immunology
Papa Kwame Pireku
Problem set 1
2.2) Antimicrobial peptides are usually produced as inactive propeptides that require cleavage by a protease to complete their activation, often by generating a cationic peptide that takes on an amphipathic structure capable of disrupting the cell membrane of a microbe. Also in neutrophils the antimicrobial agents are activated by proteolytic cleavage when these granules fuse with phagosome and encounter neutrophil elastase that has been released from primary granules. Paneth cells and neutrophils control the release of the proteases responsible for cleaving and activating these peptides.
2.4) Recognition of bacteria by mannose –binding lectin can lead to their destruction by the same mechanism as recognition by an antibody because the classical pathway can be triggered directly by a pathogen or indirectly by an antigen binding to a pathogen causing generating of active components with various effector functions.
2.5) In a healthy person hydrolysis of the thioester bond in C3 will be regulated by complement control proteins that regulate complement cascade at different points to protect host cell while allowing complement activation to proceed on the pathogen surfaces. Proteins in the first group catalyze the cleavage of any C3b OR C4b that does bind to host cells into inactive products
2.6) The key feature of the alternative pathway amplification loop is its ability to spontaneously be activated and its unique C3 convertase, the alternative pathway convertase. Plasma protein properdin, is a positive regulating protein mechanism set in place to regulate C3 also there is negative regulatory proteins like decay accelerating factor that help regulate C3. Deficient properdin patients are particularly susceptible to infection with Neisseria meningitides the main agent is bacterial meningitis.
2.7) People with deficiencies in factor 1 are susceptible to recurrent bacterial infections because of uncontrolled complement
Problem set 1
2.2) Antimicrobial peptides are usually produced as inactive propeptides that require cleavage by a protease to complete their activation, often by generating a cationic peptide that takes on an amphipathic structure capable of disrupting the cell membrane of a microbe. Also in neutrophils the antimicrobial agents are activated by proteolytic cleavage when these granules fuse with phagosome and encounter neutrophil elastase that has been released from primary granules. Paneth cells and neutrophils control the release of the proteases responsible for cleaving and activating these peptides.
2.4) Recognition of bacteria by mannose –binding lectin can lead to their destruction by the same mechanism as recognition by an antibody because the classical pathway can be triggered directly by a pathogen or indirectly by an antigen binding to a pathogen causing generating of active components with various effector functions.
2.5) In a healthy person hydrolysis of the thioester bond in C3 will be regulated by complement control proteins that regulate complement cascade at different points to protect host cell while allowing complement activation to proceed on the pathogen surfaces. Proteins in the first group catalyze the cleavage of any C3b OR C4b that does bind to host cells into inactive products
2.6) The key feature of the alternative pathway amplification loop is its ability to spontaneously be activated and its unique C3 convertase, the alternative pathway convertase. Plasma protein properdin, is a positive regulating protein mechanism set in place to regulate C3 also there is negative regulatory proteins like decay accelerating factor that help regulate C3. Deficient properdin patients are particularly susceptible to infection with Neisseria meningitides the main agent is bacterial meningitis.
2.7) People with deficiencies in factor 1 are susceptible to recurrent bacterial infections because of uncontrolled complement