Final Exam Study Guide
Final Exam Study Guide BIOL 4201
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This 12 page Study Guide was uploaded by Kayla Robinson on Thursday May 5, 2016. The Study Guide belongs to BIOL 4201 at University of North Texas taught by Dr. Goven in Winter 2016. Since its upload, it has received 106 views. For similar materials see Immunology in Biology at University of North Texas.
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Date Created: 05/05/16
Transplantation Immunology Types of Donors Cadaver donors need to be a viable match Living donors need to be a very good match Types of Grafts Autograft: self to self o Blood transfusions or skin o No rejection Isograft: twin to twin o Any tissue will work o No rejection Allograft: same species o Most common o Different MHC antigens (diff genetic material) o Rejection possible Xenograft: between species o ALWAYS has rejection Proof of Relationship Between Transplants and Immune System A) Skin Transplant Experiment o Mouse A skin transplant onto Mouse B o Primary rejection by Mouse B o Second transplant of Mouse A onto Mouse B o Secondary rejection looks like secondary memory cell response B) Transfer Immune Response o Mouse A skin transplant to Mouse B o Primary rejection by Mouse B o Take spleen cells from Mouse B, inject into Mouse C o Mouse A transplant to Mouse C o Mouse C has SECONDARY rejection—memory cells to the graft C) Tolerance o Rat babies in utero injected with rabbit cells o Rat babies learn rabbit cells as “self” o Grown rat gets rabbit cell injection—No rejection MHC genes o Chromosome 6 o 12 MHC markers- 6 class 1, 6 class 2 o Can have all 12 max different o Can have 6 different minimum if mom and dad have the same o Inheritance Percentages: o You have a 25% chance to be 100% match with sibling o You have a 25% chance to be 0% match with sibling o You have a 50% chance to be a 50% match o Share 50% with mom and 50% with dad o If you have NO MHC markers, you’re a universal donor, but will be completely immunosuppressed and die Tissue Typing MHC 1: A, B, C types HLA-A: 350 different types HLA-B: 620 different types MHC-1 Typing: We use lymphocytes to type HLA-A because they’re nice nucleated cells with MHC, NOT because they’re immune cells. Use serum to identify markers. 1. Take blood from recipient 2. Use lymphoprep to create a density gradient 3. Remove lymphocytes in the buffy coat on top 4. Make plates with indentions to hold lymphocytes, add Antibodies specific to HLA-A and complement 5. Read which Ab interact with the HLA-A 6. For instance, if a lysis reaction happens when you add A4, then the person has HLA-A4 markers Why would someone have antibodies against HLA-A types? Where do we get these for the experiment? Babies in utero have Ab against dad’s HLA Transplant patients with a non-perfect match Blood transfusion with Ab against wbc from donor MHC-2 Typing: Use lymphocytes to type for MHC-2 (HLA-D) because they’re immune cells this time in a Mixed Lymphocyte Reaction 1. Take lymphocytes from recipient and donor 2. X-ray lymphocytes from donor (now stimulant cells) 3. Add to dish and stimulate proliferation 4. If recipient T cells proliferate and make immune response against donor graft cells (bad) 5. If R T cells don’t divide, it means they’re recognizing the donor cells as self (good) 6. Measure with H thymidine, adds to DNA during replication Want HLA-A (1) and HLA-D (2) markers to match Worst if neither match Best if both match Can work if HLA-D match and HLA-A do not: there will be no T cells to cause H problems Immunosuppression Timeline 1. Induction Therapy a. Antilymphocyte serum b. Use cytotoxic drugs to reduce number of lymphocytes c. Causing immunosuppression 2. Maintenance Therapy a. Lower dose of immunosuppression b. Want to avoid dying of infection while reducing immune system function 3. Specific Treatment a. When rejection starts b. Go back to induction therapy to kill off immune system again Drugs Used 1. Corticosteroids Downregulate cytokines inhibit white cell migration stabilize wbc membrane so they can’t degranulate reduce MHC-2 expression: inhibit Thelper cells cytotoxic to T cells side effects: infection, water retention 2. Cytotoxic drugs stop DNA replication used for anti-caner fight lymphocytes (induction therapy) 3. Cytokine Inhibitors BEST Use in maintenance therapy Ex. Cyclosporine: fungus that stops IL2-R expression o No Thelper proliferation o Autocrine, can turn off only some Thelper o Very specific 4. Anti-lymphocyte Treatments Used in special therapy Anti-Thelper and anti-Tctl 5. Anti-inflammatory drugs Rejection 1. Hyperacute a. Should never happen in a medical setting b. Means you have pre-formed Ab and complement c. Immediate minute to hour reaction d. Destroys transplanted organ immediately e. Ab binds to vasculature, binds complement 2. Acute a. Not a HLA-A match b. Ab mediated inflammation of microvasculature with complement c. Tdth and Tctl and macrophages d. Slow Ab increase against transplant e. Normal tissue replaces with fibrous scar tissue f. Can be up to 3 months 3. Chronic a. Ab mediated b. Also CMI mediated c. Can take years d. NOT HLA mediated, uses other tissue markers Special Transplants Transplanting immune cells (ex. Bone marrow) Graft vs Host disease: graft rejects the host o Need 3 conditions of donor Recipient immunosuppressed Only happens when transplanting immune cells MHC differences: when the match is not perfect o New immune cells attack the host o Treatment: Suppress donor cells Will have to start over Can’t do stem cell transplant now because you destroyed them when you immunosuppressed the recipient: can only do another allogenic transplant Xenogenic transplant would solve problem (pig is similar size) Afraid of viruses we would get from pigs Primate use is unethical For leukemia or myeloma Can do stem cell transplant: self transplant, want to avoid cancer cells o Isolate stem cells from circulation or bone marrow o Add colony stimulating factor, use a cell sorter to remove cancer cells, treat with drugs o Treat recipient with chemo first Or allogenic transplant: need a tissue match o Need a perfect match donor o Treat with chemo, then add new cells Both work, can last 3-7 years o Will need to repeat, cancer will return Autoimmunity Make an immune response against healthy tissue Only a Type 2, 3, or 4 reaction (type 1 happens with allergens) Need an autoantigen- immune system recognizes self as an antigen Type of T cell receptors change, the autoantigen has always just been a part of self, now it is just read incorrectly Clonal Abortion normally protects us from autoimmunity Happens when Tctl aborts a B cell that has an anti-self receptor When this doesn’t work, you have an autoimmune disease Autoimmune Diseases A. Infection a. Rheumatic Fever i. Strep infection, make Ab response ii. Strep shares Ag with heart muscle so the Ab response damages heart iii. Treat by catching Strep early iv. Not truly autoimmune: just molecular mimicry B. Environment a. Goodpasteurs Syndrome i. Make Ab against collagen ii. Affects kidneys iii. Lungs in smokers 1. Smoke exposes basement membrane that can be attacked 2. Die of respiratory failure from destroying alveolar sacs iv. Real autoimmune disease, exacerbated by environment C. Physical Trauma a. Anterior chamber of eye i. Normally a privileged site, no vasculature, protected by blood barrier ii. Trauma causes inflammation iii. Ab against self in eye iv. Might remove the bad eye to save the other v. Happens because normally the body is not exposed to the eye “Ag” b. Vasectomy i. Snip tubes, make Ab against sperm ii. Sperm has not normally been exposed to the immune system because testis are a privileged site c. These are not exactly autoimmune: the body is just made where there are separate parts that are not normally exposed to each other D. Rheumatoid Arthritis a. Type 3 and Type 4 reaction b. Inciting agent- sometimes a virus- released into synovial fluid from blood vessel c. Causes immune response: IgG against the inciting agent d. Body makes IgM and IgG against the IgG for the inciting agent i. These are called rheumatoid factors e. Type 3 effect: bystander effect i. Neutrophils damage membrane when trying to damage Ab- Ag complex ii. Can’t get rid of Ag because it’s being made by the body (the Ab against the inciting agent) so inflammation will continue f. Type 4 effect: Tdth and Thelper meet the inciting agent, cause macrophages to come E. Pemphigus vulargis a. Skin Type 2 reaction b. Make anti-adhesion Ab in the dermis c. Ab causes inflammation at the tight junctions where the adhesion molecules are d. Cells dissociate, creating a water-filled blister e. Blister can rip off, so secondary infections are common F. Pemphigoid a. Make an Ab against basement membrane of skin b. Makes a blister of the whole skin layer c. Dermis and epidermis become thick, fewer opportunities for infection G. Diabetes Type 1 a. Childhood diabetes b. Body makes Tctl against beta cells that make insulin c. Secondary autoantibody H. Systemic Lupus Erythematosus a. 1 in 500 women b. Make IgG against cell membrane and cell components c. Type 2 and Type 3 reactions d. Type 2: Ab binds to membrane e. Type 3: Ab-Ag complexes, causes joint problems, kidney problems, skin rashes (Red Wolf Disease) Immunodeficiency Diseases 1. Primary Genetically inherited defect No immune components Multiple infections 2. Secondary Caused by immunosuppression drugs, old age, environment Places destroyed and their effects Stop T cells: Will die of viral or fungal infection, also will not make Thelper so the B cell response will be affective Stop B cells: bad, but still have T cell response Stop monocytes- no macrophages, inhibit Tdth function stop granulocytes: affects complement activity and opsonization from Ab Stop stem cell differentiation: might die Stop IgA-IgE differentiation: won’t even know Stop complement after C3, will be totally okay DiGeorge Syndrome Immune dysfunction Thymic aplasia (no thymic function) or thymic hypoplasia (very low function) No T cells Usually thyroid gland is missing, obvious physical appearance of a short neck Must live in sterile environment—no good way to treat fungal or viral infections Even with normal B cell population, will have decreased function bc no Thelper Treatment: thymus transplant o Problem: Graft vs Host o Must use fetal thymus Nezelof’s Syndrome Thymus hypoplasia No T cells but neck looks normal Can tell by infections Transient hypogammaglobulinemia Short term decrease in Ab in blood Seen in neonates and infants Have low IgG until 4-6 months for a normal baby Sick baby won’t start making IgG Mom makes Ab against baby IgG in utero Selective IgA Immunodeficiency Common No SIgA Increased repiratory infections, allergy Cross reactivity of SIgA and cow’s milk o Anti-bovine IgA reacts with SIgA in human sometimes o Remember that it’s easy to have a deficiency in SIgA because it’s so complex with the J chain and secretory component Therapy: antibiotics against infections Variable hypogammaglobulinemia Decreased production of IgG from IgM Lose ability of IgG to leave the circulation and enter the tissues Treatment: Antibiotics, Immunoglobulin infusion of IgG Severe Combined Immunodeficiency No immune response at all—WORST, will affect B and T cells 3 types o No T or B No lymphocytes at all, very rare, short life (no reproduction) o No T, have B Most B cells nonfunctional anyway because of no T helper Can sometimes see T cells, but can’t make IL-2 and IL-2R, B cells won’t proliferate o Have T and B but they don’t work Bare lymphocyte syndrome No MHC 1 or 2 Regular Phagocytosis vs Problems Regular: migration – adhesion – phagocytosis – lysosomal fusion – respiratory burst Problems adhesion deficiency: no phagocytosis lysosomal fusion: reduced killing or digestion, relatively common respiratory burst: can’t make hydrogen peroxide, can’t kill Resistance to Infection 1. Virus a. Ab and Complement, not as important b. Also Ab neutralization- blocks virus from binding to cell *** c. Tctl binds to virus, kill cell with virus inside *** 2. Bacteria a. C3a, C5a--neutrophils phagocytize b. C3b—opsonization causes neutrophils to bind c. C5b-9—bacterial lysis (not as important) d. Ab opsonization as well 3. Mycobacteria a. Tdth—macrophages b. Wall off the bacteria c. Kill cell with bacteria inside d. Phagocytosis doesn’t work well here 4. Protozoan a. Ab and complement b. If inside the cell—Tdth (like for mycobacteria) 5. Helminth worms a. If larvae: Ab and eosinophils (opsonization) b. If adults: Tdth and inflammation c. Need to kill only worms that you ingest, any replicated worms will pass through as excrement 6. Fungi a. Hard to get rid of because they’re eukaryotic b. Tdth, Tctl c. Ab not as good d. This is why you need T cells 7. Immunization a. Killed organisms: ex. Typhoid b. Attenuated organisms: ex. BCG against mycobacteria i. Make immediate Tdth response if exposed to virulent strain in the future c. Toxoids: ex. Diphtheria and tetanus i. Toxin that has been devirulated d. Inactivated virus i. Salk vaccine ii. Can give to immunosuppressed iii. Given as a shot IM iv. Make memory cells IgG in blood v. Recommended in US, fewer chance of infections, more expensive e. Attenuated virus i. Sabin vaccine ii. Can’t give to immunosuppressed iii. Given orally in solution iv. Lymph nodules in gut make IgA v. Blocks virus in the gut, but 1/750,000 can cause problems f. Site of Immunization: i. In adults: arm, has muscle and close to regional lymph node ii. In children: thigh, has muscle, close to regional lymph node, kids exercise their legs a lot
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