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Immuno. Lecture 4/5

QuestionAnswer
Helper T-cell (CD4+) -has T-cell receptors (TCR) -VDJ recombination -Educated in thymus, leave as naive T-cells -circulate -> lymph nodes -> encounter professional APC -MHCII - CD4+ communicate -Co-stimulation (TCR + CD28)
VDJ recombination -Variable, Diversity, Joining segments -slot machine -site-specific genetic recombination process in developing B and T lymphocytes that assembles unique immunoglobulin and T-cell receptor genes
Helper T-cell (CD4+) -also from APC - cytokines -tells T-cells what kind of immune response -Th1, Th2, Th17, Tfh
Th1 response (IL-2) -intracellular pathogens -viruses, intracellular bacteria -anti-viral, anti-tumor
Th2 response (IL-4) -parasites and allergens -leads to allergies -Parasites outside of the cell -allergy, tissue repair
Th17 response (IL-6, TFG-beta) -extracellular bacteria, fungi -mucosal immunity - tolerance
Tfh response (IL-6, IL-21) -stay in lymph node, help guide B-cells -Tfh = T follicular helper
Cytotoxic T-cell (CD8+) -cirrculate -> lymph nodes -> encounter APC -> costimulation (TCR + CD28) -DCs present to CD8+ cells via MHCI (antigen from inside of cell) -cross presentation -if infected -> perforin (creates holes), granzyme (cuts up proteins), apoptosis
B-cell -has B-cell receptors (BCR) -BCR does not rely on APC -binds directly to antigen -activate B-cell: 1. T-cell dependent activation 2. T-cell independent activation
T-cell dependant activation -B-cell eats the antigen present to the Th-cells on MHC II -class switch, affinity maturation (MHC communicates with TCR, not BCR)
T-cell independant activation -cross link many BCRs - strong signal - BCR + PRR = strong signal
Once B- cell activated... -2 different fates 1. short lived plasma cells - secret antibodies -pump out IgM, quick response 2. Germinal center reaction -clonal expansion -somatic hypermutation (more specific) -class-switch recombination (different response)
Germinal center reaction -clonal expansion -somatic hypermutation (more specific) -class-switch recombination (different response) -leads to long-lived plasma cells -> migrate to bone marrow, pump out antibodies continuously -leads to memory cells -> respond quickly
Natural Killer cells -innate lymphocytes (no TCR) -Germ line receptors: 1. recognize MCH I + self -> healthy; brakes 2. recognize stress ligands -> unhealthy; gas (viral infection, DNA damage, tumours -perforin, granzymes, death receptors, release cytokines
Basophil -rare (0-1%) myeloid lineage bombs (granulocytes) -activated by cytokines and IgE cross linking -once activated: release histamine (allergy rxn), release heparin (vasodilation), release cytokines (IL-4), encourage Th2 immunity and IgE response
Eosinophil -rare (1-4%) myeloid lineage bombs (granulocytes) -pink granules w/ toxic substances -T-cells recruit to deal w/ parasites (too big to phagocytose) -release granules: damage parasite membranes; drive asthma and allergic rxns -secrete cytokines
Basophil vs Eosinophil Basophil: more signalling than destruction purple on slides -> too many basophils = basphilia Eosinophil: more destruction than signalling pink on slides -> too many eosinophils = eosionophillia
Mast Cell long-lived; tissue- resident; myeloid lineage -stationed at barrier sites (skin, GI tract -gaurd against parasites, venoms, physical wounds
Mast cell activation activated by: 1. IgE cross linking (FcE receptor) 2. Complement (C3a, C5b) 3. Physical injury 4. Venoms Effects -degranulate - histamine, heparin, try-tease -Type 1 hypersensitivity -anaphylaxis
ELISA Enzyme Linked Immunosorbant Assay -Direct ELISA: known antibody, unknown antigen -Indirect ELISA: unknown antibody, known antigen -Sandwhich ELISA: secondary and tertiary antibodies
Omalizumab -anti-allergy treatment -monoclonal antibody -> targets Fc (constant region) of IgE free IgE is lowered -> FcE expression goes down -disarm mast/basophils
Created by: user-2017899
 

 



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