Freshman Vaccinations (Case 3): The Immune Response Team
Hi guys, I wrote a pretty lengthy answer but based on the feedback I could have written a more concise answer. Just for your references, (if you are referring to my answers) here are some feedback that prof. Kelly gave to me. I hope this helps!
Host Response • why is there such a poorly developed immune system in the brain tissue? • You talk quite a bit in the first section about an antibody response to S.penumoniae and N.meningitidis, but given that most of us have not previously had meningitis (and are not all carriers) what is the incidence of these antibodies existing in the general population?
Bacterial Evasion (External polysaccharide capsule) • You mention that the pneumococcal cell wall consists of peptidoglycan and lipoteichoic acid (LTA), which are of particular importance in SP virulence - in what way are these virulence factors important – what do they do? • You mention that the capsule prevents entrapment in the nasopharyngeal mucus and also inhibits effective opsonophagocytosis – how? • You mention that pneumococcal enzymes, such as neuraminidases (NanA and B), cleave glycoproteins and oligosaccharides and enhance colonization by decreasing the viscosity of the mucus – how do they decrease mucus viscosity? • You mention that pneumococcal immunoglobulin A1 protease supports nasopharyngeal colonization by inactivating human secretory immunoglobulin A and promotes attachment to host cells – how does it inactivate IgA and how doe this promote attachment?
(Complement evasion and inhibition of phagocytosis) • Release of bacterial antigens excessively activates phagocytes via toll-like receptor engagement and allow bacteria to escape phagocytosis – what is the relationship between excessive activation of phagocytes and bacteria escaping phagocytosis?
(Resistance to the complement system) • How exactly does neisserial antigenic variation and molecular mimicry work (at the molecular and cellular level)?
Outcome • You mention that both S.pneumonia and N.meningitidis can remain in the respiratory tract after the infection has subsided - what is the frequency of this occurrence in the population? • How does “the components of acquired immunity learn the best way to attack each antigen and begin to develop a memory for that antigen” • Finally, what is your prognosis for Minni after this infection?
Hi everyone, my section is up. I also came across a diagram that I thought did a pretty good job of summarizing all the different way the host damages itself and how they relate to each other. I put it up in the Google doc in case you want to use it!
Thanks Kevin! My page is up as well, but I'll look at the diagram and see if I have anything to add tomorrow.
Hey Guys, sorry for the really late reply. It seems I didn't see your replies until logging in. I'll get to work immediately.