Biochemistry II Part II PDF

BIOCHEMISTRY II PART II 1. Describe the difference between innate immunity and acquired immunity. ANSWER A) Innate immunity is the form o...

BIOCHEMISTRY II PART II 1. Describe the difference between innate immunity and acquired immunity. ANSWER A) Innate immunity is the form of immunity that is inborn in an organism and is activated immediately in response to an invading microorganism whilst acquired immunity is the type of immunity that is adapted by the body to defend the body against the invading pathogen. B) Innate immunity is generic or non-specific in nature whilst acquired immunity is specific in nature. C) Innate immunity is present from the point of birth whilst acquired immunity develops over growth. D) Aspects of innate immunity such as mechanical barriers exert their defensive mechanics irrespective of the presence or absence of an invading pathogen whilst in the case of acquired immunity, contact with a pathogen is essential to build up defensive mechanisms. E) Innate immunity is triggered immediately in response to infection whilst acquired immunity takes a while to develop and exert its effects. F) The major immune cells involved in innate defensive mechanisms are NK cells, neutrophils, macrophages, eosinophils, basophils, etc. whilst the major immune cells involved in the acquired system are majorly the lymphocytes; the B cells and T cells. 2. Briefly explain the three major immunological events that occur during an inflammatory response. ANSWERS a) Vascular changes: Blood flow increases and fluid and plasma proteins leak into the inflamed tissue. b) Cellular infiltration: leukocytes adhere to vascular endothelium and migrate through the endothelial layer to gain access to surrounding tissues. c) Chemotaxis: leukocytes follow a chemical gradient to the site of insult and unleash potent killing mechanisms. 3. State five processes involved in phagocytosis ANSWERS i. The cell that will perform phagocytosis is activated. ii. In the immune system, chemotaxis occur. iii. The cell attaches to the particle that it will ingest.  iv. The cell ingests the particle, and the particle is enclosed in a vesicle (a sphere of cell membrane with fluid in it) called a phagosome v. A lysosome fuses with the phagosome and the particle is digested. 4. Give an example of an immune cell involved in each of the following; a. Allergic response – Mast cells b. Phagocytosis - Macrophages c. Production of antibodies – B cells d. Antigen Presentation – Dendritic cells 5. Explain how complement activation would lead to lysis of bacteria. ANSWERS Complement activation results in the formation of the membrane attack complex (MAC or 5b-9; bleu) that kills Gram- negative bacteria without the help of immune cell. Influx of Ca2+ through the MAC and other electrolyte which causes the bursting of the wall a process called osmotic lysis. 6. Which Cytokines are mostly elevated in bacteria septic shock and why? ANSWER Tumour necrotic factor-alpha (TNF-α) and Interleukin-1(IL 1) are mostly elevated. Gram - negative including E-coli, K- pneumoniae, P. aeruginosa and E. aerogenes have cell wall endotoxins (Lipopolysaccharide, LPS) that stimulate macrophages to release Tumour necrotic factor-alpha (TNF-α) and Interleukin-1(IL 1) excessively, systemic levels. 7. Describe how the membrane attack complex (MAC) is formed during complement activation. ANSWER Assembly of the MAC is initiated when the complement protease C5 convertase cleaves C5 into C5a and C5b. Complement protein C6 then binds to C5b, and this complex bind to complement C7 forming a larger complex. This complex undergoes a conformation change that exposes a hydrophobic site on C7 and draws the complex into the hydrophobic lipid bilayer portion of the pathogen's plasma membrane. Subsequent binding of the C5b–C6–C7 complex to C8 exposes another hydrophobic site that further anchors the 5b–8 complex into the pathogen's lipid bilayer. Complement C8 is composed of two proteins, C8β and C8αγ. C8αγ has a hydrophobic site that draws it into the growing complex housed in the pathogen lipid bilayer and also initiates polymerization of 10–16 molecules of complement C9. This completes the transmembrane pore known as the MAC. 8. List and explain any two mechanisms employed by tumour antigens to invade immune responses mounted by the immune system. ANSWER A. Inhibiting the immune system: Tumours inhibit or evade the immune system by accumulating specific metabolites and signal factors within the TME or limiting the nutrients available to immune cells. B. Inducing T cell exhaustion: Cancer cells affect the metabolism of T cells in various ways. This could be done through the activation and proliferation of immune cells, the depletion of glucose and amino acids, high acidity and lactate, and upregulated immune checkpoint, consequently inhibiting glycolysis, thereby affecting the metabolism of T cells. 9. Describe the structure of blood group antigens and how they are formed. ANSWERS Blood group antigens are found on N-glycoproteins, O-glycoproteins, and glycolipids, both on RBCs and many other cells of the body. They’re synthesized on type 1, 2, 3, or 4 structures. Type 1 and 2 structures are Galβ1-3GlcNAc-R and Galβ1-4GlcNAc-R, respectively. Both are present on N- and O-glycoproteins, as well as on glycolipids. Type 2 structures are ubiquitous, while type 1 structures are found solely in the GI tract. Type 3 and 4 structures are all Galβ1-3GalNAc-R, however, the R group for types 3 and 4 differs. R for type 3 is serine (Ser) or threonine (Thr) of an O-glycopeptide, and R for type 4 is normally a glycolipid moiety. Synthesis of blood group antigens needs at least two steps. The first is the synthesis of H antigen, the structure corresponding to O blood type. The second is the synthesis of either A or B structure. The H antigen is formed by the addition of fucose in α1,2 linkage to a terminal galactose on a type 1-4 chain. After synthesis of the H structure, the A and B transferases, which differ by four amino acids, utilize the H structure to synthesize A and B antigens on type 1-4 chains. Two genetic loci encode the H transferase. The H loci is functional in RBCs and the secret or loci is functional in GI epithelial cells, obtaining its name for the blood group anti gens produced by secreted glycoconjugates.