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Tutorial - April 9.docx

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Immunotherapy KNOW THE PEOPLE – compare and contrast – what mouse models used?? Know the there E’s of cancer immunoediting Basis for cancer immunotherapy – know tumour ssociated antigen – what can be used or classified as such antigens? – know the techniques in which (ex, MHC peptide tetramer – what is is used for? Why used? Tool used in labs to detect CD8 T cells, etc.) Immune contexture in human tumours – know the general heading of fuzzy picture slides – know the big scope – will not ask details/specific data – know the general picture, what is each slide of data trying to convey Section 3 – most questions will focus on section three Various approaches of cancer immunotherapy – first section is the drugs – IDO – know the drug targets enzyme Know the different drugs used for different types of cancers – Ex. Cervical cancer, prostate cancer – these are specific examples used – the drugs are outlined and delineated – why the drugs – KNOW THE MECHANISMS – why are certain drugs used for certain types of cancers Cellular approaches – basic mechanisms of T cell stimulation and inhibition – CTLA4 – IMPORTANT – know the CTLA4 stuff, PD1 stuff – basis of T cell stimulation – know the drugs thtat can block stimulation, inhibition – two ways to turn on T cell – can stimulate it or prevent its inhibition – KNOW THE DIFFERENCE Adoptive transfer – know what kind of t cells are used for this therapy – and why? Why are some good for, what some aren’t? Know mechanism – most of the last bit of this lecture is data slides from the paper, do not need to focus on this- but there will be an application question from this part of the exam – APPLY what learned in lecture to a lab setting – ex., patients have harvested tumour samples, what can lab do to look for prognosis for these samples/tumours? SUM UP WHAT LEARNED IN LECTURE. - In the application question, presence of antigen-specific immune responses correlated with overall survival – this title can have something to do with the application Know the T cell grafts Clinical trials – what is required to go into phase 1, phase 2 – do not focus too much on the data, on the outcomes – Therapeutics – what Dr. Hirano cares about are the drugs (IPI – used in clinics now) – with therapeutic strategies to target MDSCs table, know three - LUPUS lecture – March 11, 2013 Skin – leads to deposition in kidney Two factors that contribute genetically and environmental Genetic factors – twins – Environmental – controversial – Apoptotic blebs NETs – neutrophil cell death results in programmed cell death – neutrophil traps – TLR receptors TLR activation bypassed BCR recognize nucleic acid or antigen associated – can recognize both – but usually associated – anergic – BCR usually recognize in lupus recognize protein associated – genetic link between protein and lupus C1q deficiency – MOUSE MODELS – know which mouse models used – significance – tells where in the specific steps that might affect – first one is Clr2 deficiency mice; other are Yaa mice; Specific mice models and what the results are Allergies – S. Berger ARTICLE PART OF THE EXAM Atopic Dermatitis – new technique is epicutanous immunization Pros and cons of why this might work? Knockout mice used – Th2 bias response – intact skin leads to Th1; stripped skin leads to Th2 response – this is more relevant to the article – Roles of Th1 and Th2 cytokines in murine model of allergic dermatitis – genotypes of mice used – wild- type versus knockouts – IL5 knockout and IFN gamma knockout doesn’t change skin thickness and when look at eosinophils, without IL5, eosinophils decrease, same with IL4; No changes in skin thickness, but decrease in eosinophilia Th1 and Th2 developed into – cytokines involved – IFNA gamma inhibits TH2 response; IL4, IL10 inhibits TH1 response – this graph is useful for other lectures as well IL4 knockout leads to decrease in TH2 responses – IGE – IL4 knockout decreases TH2 response, but knockout IFN gamma, decrease in IL4 – Intact skin and not stripped skin is crucial – paper – know the abstract EC sensitization vs. intranasal sensitization chart slide What the difference between these two sensitization lead to? What the role of IL4 does in these situations. NMDA receptor encephalitis – Patients CSF to probe rat neural tissue – binds to hippocampus HEK cells transfected to express receptors – CSF incubation – bind – reconfirm the target Target was NMDA receptor – know it – Endoderm, ectoderm, mesoderm – CORRECTION Antibody when
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