BMS 1005 Immunology Focused Study Guide Update#2 PDF

Loading...
Loading...
Loading...
Loading...
Loading...
Loading...
Loading...

Summary

This document is a focused study guide for an immunology exam. It contains questions and answers covering various immunology topics, such as hematopoiesis, immunity, and the function of different cells and components of the immune system.

Full Transcript

BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 1. What is Hematopoiesis? Occurs in bone marrow Making of WBCs 2. What is the function of Lysosomes/What do Lysosomes do? Innate Immunity Exists in some body fluids of cells in eye for example Breaks down fungi 3. W...

BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 1. What is Hematopoiesis? Occurs in bone marrow Making of WBCs 2. What is the function of Lysosomes/What do Lysosomes do? Innate Immunity Exists in some body fluids of cells in eye for example Breaks down fungi 3. What is the difference between Acquired and Innate Immunity? Acquired Immunity – has Memory and Specificity Innate Immunity – does NOT have Memory or Specificity 4. What is the function of Cytotoxic T Cell? Are CD8 & MHC I Kills intracellular bacteria Kills Cancer Cells 5. MHC I – what cells does it present Ag to? MHC I is present in all nucleated cells/all nucleated cells produce MHC I This means all nucleated cells can present Ag to Cytotoxic T Cells This explains restriction: MHC I = CD8 Tc Cells Cytotoxic T cells are restricted to only recognize MHC I 6. What are some ill effects of the Immune System? Hypersensitivity Graft Rejection Autoimmunity 7. What is the role of Fas and FasL (Death Receptors) in T cell regulation? To kill T Cells by apoptosis Programmed cell death by apoptosis They can interact on the same T cell or two neighboring T cells 8. What is the function of C5a? Chemotaxis for neutrophils Anaphylatoxic 1 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 9. What is the end product of the Compliment? MAC Component C5b678(C9)6 10. C3 Convertase that comes from the Alternative Pathway? C3bBb 11. C3 Convertase that comes from the Classical Pathway? C4b2a 12. What does it take to make C5 Convertase? C3b 13. Activator of the Classical Pathway? IgG IgM 14. What is the function of IgG? Acts as an Opsinin 15. What is the Opsinin from Innate Immunity? C3b C4b (Complement) CRP (produced by hepatocytes) 16. What is the Opsinin from Adaptive (acquired) Immunity? IgG Has feedback inhibition and will prevent B Cells from making Ab and from binding and responding to antigens IgG is small enough to cross the placenta and reach the fetal circulation and provides protection during the first few months of baby’s life. 17. What immunoglobulin is found in breast milk and is dimeric? IgA 2 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 18. What immunoglobulins act as a receptor for B Cells? IgD IgM – when IgM is a receptor it will be a monomer (inserted into the plasma membrane of the B Lymphocytes/B Cells and can detect the Ag – which is why it’s still part of the B Cell) 19. When is IgM Pentameric? When it functions as an effector IgM at this time is capable of mediating host defenses invading pathogen At this time IgM is produced by plasma cells and secreted as soluble pentamers 20. Which Ab and which WBC are antiparasitic? IgE Eosinophils 21. What is another effect of Eosinophils besides acting as an antiparasitic? Releases histaminase (an enzyme that breaks down/degrades histamine) which can help limit the severity of allergic reactions Releases Arylsuphatase ( an enzyme that degrades SRS-A [slow-reacting substance of anaphylaxis] – which is a mixture of leukotrienes) which can limit the severity of allergic reactions Eosinophils are important to chemotactic factor 22. What type of hypersensitivity IgE involved in? Type I – Immediate Type Hypersensitivity 23. What is a drug associated with hypersensitivity? Penicillins (PCN) PCNs act as hapten Hapten - small molecule that elicits an immune response only when attached to a large carrier such as a protein (conjugated to a host protein) – can attach to surface proteins on RBCs. Again: Haptens have to bind to proteins of a larger molecule in order to become immunogenic 3 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 24. Which Anaphylactoid Reaction? Induce by certain drugs such as Non IgE mediated It does not involve/is not caused by IgE, but has a similar effect 25. What is the difference between: Rheumatic Fever & Poststreptococcus Glomerulonephritis (PSGN) aka Paranephritis? Rheumatic Fever Type II Hypersensitivity/Autoimmune Disease: Ab-Mediated Disease Anti-streptococcal A Ab cross-reacts with Cardiac Ag and cause Rhuematic Fever Ag and Ab already circulating PSGN/Paranephritis Type II Hypersensitivity: Immune Complex Hypersensitivity Ag-Ab complexes induce an inflammatory response 26. What is the Rheumatoid Factor? IgG and IgM bound to Fc fragment of normal IgG Used to test for Rheumatoid Diseases Patient is positive for Rheumatoid Disease (RA) if serum and synovial fluid contain Rheumatoid Factor 27. What medication should those with Type I Hypersensitivity have at their fingertips at all times? Epinephrine (EpiPen) to avoid anaphylactic shock 28. What is meant by Neonate Tolerization? (See PPT # 6 Slide #6) Scenario I Adult Mouse CBA (Donor) gives graft to Adult Mouse A (Recipient) Result: Graft is rejected Scenario II Adult Mouse CBA (Donor) gives spleen antigens to Neonate Mouse A (Recipient) (has not yet developed tolerance) then; Neonate Mouse A will mature then; 4 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 Graft given to Mature Mouse Result: Graft will survive because the Neonate Mouse A will become mature and d/t the encounter of being given the spleen cells in the Neonate stage, he/she will: Mature Become tolerant Be able to accept the graft 29. If we develop tolerance to B or T Cell, which one will last longer? Tolerance to T Cell lasts longer Rationale: T Cells start in the bone marrow T Cells then migrate to the thymus gland to develop or mature Thymus gland begins making T Cells for you are born and keeps producing T Cells until puberty After puberty thymus gland begins to slowly decrease in size (involution) and is replaced by fat Because of this we have a stockpile of memory T Cells 30. What is Xenograft? A type of rejection (the strongest type of rejection) Cross species barrier (i.e. Pig’s heart to human = Strong Rejection) Txmnt for Stabilization of Graft to Prevent Rejection: Cyclosporin (Tacrolimus) 31. Mixed Lymphocyte Reaction (MLR) A way to test and show safety of a drug or implantable material. Test to show for example if donor and recipient are a match for implantation of organs, mixing of WBCs, etc. What would you do if you were a surgeon and the WBC of the donor and recipient had no reaction? It means you can go ahead with the transplant. 32. What is Hyperacute Rejection? Rejection is fast Preformed antibodies react with: Alloantigens on the vascular endothelium of the graft Activate complement Trigger rapid intravascular thrombosis and necrosis of the vessel wall 5 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 33. What is Acute Rejection? Rejection takes a little longer than hyperacute rejection T cells and newly activated immune response Mostly CD8+ T lymphocytes cell-mediated immunity CD8+ T lymphocytes are reactive with alloantigens on graft endothelial cells and parenchymal cells cause damage to these cell types Endothelium inflammation is sometimes called “Endothelialitis” Alloreactive antibodies may also contribute to vascular injury 34. What is Chronic Rejection? Takes months or years after transplant Cells deposited in the blood vessel wall; Type IV - Delayed type hypersensitivity (DTH) Cell-Mediated Immunity plays a significant role – T cells, particularly Cytotoxic T Cells recognize and attach the transplanted tissue leading to destruction Ex: Kidney transplant rejection (gradual loss of kidney fx) Lack of blood supply eventually leads to rejection 35. Evasion of the immune system by tumor? Down-regulation of MHC I 36. Effect of down regulation of MHC I Can’t interact with the T Cells/Can’t present to T Cells Reduced recognition by the cytotoxic CD8 T Cells 37. What happens when you have APC presenting to Antigens without co-stimulation? Normally (normal response): Costimulation between B7 and CD28 will produce IL2 and the result of binding of IL-2 will be T Cell production/Activation of Naïve T Cell and co- stimulation (IL-2 has a receptor on the T Cell gives a life signal and will produce more active cells) But when co-stimulation is not there: B7 to CD8 interaction is not there T Cell will not be activated and will be anergic 6 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 Also, if we have CTLA-4 on the T Cell binding B7 we won’t have production of IL-2 – In this case: the T Cell will not be activated and instead will die Co-stimulation is very important for activation Anergic refers to: lymphocytes that exhibit an inability to react to Ag or allergens 38. What is LAK (Lymphokine Activated Killer)? NK Cell activated with IL-2 39. What is the function of NK Cells? Surveillance for Cancer Cells Can kill without the need for MHC I therefore is very important 40. What is the lymphocyte of innate immunity? NK Cells 41. What is the lymphocyte of acquired immunity? B and T Cells 42. What occurs when we have a def. in enzyme ADA (Adenosine Deaminase Deficiency Leads to SCID (Severe Combined Immunodeciency) 43. What happens when there is a deficiency in the gamma chain of IL-7 receptor? Causes SCID by inhibiting involvement of T Cells The deficit is X-linked in the X Chromosome and males as a result will suffer more than females because males only have one X Chromosome. 44. What is the disease called when a child is born with no thymus? DiGeorge Syndrome 45. What is chimeric monoclonal Ab? Has 2 things close together/2 parts which are: Fc part from human Fab portion from mouse 7 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 Overall: we want to reduce adverse immune effects when putting two unlike things together. 46. What is the Magic Bullet? mAb + Ricin 47. How can the side effects of chemotherapy with mAb be reduced? Conjugate an enzyme that will activate the inactive Pro-Drug at the site of Cancer 48. What is extravasation? Polymorphonuclear Leukocytes (PMNs) leaves blood circulation via/by adhering to the endothelium and leaks out into surrounding tissues 49. What happens if extravasation is deficient? Selectins and integrins are deficient 50. What is Graves Disease (Hyperthryroidism)? An Ab-mediated autoimmunity The Thyroid Stimulation Hormone (TSH) is the target antigen Causes hyperthyroidism which is when the thyroid gland makes too much thyroid hormone 51. What is Myasthenia Gravis (MG) IgG Ab attack acetylcholine receptors (AChR) In other words: Ab inhibits AcH binding to the AcH receptor (down-modulates receptors) 52. What is Transient Myasthenia Gravis (MG)? IgG is a small molecule that can cross the placenta resulting in baby acquiring MG this way hence Transient MG. 53. What is the function of the spleen? Encapsulated bacteria is involved Ab mediated phagocytosis is involved Therefore: When you have a capsule it is usually difficult to phagocytosis the neutrophil and will be exposed to infection 8 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 54. What is affinity maturation? Affinity will increase with increased exposure Happens because mutations occur on the variable chains & variable domains of light chains and heavy chains 55. Which Ab is responsible for protection of mucosa surfaces? IgA IgA is a monomer in serum IgA is a dimer if not in serum 56. Which Ab has no effector function? IgD 57. What function does IgD have? B Cell Receptor (BCR) 58. Which immunoglobulin is a monomer in the serum? IgA 59. What immunoglobulin has feedback inhibition? IgG 60. What immunoglobulin is opsonin? IgG 61. What is the restriction when have the interaction between the B Cell and the TH2 Cell? MHC II Restriction 62. What is the restriction when B Cell interacts with Cytotoxic T Cell? MHC I Restriction To effectively help with immune defense, B Cell needs MHC I to go to cytotoxic T Cell to kill, so In the case of reduced/restricted MHC I, the B cell acts just like any other infected cell EBV (Epstein Barr Virus) is a condition that happens as a result of MHC I Restriction 63. What deficiency does a patient have when they are infected with Mycobacterium Lepra? TH1 deficiency 9 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 64. What are the 2 forms of Mycobacterium Lepra? Tuberculoid Leprosy Mild Form TH1 and cell-mediated immunity is intact Lepromatous Leprosy Severe Form TH1 deficiency -> Cell -mediated immunity is deficient 65. What is Mycobacterium Tuberculosis? An intracellular infectious agent that lives inside the macrophage Macrophage will have lysosomes that will fuse 66. How can Mycobacterium Tuberculosis evade being killed by the innate immune cells? By inhibiting phagolysosome (phagosome and lysosome) fusion: cord factor. 67. What is ADCC (Ab-Dependent Cellular Toxcitiy)? The NK cells are activated and kill the Ab-coated cells (the effector cells kill the target cells) Receptor cell is a cytotoxic cell that will release cytotoxic granules and kill the target cell CD8 T cells release granules containing granzymes and perforins at the target cell Perforins will make holes in pores and through these pores the granzymes (enzymes) will enter and kill/trigger apoptosis Facilitated by Ab Process is similar to opsonization and phagocytosis 68. Which cells produce histamine? Basophils (blood) Mast cells (tissue) 69. What is a neutrophil? Part of innate immunity Major phagocyte Most common/makes up largest portion of WBCs (this makes them very important) 10 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 70. What is C3bBb? C3 convertase for alternative pathway Breaks down C3 into C3a and C3b 71. What is a committed B Cell? Bound to a specific Ag/committed to certain epitopes and has a receptor that recognized certain epitopes Ag-independent differentiation 72. What type of defense mechanisms are acidic pH of the stomach, skin, lysozyme, microflora, enzymes, etc.? Natural defense mechanisms 73. What is Graft Vs Host? The graft rejects the host (incompatibility) Ex: Occurs after bone marrow transplantation Graft cells are immunocompetent Recipient is immunoincompetent 74. When you vaccinate someone is it acute or passive immunization? Active immunization Ex: Flu shot 75. What is Acute Desensitization? Involves administration of very small amounts of Ag in 15 minute intervals Ex: Penicillin (PCN) – if someone is allergic/hypersensitive to PCN, but there is no other drug alternative acute desensitization can be implemented Temporary – once done with acute desensitization, patient becomes allergic again to the PCN for instance 76. What is a tumor marker? A marker for cancer, which is anything present in or produced by cancer cells or other cells of the body in response to cancer 11 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 77. What is a type of cancer? Colon cancer – cancer that begins in the large intestine (colon) which is the final part of the digestive tract Colon cancer, however, can occur in any part of the colon 78. What is CALLA? Ag associated with childhood leukemia 79. How can a bacterial infection cause/trigger autoimmunity? We have a B cell that is potentially anti-self, but because there is no T helper cell to activate the B cell, the B cell remains inactive (doesn’t do anything) Now there is an infection with a bacterium that has one peptide (that’s recognized by the bacteria) that has a T helper cell that can now activate the B cell to fight the bacteria But it makes an Ab that has the same specificity as the Ag from the bacteria The Ab will be specific to the epitope which is similar to the self-epitope, therefore; The B cell will produce Ab that will be active against the bacteria The bacteria will be eliminated after 1-2 weeks; however, the B cell will remain active against the self-antigens and this is an autoimmune reaction This is called Cross-Reaction – when an Ab that was made against the bacteria mistakenly recognizes the other one because of similarities in epitopes 80. What blood group is the universal acceptor/recipient? AB+ 81. What blood group is the universal donor? O- 82. Which type of hypersensitivity is mediated by immune complexes? Type III 83. What type of hypersensitivity is it when you get a bee sting? Type I Hypersensitivity (Immediate) 84. What is the mechanism of Type IV Hypersensitivity? Called delayed because it starts hours or day after contact with the Ag 12 BMS 1005 Exam 1 (Immunology) Focused Study Guide Update#2 Lasts for days CD4 & TH1 is required to activate the macrophages Has INDIRECT effector function so the macrophages will do the damage 85. What is an example of Type IV Hypersensitivity? Poison Ivy Poison ivy acts a hapten which is a small molecule that when combined with a larger carrier such as a protein When absorbed through the skin from a poison ivy plant, urushiol undergoes oxidation in the skin cells to generate the actual hapten, a reactive molecule called a quinone, which then reacts with skin proteins to form hapten adducts. Result: Body becomes immunogenic/allergic 13

Use Quizgecko on...
Browser
Browser