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Tutorial notes - February 19, 2013.docx

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Department
Immunology
Course
IMM250H1
Professor
All Professors
Semester
Winter

Description
KNOW THE PAPERS; but knowing the abstract is sufficient LECTURE ONE Know why the finding is the first of its kind T cell receptor – KNOW what the variable, invariant parts are – be able to know the material well enough – if knock out that chain, would person still have T cells Do not know the T delta pathway What is SCID? What it stands for – if a child comes in with a symptoms B cell antibody production – ability to kill and lyse target cells as assay – looking at aperipheral T cells – how much they expand, they grow – what cytokines they produce – tell you the functional assays and looking at Tregs and how these cells are good at suppressing cells – Treg suppressor cells Sort out the Foxp3 high cells – culture different ratios of Tregs with T effector cells – also in MS lecture – MS patients Treg may not be working as well – KNOW THE TREGS (in almost every lecture) Indirect measures of thymus function 1. Flow cytometry using markers that mark memory and naïve cells 2. Or look for recent thymic immigrants – looking for TREC circles – when naïve T clel – when T cell receptor rrearranged, the junk DNA stays as circle – these mark the ones that have just left the thymus – KNOW THIS Defect in CD3 chain – in the paper – know the details of the paper Leaky phenotype discussed in the paper – some T cells preserved, while others did not form – delta cells have an advantage – alpha beta needed that signal and was unable to get past developmental checkpoint – some T cells still formed – late onset TCD Treatment is supportive and curative – the latter, ex transpantion with _________ Who is the best donor? See the paper published by him in JAMA 2006 – haploidentical donor is third best; matching is the HLA Do not worry bout strategies Gene therapy – KNOW THIS What the patients ook like when presented with SCID; what does SCID look like; curative and supportive LECTURE 2 – transplantation Types of rejection History not important Dates not important HLA – know it is the major thing when used to match up appropriate donors – antibodies developing against HLA – not chosen for transplant Mechanisms of rejection slide – KNOW THIS - Mchanisms = direct or indirect o Direct is when APC is from the actual organ from donor – this organ has antigen presenting cells that is presenting directly to T cell – cytotoxic T cell can lyse the tissue o Indirect – akes longer to come about – the recipient APC picking up antigen and presenting antigen on class one or class two to receipient T cells - KNOW THE CHART on the next slide - Types of rejection =/= mechanisms CD8 cells in direct approach can lyse target tissue – specific for class one of host – in the second one, not able to recognize class one on the organ does not lyse the tissue For the CD8 to lyse something, must see class 1 it recognizes – only see in allorecognition – cause rapid tissue destruction B cells Immunosuppressive therapy – KNOW THE DRUGS Know the mode of action/mechanisms of the drugs What is the same and different between the drugs Antibody therapy – what is given to patient immediately following transplant – called induction agaents Highest chance of rejection after transplant Biopsies – to measure drug in the blood – if quantities are excessive – monitoring drug levels; also do biopsies Types of rejection – Hyperacute – does not happen very often because screened HLA of donor and recipient – Acute cellular rejection – diagnose with biopsy see immune cells infiltrate the tissue – purple dots are immune cells coming in If more foxp3 positive cells in graft, that’s good – they are inhibiting immune system – protective against any rejection Acute cellular rejection – know Antibody-mediated rejection is third type – takes a bit longer – generally have antibodies and complement detected in biopsy – blood vessels start to get vasculopathy – get thicker – sometimes can lead to blood vessel wall – smooth muscle wall are proliferating – antibody mediated rejection – Tolerance – central has to do with the thymus; do mixed chimerism KNOW THIS – basically, ablation, followed by transplant of a bit of marrow from donor; then do heart transplant; to educate the T cells that these cells are self antigens – negative selection , T cells die; if not dangerous, T cells can exit the thymus – so when the recipient gets the tranplsant, they – KNOW THIS Costimulation – CTLA 4 LG – one method that is successful – binds B 7.1 – prevents from binding _______ so causing anergy of the T clel – if get signal one without two Expand others Tregs and fusing them back in DO NOT STUDY THE CASE STUDY Ex. If did biopsy and it showed evidence of this, what is this? What would you do? – just know hyperacute/acute/ - types and mechanisms of rejection known – MEMORIZE THE MECHANISMS OF DRUGS LECTURE 3 Classify autoimmune diseases – KNOW THIS Organ specific vs systemic or by the type of immune effector mechanisms – KNOW THE TABLES Type 2 – Graves’ disease – autoantibodies produced in both examples – autoantibodies causing tissue damage – ine one cas,e autoantibodies oversitulating receptor in thyroid gland that causes Graves disease Know How it is antibody mediated disorder – Myasthenia Gravis – antibodies blocking in this case instead of stimulating – antibodies can be antagonist or stimulating dpending on how it is binding How to manage antibody disorders – antibody mediated rejection – same ways to mediated antibody mediated rejection also used to deal with antibody mediated autoimmune – long term management, plasma cleansing, rituximab, - some agents used for multiple conditions MS – Know the history – not the dates but know Diagnoistic criteria can be tested – must have two attacks – either two lesions in space or time Two forms of the disease – relapsing remitting – most patients convert to secondary progressive form Inflammatory attack on the myelin and appearance of galalinium enhancing lesions on MRI – ex. What would you see on the MRI? Secondary progressive – see brain atrophy which is seen on MRI Acute lesion – Chronic plaques – lesions may come back to same area – shadow plaques, so limited remylenatino, and with time, no more remyeliation occurring Early MS vs later MS – KNOW THIS KNOW THE TAKE HOME MESSAGES EAE – KNOW THIS Do not know the scoring – know how induce the disease = myeline antigen plus adjvant Active immunization vs adoptive transfer Know this is T cell mediated, so Type 4 – transfer T cells, transfer disease – KNOW Three animal models – 1. EAE – myelin and adjuvant mixed up; or T cells from sick mouse into healthy mice 2. Or overexpress mice T cell receptor – so respond to certain germs in facility KNOW THESE THREE MODELS Is EAE good model or not? Immunopathogenesis – T helper cells – these ones initiate the disease – know the different pathways TH1, TH2, and TH17 – know what he major transcription factors that define these cells and what cytokines make these cells – know the T helper differentiation slide TH17 cells – neutrophilic activation – now basic TH17 pathway TH17 do in MS – T regulatory cells – see in every lecture – there is one autoimmune disease that involves people missing Foxp3 – called IPECs – Suppressor assay – coculturing Tregs with T effector cell – get idea of how well Trgs are suppressing – curve indictes degree of suppression – B cells in MS kNOW THIS What are they doing? Good? Bad? Ugly? Can be suppressor and activate autoimmune responses Know how to target B cells Treatments – know what they are, how they work. How to name. steroids, interferon beta – glatiramir acetate – know how they are working Do not study the emerging therapies and stuff beyond LECTURE 4 Apoptosis 6 major concepts 1 – types of cell death – apoptosis, necrosis Something about C elegans being first organism to be used to study cell death, homology of genes in cell death in mammals and c elegans – know this 2 – mechanisms of cell death Two – cell death receptor and mitochondria triggered pathways – know this Caspase – BCL2 family – these two discussed later; mitochondria pathway, release of cytochrome c and formati
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