MICR221 Module 4
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53 terms
Terms | Definitions |
|---|---|
 Immune response | bacteria-->endocytosis-->DC,Macrophage-->CD8+ (T cyctotoxic cell) or CD4+-->TH1 or TH2-->B cell-->memory cell or plasma cell |
| cell differentiation- myeloid precursor | bone marrow stem cell-->myeloid precuror-->graulocytes(-->neutrophil or mast cell) or monocyte(-->DC or macrophage) |
| granulocytes | contain granules which contain toxins or enzymes that are releases to kill target cells |
| neutrophil | phagocytosis |
| mast cell | -degranulation -allergy symptoms and inflammation |
| PAMPs | -Pathogen-Associated-Molecular-Patterns -e.g. lipids, proteins, dsRNA -these make antigen |
| Antigen Presenting Cell (APC) | -DC and macrophages -MHC-I -MHC-II -both have PRRs (Pattern Recognition Receptors) which are --TLCs -TLC signaling--> interact with PAMPs, gene transcription and translation and activates phagocytes--> increases phagocytosis |
| effects of TLC signaling | -increase phagocytosis ability -increase immunostimulatory capacity of APC -enhance T cell stimulation and better 'memory' response |
| Dendritic Cell (DC) | -dedicated APC -phagocytosis (innate response) -migration to lymph nodes once presented with antigen -communicate with other cells |
| macrophage | -found in almost all tissues -present antigen to T cells -first line of defense and are very effective because they interact with PAMPs -phagocytosis (innate response) |
| MHC | must have antigen bound to their antigen binding site to be stable so most of the time they bind 'self antigen' so when non=self antigen is bound it's obvious |
| MHCI | -membrane embedded alpha chain, B2M -specific antigen -all nucleated cells -9-10 amino acids -antigen bound within ER and then the peptide bound MHCI is transported to the cytoplasmic membrnae -MCHI interacts with TCR and CD8+ is activated (T cytotoxic) |
| MHCII | -alpha chain, beta chain -native antigen -just APC -11-15 amino acids -antigen enters via phagocytosis MHCII is transported from the ER to lysosomes via Ii protein (invariant chain), a phagolysosome is made and the antigen presented to MHCII peptide bound MHCII is then transported to cytoplasmic membrane -MHCII interacts with THC (CD4+)--> B cell activation -DM dislodges CLIP (leftover Ii) and puts the peptide in MHCII |
| Invariant chain | -Ii protein -stabalise MHCII prepeptide bound |
| endogenous antigen | -intracellular antigen-degraded in cytoplasm |
| CD8+/T cyctotoxic cells | -attack and destroy antigen bearing cells -releases granzyme and perforin into antigen bearing cells which kills them -TCR activates CD95L which binds to CD95 on target cell which initiates apoptosis |
| perforin | perforin forms a polymeric cylindrical structure in the lipid-bilayer |
| granzyme | enters cell via perforin pore, it's a protease that cleaves target cell proteins initiating apoptosis |
| exogenous antigen | extracellular antigen- phagolysosome, degrade |
| CD4+/ THC | T Helper cell TH1-IFN-y TH2 |
| TH1 | IFN-y increases macrophage activity and so phagocitosis of pathogenic cells increases and bacterial infections are eliminated |
| TH2 | releases cytokines which interact with cytokine receptors on B cells that release antibodies and proliferate into plasma cells |
| B cells (in immune response) | -IgM/IgD antigens on them and then they can switch to IgG, A, E -recognise native antigen -have immunoglobulins on their surface which recognise antigen -IgM (once B cell activated) is pentameric |
| plasma cell | -differentiated B cells specialising in antibody release -secondary immune response -release Ig's -short life time |
| memory cells | -specialised in creating memory immune response -don't secrete antibodies, express antibody as BCR -membrane bound -triggered once they see antigen in blood/lymphatic systems -respond rapidly and become plasma cells -long life time |
| cell differentiation- lymphoid precursor | Bone marrow stem cell--> lymphoid precursor--> T cell or B cell |
| T cells | -origin: bone marrow -mature: thymus -T cell central tolerance: death by neglect, positive selection, negative selection -activated: T cell periferal tolerance -types of T cells: CD4+/T helper cell, CD8+/T cytotoxic cell, natural killer cells -death: apoptosis |
| T cell central tolerance | -death by neglect -positive selection -negative selection |
| death by neglect | don't/can't recognise antigen- cTEC, if cell scanned doesn't react positively it will die via apoptosis |
| positive selection | the naive T cell shows moderate signal towards mTEC cell and then it gets activated |
| negative selection | shows very strong reaction to mTEC cell and potential to autoimmune so dies via apoptosis |
| T cell periferal tolerance | 1. bind to MHC-foreign peptide complex to their TCR 2. interaction between B7 protein on APCs and CD28 o T cells - to maintain anergy any T cell that comes into a non-APC while its naive will never be activated and die in apoptosis |
| natural killer cells | -detect altered MHC expression and lysis or -low or absent expression of MHC-I triggers NK activation leading to killing of target cell |
| T cell receptor | alpha chain- DNA V(70 genes)-J(61)-C(1) beta chain- DNA V(52 genes)-D(2)-J(13)-C(2) 2 variable regions |
| B cells | -origin: Bone Marrow -mature: bone marrow- b cell central tolerance, BCR rearrangement -activation: B cell periferal tolerance -isotope switching: IgM/IgD--> other Ig's |
| B cell central tolerance | -bone marrow- check to determine if they bind to self antigen--> autoreactive immature B cell-->apoptosis -BCR rearrangement-makes distinctive antigen receptors. Then travels to blood |
| B cell activation/ B cell periferal tolerance | 1. antigen binding and cross linking of surface immunoglobulin 2. CD40 is expressed on B cell and MHCII/TRC ineractions results in CD40L being expressed. When CD40 interacts with CD40L cytokines are released from T cell and activate B cell |
| isotope switching | IgM/IgD are produced, looping out of the unnessary genes and then whatever isotope is needed is produced leaving particular sequence of genes e.g. IgG |
| IgG | -found in blood -high conc. in secondary immune response -functions: opsonise/neutralise, target viruses/bacteria, neonatal immunity because paces through placenta |
| IgA (dimer) (J chain) | -found in secretions e.g. mucus, saliva, breast milk -functions: neonatal immunity, defense of mucosal membrane, target virus/bacteria |
| IgM (pent) (J chain) | -primary immune response -expressed on naive B cells -functions: activates complement, targets extracellular bacteria, BCR |
| IgE | -present in blood -functions: bound to mast- allergic, paracitic immunity |
| IgD | -present on naive B cells and memory cell - no known function |
| complement | -antibody mediated destruction -form a pore in cytoplasm which lysis the cell, ineffective against gram +ve bacteria -can be attracted to cell wall where complement receptors (C εR) on phagocytes enhance opsonisation--> faciliatate uptake of antigen |
| antibody structure | -heavy chain- DNA V(~50 genes)-D(~25)-J(~5)-C. constant domain, has specific non-changing isotopes -light chain- DNA V(~50 genes)-J(~5)-C. has different affinities (it's ability to bind anitgen) between Ig's. variable domains -antigen binding site -disulfide bonds -IgM/IgD has a extra heavy chain -some have J-chain |
| Neonatal tolerance | caused by: - supressor cellls: Tregs, there is a big wave of them produced in the neonatal their fxn is to dampen immune response -highly active central tolerance- huge output from the thymus (huge -ve selection) -IgA/IgG is given to child from mother via breast-feeding (IgA) and while the baby is in the womb (IgG) -tolerance is more heavily used then immunity because neonates are lymphobinic (have no lymph system) |
| Treg | -suppress activation of immune system and prevent autoimmune diseases -they differentiate between self and non-self supressor and regulatory activities -could be useful in preventing AIDs or cancer |
| Tolerance | -acquired inability to make an adaptive immune response directed to self antigen because all macromolecules are potential antigens -developed capacity to discriminate between foreign and host antigen |
| Hypersensitivity | -IgE/Mast cell interaction antigen-->APC-->TH2-->cytokines-->cytokine receptors on B cell-->IgE- Fcε binding region-->mast cell- FcεR (receptor)-->antigen cross links two antibodies on mast cell--> degranulation-->releases allergic mediators e.g. histamines and seratonin-->symptoms= hayfever and asthma |
| innate response | -non-specific -born with -narrow range of receptors (toll-like receptors) -instant response (within hours) -barrier defenses- skin, mucus, stomach acid, secretions -internal defenses- phagocytes, complement, natural killer cells |
| adaptive response | -specific -acquired, memory -delayed response-maybe days -broad range cells- T cells, B cells -humoral response-antibody production -cell-mediated (CD8+ activation, cytotoxic T cell) -MHC dependent-highly polymorphic |
| Blood and lymph systems | -primary lymphoid organ: bone marrow and thymus -bone marrow-->stem cells-->WBCs under influence cytokines -increase neutrophil -circulating system-blood lymph -connecting between lymph and blood systems -blood flow from veins to heart, lungs-->arteries-->tissues -lymph drains from thoracic duct into left subclavian vein of blood circulatory system -thymus-educates T cells, selection get rid of autoimmune |
| Secondary lymphoid systems | -spleen- filter blood, contain phagocytes and lymphocytes -lymph-drains from extravascular tissues into lymphatic capillaries-->lymph ducts-->lymph nodes. filter lymph, collecting pt, DCs, antigen, lymphocytes, phagocytes, APCs--> T cells-->B cells-->cells and antibodies-->left subclavian vein-->blood vessels -Mucosal Associated Lymphatic Tissues (MALT)- lungs, genital, intestinal tract. interacts with antigens and microorganisms in gut, bronchi other mucous membranes |
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