Fichas
Immune response
Fichas del conjunto (117)
- 1PRRsPattern recognition receptors
- 2PAMPsPathogen associated molecular patterns
- 3Transcription factors turned on by MyD88 dependant and independant signallingDependant - NFkB, JNK, p38
Independant - NFkB and IRF3 - 4C-type Lectin receptorsDectin 1, Dectin 2 and mannose receptors
all recognise candida and all lead to Th17 adaptive immune response - 5MincleA C-type lectin receptor which recognises malassezia spp, recognises trehalose dymycolate from Mtb
- 6RIG-1 like receptorsRIG-1 - recognises retinoic acid-inducible gene 1, ss RNA, short blunt end of dsRNA.
MDA5 - melanoma differentiation associated genes, recognises dsRNA. - 7Th1 Tcell what activates it what response does it produceIL-12
Produces IFN-y
Macrophages increased phagocytosis
CD8Tcell kill infected cells
B cell make antibody to enhance phagocytosis - 8Th2 CD4 TcellsIL-4 from APC
Starts making IL4, IL5, IL13
Makes mast cell destroy worms CD4 Tcell produce more IL4, IL5, IL13 and Bcell make antibody to bind pathogen. - 9What does MyD88 independant signalling use instead of MyD88?TRIF
- 10Explain the structure of a BCRNotes
- 11Explain the structure of a TCRnotes
- 12What are two other sources of variation for the Bcell receptor other than rearrangment?1. Exact point of splicing between V and D and D and J
2. extra nucleotide can insert at these joints called N region - 13RSSRecombination single sequence
Recognised by RAG-1 and RAG-2 for recommbination - 14RAG-1 and RAG-2Recognise RSS and cut both strands of DNA.
- 15How is RAG-1 and RAG-2 cutting repaired?Regular cellular machinary, Tdt
by nonhomologous joining, the two ends are ligated to form a coding joint V-DJ on heavy chain and VJ on light chain - 16Allelic exclusionOne chromosome makes a defective BCR then the other one is used. If both defctive then death occurs.
- 17Where does Negative and positive selection of Tcells occurThymus
- 18Negative selectionCells that bind MHC to strongly are killed
- 19Positive selectionCells that bind MHC at the right level survive
Cells that don't bind enough, death by neglect - 20Features of cytokinesSouble intercellular signalling molecules
picomolar and nanomolar concentrations
acts through specific receptors
Acts locally - 21PleiotrophicMore than one effect, cytokines
- 22Why are cytokines tightly regulated and how?Extremely potent and through receptor expression
- 23What does sustained of systemic production of cytokines lead to?Pathogenesis and disease
- 24IL-2, IL-6, TNFalphaProinflammatory cytokines
- 25Endogenous pyrogensIncrease the thermoregulatory set point in the hypothalamus
- 26What are effects of pro-infammatory cytokinesEndogenous pyrogens
upregulate synthesis of pro-inflammatory cytokines
Stimulate production of acute phase proteins
attract inflammatory cells - 27Cytokine stormLarge quantities of cytokines released, uncontrolled high fever, local edema, severe swelling, septic shock
- 28Anti-inflammatory cytokinesIL10, TGFbeta
- 29IL-10 effectsStops macrophage production of TNFalpha
suppressive functions in the immune response - 30ChemokinesProteins active over 1-100mg/ml concentration range
stimulate and sustain inflammatory response
short lived - 31Describe overall chemokine structureConserved cysteine residues that form disulphide bonds in tertiary structure
- 32CXC chemokinesBind to CXCR receptors
produced mainly by macrophages
primarily effect neutrophils - 33CC chemokinesTwo adjacent cystienes
Bind to CCR receptor
Produced mainly by macrophages and t cells
primarily attract monocytes
Can also attract tcells, eosinphils and basophils - 34C chemokinesOnly one cystiene bond
bind to XCL receptors
Attract pre cursor tcells in thymus - 35CX3C chemokinesHave cysteines separated by three amino acids
Attract tcells and monocytes - 36Structure of a chemokine receptor?All have seven span transmembrane proteins
Signal through G-coupled receptor - 37IL-8CXCL8
Produced by monocytes, macrophages, fibroblasts, keratinocytes - 38Antigen specificMHCI/II and TCR
- 39CoreceptorCD4/8
- 40AdhesionLFA1 - ICAM
- 41Co-stimulationCD28/CD80
- 42What inflammatory signals does the APC give the Tcell?IL-12
- 43CTLA-4Competes with CD28 to bidn with CD80 from APC
- 44p-SMACThe peripheral ring of contact all but ICAM and LFA are in this cirle
- 45Describe the intracellular process of TCR activationNotes
- 46Outcome of TCR activationIl-2 - Tcell proliferation
Tcell cytotoxic function CD8
cytokines -> anitbody production
IFNgamma activates macrophages - 47ThT helper cell
CD4 Tcell subsets - 48TcCytotoxic Tcell
CD8 subsets - 49What do CD4 Tcell subsets do?Activate macropahges to make cytokine
- 50What do CD8 Tcell subsets do?Release perforins and granzymes
Cell death of target cell - 51CD4 Th1IL-12 from APC activates them
They create IFNy
Increase macrophage phagocytosis, induce CD8 cells to kill infected cells, Bcells make antibody to enhance pahgocytosis
Intracellular infection - 52CD4 Th2IL-4 activates them
Make IL4, IL5, IL13
Mast cell and eosinohil destory worms, CD4 tcell produce more IL4,5,13
Bcell make antibody
Worms and parasites - 53What can result from Th1 and Th2 if things go wrong?Th1 - autoimmunity
Th2 - allergies - 54IL-12IFN-y production
- 55IL-23IL-17 production
- 56Th17 immune cellscauses neutrophils, inflammation, CD4 tcells to make IL22, autoimmunity
- 57TfhStimulate B cells
- 58Th9Activated by IL-4, TGFb
Makes pro-inflammatory IL9 and Anti-inflammatory IL-10 - 59Type 1 response CD8IL-12 activated
IFNy production - 60Type 2 responses CD8IL4 activated
Makes IL4, IL5, IL13 - 61Non conventional TcellsWithin gut epithelium
gamma sigma not alpha beta TCR
Recognise antigen directly, innate like - 62Non convential Tcell NKNatural killer cells
Respond very fast
express restricted alphabetaTCR and NK markers
Recognise lipid antigen on MHC like molecules
Innate like - 63What two types of transcription factors are needed in Tcell activation?One to turn on genes STAT
One to keep them on - 64Th1IL12 Activation
STAT3 turn on genes
Tbet keep genes on
INFy produced - 65Th2 cellsIL4 activator
STAT6 turns genes on
GATA3 keeps genes on
IL4, IL5 IL13 produced - 66Th17 cellsIL-23 activator
STAT3 turns genes on
RORyt keeps genes on IL17 produced - 67What are the five ways of keeping a tcell subset that subset?1. transcription of cytokine genes (positive feedback)
2. Inhibit expression of other cytokine receptors
3. Hisotne modifications to prevent other transcription factors binding
4. DNA methylations to prevent other genes being transcribed
5. micro RNAs
HERITABILITY OF DIFFERENTIATION - 68What controls the speed of response?Amount and availability of antigen
costimulation
cytokines - 69What controls the magnitude of a response?The amount and availability of antigen
costilumaltory molecules
cytokines
naive precursor frq - 70What drives the resolution of a responsedecreased cytokines
antigen/pathogen cease to bind
decreased cytokines - 71TregsSuppress the Tcell activation, proliferation and differentiation
- 72Natural TregsDevelop in the thymus
10% of all CD4 T cells - 73Induced TregsAre induced in the periphery
- 74What do Tregs express?FoxP3
IL2 receptor and alpha chain CD25
Co-inhibiting molecule CTLA4 - 75Foxp3Expression in induced Tregs can be driven by TFGb
Interferes with IL-2 production by uptaking and degrading it as well as stopping Tcells produce it - 76Foxp3Expression in induced Tregs can be driven by TFGb
Interferes with IL-2 production by uptaking and degrading it as well as stopping Tcells produce it - 77Foxp3Expression in induced Tregs can be driven by TFGb
Interferes with IL-2 production by uptaking and degrading it as well as stopping Tcells produce it - 78Foxp3Expression in induced Tregs can be driven by TFGb
Interferes with IL-2 production by uptaking and degrading it as well as stopping Tcells produce it - 79IL-10 secretion by TregsSuppresses Tcell cytokine production and reduces MHC expression in APCs
- 80TGFb expression by TregsBlocks Tcells cytokine production stops cell division and killing ability
- 81CTLA-4 and TregsBinds with high affinity to CD80 on APC stopping binding with Tcells
It also induces DC to porduce molecules that are toxic to Tcells - 82IPEXSystemic autoimmunity
Foxp3 mutation
Will die within 1-2 years without treatment
symptoms gut inflammation, autoimmunity, type 1 diabetes, thyroid disease, dermititis - 83M2Regulatory macrophages
Produce TGFb
Antiinflammatory
promote wound healing and tissue repair - 84What do B cells do?Secrete antibody
act as APC
Establish a memory population - 85Tcell dependant antibody productionBcell takes up pathogen and presents it, Tcell bind, activate tcell to produce cytokines, B cell develops into a plasma cell
- 86CD40LBcell uptakes pathogen, presents it and upregulates CD40L. Tcell activated and also upregulates CD40L which binds CD40L on Bcell
Bcell develops into plasma cell - 87CD40LBcell uptakes pathogen, presents it and upregulates CD40L. Tcell activated and also upregulates CD40L which binds CD40L on Bcell
Bcell develops into plasma cell - 88SpleenBlood filter
Red and white pulp - 89White pulpBcells and Tcells are organised into discrete regions of the white pulp.
Bcells in follicles, Tcells in PALS
Marginal zones contain macrophages and DCs - 90Germinal centresFound in Bcell region of lymphnode or spleen
Naive Bcells which encounter antigen moves to the boundary with Tcell areas
Activated cells move to the follicle to form a germinal centre - 91Role of antibodiesCan neutralise toxins
opsonisation to help ingestion by macrophage
cause compliment activation - 92Somatic hypermutationOccurs after antigen driven activation as part of the germinal centre response
Point mutations, 50% of mutation in antibody at each division
Requires AID - 93AIDActivation inducedcytidine deaminase
- 94Affinity maturationGood mutations then the Bcell survives
Bad mutation apoptosis - 95Where does somatic hypermutation and antibody class switching occurGerminal centres
- 96Antibody classesDifferent isotypes of constant regions of heavy chain
- 97What three forms does antibody come in?Monomer 2 sites
dimer 4 sites
pentamer 10 sites - 98IgM1st antibody after immunization
strong activator of complement
generally low binding strength - 99IgGMonomer
Can cross the placenta
in blood, lymph and ecf
major circulating antibody
activate complement - 100IgDAbdundant on Bcell surface like IgM
Secreted function unknown - 101IgAIn blood, saliva, tears, breast milk, mucous
dimers linked by jchain peptide - 102IgEMost bound to receptors on granulocytes
binding to Ige bound to mast cells causes degranulation and allergies - 103What drives class switching?Tfh
- 104What is initally produced in an immune response followed by what?IgM
IgA and IgG - 105What isotype do naive b cells express?IgD and IgM
- 106What is immunological memory?Cells more specialised and more of them
- 107Immunology memory isA pool of specialised memory cells that develop during an immune response and persist without the antigen available naymore
- 108Where do short lived plasma cells residelymph node or spleen
- 109Long lived plasma cells reside in?Bone marrow
- 110What are long lived plasma cells a sourceHigh affinity class switched antibody
- 111Where do memory Bcells arise from?The germinal reaction
- 112Features of a memory BcellExpress higher levels of MHCII and co-stimulatory molecules than naive Bcells
Divide very slowly if at all
Express surface IgG but do not secrete it
Quickly regenerate antibody when they reencounter it - 113T memory cellslong lived cells that survive after the contraction of the effector phase
- 114Features of T memory cellsDivide more frequently than naive t cells
balance of proliferation and death dictates memory pool size
IL7 and IL15 needed for survival - 115Why are T memory cell better?They divide more and to lower antigen doses
require less costimulation
produce cytokine faster
may be strategically positioned in tissue where infection might occur - 116Central memoryExpress lymphnode homing molecules
slower than effector memory cells to produce cytokine - 117Effector memoryLack lymphnode homing molecule
rapidly produce cytokine upon antigenic stimulation
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- MICR223 Fichas sobre Immune response, creado por ruby.white94 el 13/10/2013.
- Creado por
- ruby.white94 · oct 2013
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- 19 feb 2016
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