Complement System Flashcards
What are the major functions of complement system?
A) protection of host cells
B) Non-inflammatory removal of cancerous cells
C) Removal of infectious microorganisms
D) Development of innate immune response
E) All of the above
F) All answers are correct except D
G) All answers are correct except B
H) Only A and C are correct
G) All answers are correct except B
Which of the statements is not correct?
A) Complement system is present in blood serum
B) Complement system induces allergic reactions
C) Complement system does not fight against helminths
D) Complement system is comprised by number of different enzymes.
E) Complement is a strictly regulated system.
C) Complement system does not fight against helminths
Which of the following statements is not correct?
A) Cleavage of C3 results in C3a and C3b
B) C3a and C5a are anaphylatoxins and both induce inflammation
C) C3a participates in opsonization
D) C4 and C2 are not C3 convertases
C) C3a participates in opsonization
What is Lipofuscin?
A) An enzyme that is found in many body organs and contributes to aging process.
B) A molecule that is found only in retinal pigment epithelium and accumulates as person ages.
C) A pigment that highly increases in number in RPE with aging process and contains A2E compound.
D) A lipid-protein aggregate that is cytotoxic in RPE and gets accumulated in extracellular matrix over time.
C) A pigment that highly increases in number in RPE with aging process and contains A2E compound.
What are the risk factors for development of macular degeneration?
A) Unhealthy lifestyle, normal aging process, loss of RPE cells.
B) Smoking, normal aging of cells, insufficient blood supply to RPE
C) Environmentla factors, high number of carotenoids, Lipofuscin accumulation
D) Environmental factors load of reactive oxygen species, loss of complement cells
A) Unhealthy lifestyle, normal aging process, loss of RPE cells
Why does thickening of Bruch’s membrane occur?
A) Water and other important molecules cannot cross the membrane and this causes lipid accumulation in it.
B) Cell debris accumulates under epithelial membrane and this results in thickening of Bruch’s membrane
C) Drusen start to form and occupy RPE, which causes thickening of Bruch’s membrane.
D) Lipid drops start to accumulate under basal linear membrane and form Drusen that result in thickening of Bruch’s membrane.
D) Lipid drops start to accumulate under basal linear membrane and form Drusen that result in thickening of Bruch’s membrane.
Poor regulation of complement system results in:
A) Over-activation of classical pathway which causes inflammation in RPE and leads to Macular degeneration.
B) Increased amount of C3b which causes anaphylactic reaction in RPE and leads to Macular degeneration.
C) Reduction of efficiency of other inhibitory complement regulators which causes formation of Drusen and leads to Macular degeneration.
D) Increase of TCC complex which attacks RPE and leads to macular degeneration.
D) Increase of TCC complex which attacks RPE and leads to macular degeneration.
What are the physiological functions of the complement system?
1) Regulators - Protection of host cells
2) Regulators - Non-inflammatory removal of modified host cells
3) No regulators - Complement activation and removal of infectious microorganisms
What are the pathological functions of the complement system?
1) No or defective regulators - inappropriate action of regulators leads to host cell damage
2) No or defective regulators - Inefficient removal of modified host cells can lead to pathology
3) Acquired regulators - Pathogens acquire host regulators and avoid complement attack.
What are the two C3 convertases?
C3bBb and C4bC2b
What leads to “switched” microglia?
Acute neurodegradation, chronic neurodegeneration with extracellular protein misfolding, chronic neurodegeneration with intracellular protein misfolding + systemic inflammation. Reverse is true as well.
What are the visual functions of the Retinal Pigment Epithelium?
1) Light absorption
2) Epithelial transport - Cl ions, and H20 in, Glucose and Vitamin A out
3) Glia - K+ in and out
4) Visual cycle - 11- cis retinal changes conformation here
5) Phagocytosis
6) Secretion - PEDF out, VEGF in
How is the RPE in an environment of oxidative stress?
Light focused through a lens, phagocytosis and retinal metabolites enter through the retina onto the RPE, which produces lipofuscin and then you get a decrease of oxygen and venous blood O2 saturation drops down to 90%
How is there protection against oxidative damage in the RPE?
To maintain here needs to be more protective elements to outweigh the reactive oxygen species present in the RPE. Protective elements include melanin, cartenoids and enzymes, while reactive oxygen species include blue light, phagocytosis, O2 and retinal. Having more reactive oxygen species present can contribute to RPE damage and contribute to macular degeneration.
When does lipofuscin accumulation peak in the RPE?
Around 70 years of age
What are the cytotoxic effects of A2E?
When A2E is mixed with blue light and O2, the resultant is A2E-Epoxide which then makes Mitochondria and Lysosomes. The destabilization of mitochondria and lysosomes, leads to lysosomes making more A2E.
What happens when there is an imbalance between protective factors and damaging factors?
When there is lots of oxidative stress like smoking, normal aging of cells and the loss of RPE cells, the load of reactive oxygen species such as blue light, phagocytosis, O2 and retinal increases and outweighs the protective factors. This in turn results in more lipofuscin accumulation and RPE damage in the form of macular degeneration.
How does the hydraulic connectivity of Bruch’s membrane change with age?
It decreases with age at the maular, peripheral and AMD levels.
What are drusen?
Accumulations of lipid deposits in the bruch’s membrane that are precursosrs to age related macular degeneration.
Complement proteins and regulators were found in drusen. Complement factor H (CFH).
What does factor CFH contribute to in the complement system.
Reduced inhibitory efficiency targeting C3 cnvertase in the lectin pathway and the classic pathway as well as C3b.
What does CF3 do in the complement system?
Increase activity of C3b, and C3a opsonization and C3a inflammation
What is the hypothesis concerning the complement system’s involvement in macular degeneration?
Reduced control of the alternative pathway leads to increased amount of terminal complement complex (TCC) which attacks the Retinal pigment epithelium (RPE) and leads to macular degeneration.
True or False, COmplement activates free cytosolic Ca2+
True
True or false, there is increased VEGF secretion through the complement system and oxidative stress.
True
