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Immune response

ruby.white94 MICR223 Englisch 117 Karten

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  1. 1PRRsPattern recognition receptors
  2. 2PAMPsPathogen associated molecular patterns
  3. 3Transcription factors turned on by MyD88 dependant and independant signallingDependant - NFkB, JNK, p38
    Independant - NFkB and IRF3
  4. 4C-type Lectin receptorsDectin 1, Dectin 2 and mannose receptors
    all recognise candida and all lead to Th17 adaptive immune response
  5. 5MincleA C-type lectin receptor which recognises malassezia spp, recognises trehalose dymycolate from Mtb
  6. 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.
  7. 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
  8. 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.
  9. 9What does MyD88 independant signalling use instead of MyD88?TRIF
  10. 10Explain the structure of a BCRNotes
  11. 11Explain the structure of a TCRnotes
  12. 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
  13. 13RSSRecombination single sequence
    Recognised by RAG-1 and RAG-2 for recommbination
  14. 14RAG-1 and RAG-2Recognise RSS and cut both strands of DNA.
  15. 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
  16. 16Allelic exclusionOne chromosome makes a defective BCR then the other one is used. If both defctive then death occurs.
  17. 17Where does Negative and positive selection of Tcells occurThymus
  18. 18Negative selectionCells that bind MHC to strongly are killed
  19. 19Positive selectionCells that bind MHC at the right level survive
    Cells that don't bind enough, death by neglect
  20. 20Features of cytokinesSouble intercellular signalling molecules
    picomolar and nanomolar concentrations
    acts through specific receptors
    Acts locally
  21. 21PleiotrophicMore than one effect, cytokines
  22. 22Why are cytokines tightly regulated and how?Extremely potent and through receptor expression
  23. 23What does sustained of systemic production of cytokines lead to?Pathogenesis and disease
  24. 24IL-2, IL-6, TNFalphaProinflammatory cytokines
  25. 25Endogenous pyrogensIncrease the thermoregulatory set point in the hypothalamus
  26. 26What are effects of pro-infammatory cytokinesEndogenous pyrogens
    upregulate synthesis of pro-inflammatory cytokines
    Stimulate production of acute phase proteins
    attract inflammatory cells
  27. 27Cytokine stormLarge quantities of cytokines released, uncontrolled high fever, local edema, severe swelling, septic shock
  28. 28Anti-inflammatory cytokinesIL10, TGFbeta
  29. 29IL-10 effectsStops macrophage production of TNFalpha
    suppressive functions in the immune response
  30. 30ChemokinesProteins active over 1-100mg/ml concentration range
    stimulate and sustain inflammatory response
    short lived
  31. 31Describe overall chemokine structureConserved cysteine residues that form disulphide bonds in tertiary structure
  32. 32CXC chemokinesBind to CXCR receptors
    produced mainly by macrophages
    primarily effect neutrophils
  33. 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
  34. 34C chemokinesOnly one cystiene bond
    bind to XCL receptors
    Attract pre cursor tcells in thymus
  35. 35CX3C chemokinesHave cysteines separated by three amino acids
    Attract tcells and monocytes
  36. 36Structure of a chemokine receptor?All have seven span transmembrane proteins
    Signal through G-coupled receptor
  37. 37IL-8CXCL8
    Produced by monocytes, macrophages, fibroblasts, keratinocytes
  38. 38Antigen specificMHCI/II and TCR
  39. 39CoreceptorCD4/8
  40. 40AdhesionLFA1 - ICAM
  41. 41Co-stimulationCD28/CD80
  42. 42What inflammatory signals does the APC give the Tcell?IL-12
  43. 43CTLA-4Competes with CD28 to bidn with CD80 from APC
  44. 44p-SMACThe peripheral ring of contact all but ICAM and LFA are in this cirle
  45. 45Describe the intracellular process of TCR activationNotes
  46. 46Outcome of TCR activationIl-2 - Tcell proliferation
    Tcell cytotoxic function CD8
    cytokines -> anitbody production
    IFNgamma activates macrophages
  47. 47ThT helper cell
    CD4 Tcell subsets
  48. 48TcCytotoxic Tcell
    CD8 subsets
  49. 49What do CD4 Tcell subsets do?Activate macropahges to make cytokine
  50. 50What do CD8 Tcell subsets do?Release perforins and granzymes
    Cell death of target cell
  51. 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
  52. 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
  53. 53What can result from Th1 and Th2 if things go wrong?Th1 - autoimmunity
    Th2 - allergies
  54. 54IL-12IFN-y production
  55. 55IL-23IL-17 production
  56. 56Th17 immune cellscauses neutrophils, inflammation, CD4 tcells to make IL22, autoimmunity
  57. 57TfhStimulate B cells
  58. 58Th9Activated by IL-4, TGFb
    Makes pro-inflammatory IL9 and Anti-inflammatory IL-10
  59. 59Type 1 response CD8IL-12 activated
    IFNy production
  60. 60Type 2 responses CD8IL4 activated
    Makes IL4, IL5, IL13
  61. 61Non conventional TcellsWithin gut epithelium
    gamma sigma not alpha beta TCR
    Recognise antigen directly, innate like
  62. 62Non convential Tcell NKNatural killer cells
    Respond very fast
    express restricted alphabetaTCR and NK markers
    Recognise lipid antigen on MHC like molecules
    Innate like
  63. 63What two types of transcription factors are needed in Tcell activation?One to turn on genes STAT
    One to keep them on
  64. 64Th1IL12 Activation
    STAT3 turn on genes
    Tbet keep genes on
    INFy produced
  65. 65Th2 cellsIL4 activator
    STAT6 turns genes on
    GATA3 keeps genes on
    IL4, IL5 IL13 produced
  66. 66Th17 cellsIL-23 activator
    STAT3 turns genes on
    RORyt keeps genes on IL17 produced
  67. 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
  68. 68What controls the speed of response?Amount and availability of antigen
    costimulation
    cytokines
  69. 69What controls the magnitude of a response?The amount and availability of antigen
    costilumaltory molecules
    cytokines
    naive precursor frq
  70. 70What drives the resolution of a responsedecreased cytokines
    antigen/pathogen cease to bind
    decreased cytokines
  71. 71TregsSuppress the Tcell activation, proliferation and differentiation
  72. 72Natural TregsDevelop in the thymus
    10% of all CD4 T cells
  73. 73Induced TregsAre induced in the periphery
  74. 74What do Tregs express?FoxP3
    IL2 receptor and alpha chain CD25
    Co-inhibiting molecule CTLA4
  75. 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
  76. 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
  77. 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
  78. 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
  79. 79IL-10 secretion by TregsSuppresses Tcell cytokine production and reduces MHC expression in APCs
  80. 80TGFb expression by TregsBlocks Tcells cytokine production stops cell division and killing ability
  81. 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
  82. 82IPEXSystemic autoimmunity
    Foxp3 mutation
    Will die within 1-2 years without treatment
    symptoms gut inflammation, autoimmunity, type 1 diabetes, thyroid disease, dermititis
  83. 83M2Regulatory macrophages
    Produce TGFb
    Antiinflammatory
    promote wound healing and tissue repair
  84. 84What do B cells do?Secrete antibody
    act as APC
    Establish a memory population
  85. 85Tcell dependant antibody productionBcell takes up pathogen and presents it, Tcell bind, activate tcell to produce cytokines, B cell develops into a plasma cell
  86. 86CD40LBcell uptakes pathogen, presents it and upregulates CD40L. Tcell activated and also upregulates CD40L which binds CD40L on Bcell
    Bcell develops into plasma cell
  87. 87CD40LBcell uptakes pathogen, presents it and upregulates CD40L. Tcell activated and also upregulates CD40L which binds CD40L on Bcell
    Bcell develops into plasma cell
  88. 88SpleenBlood filter
    Red and white pulp
  89. 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
  90. 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
  91. 91Role of antibodiesCan neutralise toxins
    opsonisation to help ingestion by macrophage
    cause compliment activation
  92. 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
  93. 93AIDActivation inducedcytidine deaminase
  94. 94Affinity maturationGood mutations then the Bcell survives
    Bad mutation apoptosis
  95. 95Where does somatic hypermutation and antibody class switching occurGerminal centres
  96. 96Antibody classesDifferent isotypes of constant regions of heavy chain
  97. 97What three forms does antibody come in?Monomer 2 sites
    dimer 4 sites
    pentamer 10 sites
  98. 98IgM1st antibody after immunization
    strong activator of complement
    generally low binding strength
  99. 99IgGMonomer
    Can cross the placenta
    in blood, lymph and ecf
    major circulating antibody
    activate complement
  100. 100IgDAbdundant on Bcell surface like IgM
    Secreted function unknown
  101. 101IgAIn blood, saliva, tears, breast milk, mucous
    dimers linked by jchain peptide
  102. 102IgEMost bound to receptors on granulocytes
    binding to Ige bound to mast cells causes degranulation and allergies
  103. 103What drives class switching?Tfh
  104. 104What is initally produced in an immune response followed by what?IgM
    IgA and IgG
  105. 105What isotype do naive b cells express?IgD and IgM
  106. 106What is immunological memory?Cells more specialised and more of them
  107. 107Immunology memory isA pool of specialised memory cells that develop during an immune response and persist without the antigen available naymore
  108. 108Where do short lived plasma cells residelymph node or spleen
  109. 109Long lived plasma cells reside in?Bone marrow
  110. 110What are long lived plasma cells a sourceHigh affinity class switched antibody
  111. 111Where do memory Bcells arise from?The germinal reaction
  112. 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
  113. 113T memory cellslong lived cells that survive after the contraction of the effector phase
  114. 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
  115. 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
  116. 116Central memoryExpress lymphnode homing molecules
    slower than effector memory cells to produce cytokine
  117. 117Effector memoryLack lymphnode homing molecule
    rapidly produce cytokine upon antigenic stimulation

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Beschreibung
MICR223 Karteikarten am Immune response, erstellt von ruby.white94 am 13/10/2013.
Erstellt von
ruby.white94 · Okt 2013
Aktualisiert
19 Feb 2016
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