Karteikarten
Week 9
Karten in diesem Stapel (44)
- 1Where are lymphocytes mostly located?Spleen
- 2Describe the pathway of lymphocyte re-circulation-Naive/memory T and B cells lymphcytes, enter lymph nodes via HEVs
-If they don't encounter antigen in lymphoid tissue in a day they exit via the efferent lymphatics
-They re-enter the circulation where the thoracic duct enters the left subclavian vein - 3Describe the arrangement of T/B cells in a lymph node-T cells migrate to the paracortex section of a node along with dendritic cells
-B cells migrate to the cortex along with follicular dendritic cells
-Dendritic cells enter the node via the afferent lymphatic vessel
-Effector T/B cells migrate to the cortex/paracortex border and interact
-Plasma cells migrate down to the T zone and exit via the efferent lymphatic vessel - 4Describe the overall arrangement of a geminal centre-In the cortex of a lymph node
-Dark zone is densely packed with proliferating cells
-Light zone is the site of selection, differentiation and re-circulation - 5What happens in the dark zone in the germinal centre?Somatic hypermutation
-Point mutations are randomly inserted into the genome
-This creates many different variable regions on the antibody
-This process is driven by AID enzymes - 6What happens in the light zone in the germinal centre?-Selection of antibodies
-Apoptosis of useless B cells occurs
-Differentiation of B cells
-Class switching
-Light/dark zone re-circulation - 7How does selection of antibodies occur?-Follicular dendritic cells (FDC) present antigen complexes to test antibodies
-Higher affinity antibodies outcompete less effective ones
-Less effective B cells are apoptosed - 8What cell types do B cells differentiate into?-Plasma cells (class switched antibodies)
-Memory B cells - 9What molecule is involved in TFH and B cell interactions?-CD40 ligands on TFH cells bind to CD40 on B cells
-This drives class switching from IgM to higher affinity antibodies - 10What process does CD40/CD40 ligand interactions drive?-Selection
-Class switching
-Further mutations via light/dark zone re-circulation - 11What does antibody secretion by plasma cells do?-Neutralisation
-Opsonisation
-Complement activation via classical pathway - 12How do conjugate vaccines work?-B cells bind to polysaccharide epitopes bound to pathogen
-Antigen is internalised
-Peptides from protein are presented to the T cell
-Class switching occurs and antibodies are secreted - 13What are natural antibodies?-Mostly IgM
-Not undergone somatic hypermutation
-Provide resistance in first 48 hours
-Sticky and bind to many bacteria
-Produced b B1 cells in peritoneal and pleural cavities - 14How do T cell independent antibodies work?-Stimulated by bacterial polysaccharides which have repeating structures
-Low affinity IgM antibodies are produced quickly
-No immune memory - 15What is the prodromal response to infection?The first set of symptoms of infection. They are caused by a direct cascade of interferon induced responses
- 16What do Interferon Stimulated Genes do?-Limit pathogen growth by causing apoptosis
-Can clear infection without the help of the adaptive immune system - 17What is the role of cytotoxic T cells in anti-viral immunity?-Releases perforin, granzyme and granulysin
-FAS ligand binds to FAS on target cells and triggers apoptosis - 18What is the role of natural killer cells in anti-viral immunity?-Triggered by lack of MHC I on cells caused by viral infections
-Releases IFN(gamma)
-Releases perforin and granzyme
-Apoptosis via Fas/FasL
-Migrates along IL-12 gradients - 19What is Antibody-Dependent Cell Cytotoxicity (ADCC)?-NK cells express an Fc receptor which binds to the Fc part of IgG antibodies which are bound to the surface of infected cells
-Even non-neutralising antibodies can induce killing of any virion they bind to - 20How is T cell tolerance maintained?-Thymic positive/negative selection
Peripheral:
-ignorance
-anergy
-cell death
-suppression - 21How is B cell tolerance maintained?Early antigen encounter pre-lymphoid tissue
Lack of T cell help peripherally - 22How does loss of tolerance develop?-Ignorance at sites such as the eye/testis
-impairment of Treg cells
-Inappropriate antigen presentation resulting in anergy/apoptosis of T helper cells - 23What are the 5 main mechanisms by which autoantibodies can produce autoimmune disease?-Complement dependent lysis of the target cell
-Opsonisation
-Formation of immune complexes
-Blockade of receptors for physiological ligands
-Stimulation of cell surface receptors - 24Where is the site of tissue specific autoimmunity in: -Graves/Hashimoto's disease -Goodpasture's syndrome -Diabetes mellitusThyroid and ocular connective tissues
Kidney/lung basement membrane
Bet cells of the pancreas - 25Where is the site of tissue specific autoimmunity in: -Pernicious anaemia -Addison's disease -Myasthenia gravisParietal cells/IF
Adrenal glands
Acetylcholine receptor - 26How does autoimmunity related to RA occur?-Antibodies form against the Fc portion of IgG which is a rheumatoid factor
-Anti-CCP antibodies (more erosive disease) - 27What are some features of RA?-Affects women more
-Joints in hand, wrist and feet become painful, swollen and stiff
-Can be an erosive disease where bone/cartilage destruction leads to joint deformity
-Is a systemic disease
-Can result in severe disability - 28How do IgG and IgM levels change with primary and re-exposure to inoculum?IgM rises rapidly in the primary inoculum phase, but on re-exposure there is a little increase
IgG rises with a delay on primary inoculum, but on re-exposure it rises rapidly - 29At what stage of the disease stage do vaccines work?When the infection is being established. There are fewer numbers of bacteria so there is less resistance, and it stops bacteria from replicating
- 30When looking at a sample of B cells from an unimmunised donor: -what isotope of antibody is produced? -affinity of antibody? -somatic hypermutation?-Mostly IgM (more than IgG)
-Low affinity
-Low somatic mutation - 31When looking at a sample of B cells from an immunised donor: -what isotope of antibody is produced? -affinity of antibody? -somatic hypermutation?-IgG and IgA
-High affinity
-High somatic hypermutation - 32What are features of the ideal vaccine?-Not cause illness/death
-High efficacy
-Protection lasts several years
-Produce neutralising antibodies against infections that target irreplaceable cells
-Low cost
-Stable in different environments
-Easy to administer
-No s/e's - 33How is passive immunity different from active?Passive: donating immunity
Active: activating the host to develop immunity - 34What is passive immunophylaxis?-Donating IgG antibodies which are high affinity and opsonising
-Immediate protection (no 2 week lag)
-Specific antibody to disease
Cons:
-short lasting
-espensive
-short half-life (14-21 days) - 35What are the different forms an active vaccination can be found?Whole micro-organism:
-live-attenuated
-dead (less effective but safer)
Subunit of micro-organism:
-inactivated toxin
-recombinant proteins
-polysaccharide
-conjugate vaccines polysaccharide combined with pathogen - 36Describe a bacterial capsule-Outer capsule made out of polysaccharide
-Hides surface molecules from immune system
-Poorly immunogenic
-T-independent antigen responses are needed - 37What are some disadvantages to T independent antigen responses?Lack of T cell help means:
-lack of affinity maturation in germinal centres
-poor memory induction
-Poor response in under 2yrs - 38How do conjugate vaccines work?-Polysaccharides are conjugated to protein antigen
-The vaccine is internalised by APC
-Peptide presented to CD4+ T helper cell
-T cell recognises protein/polysaccharide
-Triggers polysaccharide-specific B cell to produce antibody - 39What are adjuvants?A substance that enhances the immunogenicity of substances mixed with it
- 40How do adjuvants work?-Convert soluble antigens to particulate material to increase APC uptake and slow release of antigen
-Include bacterial products which leads to up-regulation of co-receptors and cytokines
-Toll receptor agonists for tumour vaccination - 41Define herd immunityWhere enough of a population is vaccinated against an infectious organism
- 42What factors affect herd immunity?-Coverage rates
-Susceptibility of hosts
-Vaccine effectiveness
-Force of transmission
-Crowding
-Nasopharyngeal carriage - 43How can an egg allergy affect flu vaccination use?Flue vaccine is developed in eggs. Small ovalbumin (egg white) content is found in the vaccine.
RIsk of anaphylaxis - 44How can vaccines be used in cancer prevention?Some cancers develop as a result of viral infection eg. HPV and cervical cancer, HBC/HCV and hepatic cancer
Informationen
- Beschreibung
- B and T cell co-operation Cytotoxic T cells and antiviral killing Clinical autoimmunity Vaccination
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- Dolu Falowo
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