial products to kill or immobilise microbes
MAST degranulation = release potent inflammatory mediators, drive allergic response =
pathogen expulsion
Complement Deficiencies
1. Classical = immune-complex disease
2. MB-lectin = bacterial infection
3. Alternative = Pyogenic + neisseria infection, no immune-complex disease
4. C3 = pyogenic + neisseria and sometimes immune-complex disease
5. MAC = neisseria infection only
Phagocyte Deficiencies
1. Leukocyte adhesion def. (LAD) = neutrohpils fail to migrate, Type 1 = no firm
adhesion, Type 2 = no rolling adhesion
2. Chronic granulomatous, Chedaik-higashi = failure of ROS production, failure of
phago/lysosome fusion.
Acute Inflammation
Immediate, WBC -> site, plasma + soluble mediators leak into site
Diseases: sepsis, trauma
Chronic Inflammation
Long term, macrophage + WBC inflitration, macrophage + granulocyte products = tissue
destruction
STERILE INFLAM = no infectious agent
Diseases: rheumatoid arthritis, chron's disease
Self vs Non-self Hypotheses
WITH COMPLETE SOLUTIONS VERIFIED
Immune Cell Recruitment
Rolling adhesion -> Firm Adhesion (ICAM-1 - LFA-1) -> Diapedesis (immune cell
squeezes through endothelium) -> Migration (along chemokine gradient to infection site)
Complement System
1. Classical: Ag:Ab complex activates = recruits inflammatory cells
2. MB-Lectin: lectin - sugars on pathogen activates = opsonisation with C3b
3. Alternative: hydrolysis of C3 lets complex bind pathogen = activates = killing by MAC
(contains C9, degrades membrane)
Function of Reactive O2 and N2 Species
1. inactivate key enzymes
2. destroy protein structure
3. lipid and DNA oxidation = cytotoxicity
4. solubilise proteases
Macrophage Pathways
Immediate = reactive O2 species, proteases, acidification
Delayed = NO production, anti-microbial peptides, nutrient depletion, macrophage death
Neutrophil and MAST cell responses
, NETs = contain chromatin and anti-microbial products to kill or immobilise microbes
MAST degranulation = release potent inflammatory mediators, drive allergic response =
pathogen expulsion
Complement Deficiencies
1. Classical = immune-complex disease
2. MB-lectin = bacterial infection
3. Alternative = Pyogenic + neisseria infection, no immune-complex disease
4. C3 = pyogenic + neisseria and sometimes immune-complex disease
5. MAC = neisseria infection only
Phagocyte Deficiencies
1. Leukocyte adhesion def. (LAD) = neutrohpils fail to migrate, Type 1 = no firm
adhesion, Type 2 = no rolling adhesion
2. Chronic granulomatous, Chedaik-higashi = failure of ROS production, failure of
phago/lysosome fusion.
Acute Inflammation
Immediate, WBC -> site, plasma + soluble mediators leak into site
Diseases: sepsis, trauma
Chronic Inflammation
Long term, macrophage + WBC inflitration, macrophage + granulocyte products = tissue
destruction
STERILE INFLAM = no infectious agent
Diseases: rheumatoid arthritis, chron's disease
Self vs Non-self Hypotheses
