Immunology Flashcards

1
Q

Summarise the two basic strategies used by the immune system to recognise danger and initiate a response

A
  1. One gene codes for one receptor protein (germ-line encoded), hundreds of genes–> detect molecular pattern Many cells same receptor

–> fast but not as efficient

  1. Random recombination of gene fragments give many different receptors –> detect specific structure efficient but slow, potential for autoimmunity
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2
Q

Name two types of triggers (PRR - pattern recognition receptors) for germ-line detection

A

PAMPs –> Pathogen-Associated Molecular Patterns (e.g. specific surface proteins)

DAMPs –> Damage-Associated Molecular Patterns (e.g. intracellular/ extracellular components wrong)

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3
Q

Antigen Specific receptors on lymphocytes

A

B: antigen binds intact antibody

T: two chains forms T cell receptor, bind to processed antigens –> One lymphocyte: many copies of same receptor on surface

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4
Q

Epitope

A

Binding site on Antigen

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5
Q

Innate immunity characteristics

A

Uses germ-lined antibodies

  • independent of previous exposure
  • fast
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6
Q

Innate immunity tasks

A
  • destroys invading Nucleic Acids (Viruses)
  • initiates inflammatory response + signals calling for help

–> buys time and directs further response

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7
Q

Adaptive Immunity characteristics

A
  • slow
  • specific
  • able to form memory –> secondary response much faster and more effective
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8
Q

Time innate vs adaptive immunity

A
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9
Q

Major Components of Immune respnse

A
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10
Q

Clonal Selection

A

Antigen binds to surface receptor on the B cellor the T celland causes selective expansion of that clone = clonal selection

Binding of lymphocyte to Antigen causes proliveration and survival

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11
Q

Primary Lymphoid organs

A

Organs Where Lymphcytes are produced:

Thymus (T-lymphoctes)

Bone Marrow (B-lymphocytes)

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12
Q

Secondary Lymphoid organs

A

Spleen

lymph nodes

mucosal associated lymphoid tissues (MALT)

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13
Q

Thymus

  • sturcure + function
A
  • production and proliveration of T-lymphocytes (output gets less over time)
  • two lopes with several lobules

Lobules:

dark staining areas outside (Cortex)

Brighter in middle (Medulla)

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14
Q

Lymph node

A

Germinal center –> occur with infection, proliveration of B-cells

Filter antigens in Lymph

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15
Q

Lymphocytre recirculation

A

L. circulate in Vessels –> into secondary lymphativ organs via

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16
Q

HEV

A

High endothelial venule

Site of Extravasation

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17
Q

Extravasation of naive lymphocytes

A
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18
Q

Explain CD

A

CD Markers (cluster of differrentiation) bind to important cell surface receptors for cell, different cells express different CD markers

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19
Q

CD makers of T-lymphocytes

A

All: 3

CD4–> T-helper cells

CD 8 –> cytotoxic T -cells

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20
Q

CD markers of B - lymphocytes

A
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21
Q

Recall physical barriers in immune defence

A

Skin

Muscous membranes (secretion traps 🦠, cilia transport them out)

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22
Q

Recall physiologial barriers (chemical)

A

Body temperature / fever

Low pH (gastric acid)

Chemical mediators (Lysosomes etc)

Phagocytic:cells ingest material

Inflammatory:local vascular permeability increases

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23
Q

Major Cell types of immune system

A
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24
Q

Neutrophil (distinction, function) , killing mechanism

A

Distinction: polymorphonuclear (nucleus several)

phagocytosis and killing of microbes

Oxygen in-dependent: enzymes, lyssomes, other peptides

Oxygen dependent: respiratory burst –> radicls, peroxydes, superoxides

40-70% of cells, circulating, first to go into infected or damaged tissue

Can form NET (Neutrophil, extracellular trap), network of neutrophils fibres and protein, tries to catch microorganisms

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25
Q

Eosinophil (distinction, function)

A

halbrunder zellkern

phagocytosis

granule release

defence against parasitic infections

help B cell responses in GALT (IgA production)

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26
Q

Basophil (distinction, funtion)

A

Stain dark,

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27
Q

Monocyte /Macrophage (distinction, function)

A

Present in Tissues, signal infection by release of solouble mediators, phagocytosis and killing, APC

Macrophage = activated Monocyte

28
Q

Macrophage

A
29
Q

Mast cell (disginction, function)

A

granule release (pro inflammatory)

30
Q

Dendritic cell

A

Anitgen capture and presentation

Secrete Cytokines

31
Q

Natural killer cell (NK)

A

lysis of infected cells

32
Q

Movement of neutrophils into tissues

A
33
Q

Opsonisation

A

Coating of microorganisms into proteins

–> easier for phagocytosis (Monocytes bind to Microorganism thoruigh osonins)

34
Q

Opsonins

A

molecules that bind to antigen and phagocytes, proteins that coat microorganisms

Can be antibodies and complements

35
Q

Cytokine definition

A

Small proteins, messengers of immune System, generally act locally

Highly effective at low dosage –> short life span

36
Q

Structure of antibody

A

2 light, 2 heavy chains (each always identical)

Fab, FC domain (Fab = interaction)

Constant part and variable part (binding to antigen, 3 hypervariable regions)

37
Q

complementarity determining regions (CDR’s)

A

3 hypervariable regions on Antibodies that bind to Antigen

38
Q

Antibody Affinity

A

numbers and strenght of non-covalent interactions of one single antibody binding site with a single epitope

39
Q

Antibody Avidity

A

overall strenth of antibody binding as a summ of multiple Antibody binding sites binding to multiple Antigen epitopes

40
Q

Antibody cross reactivity

A

One Antibody may bind to other Antigen (which it was not produced for)

41
Q

IgG Antibodies

A

4 Subclases

–> transported across placenta for protectin of baby

–> blood + extracellular fluid

–> classic complement activation

42
Q

IgA Antibodies

A

dimer, linkes through joining chain + disulphide bridges

secreted in muscus

defence from bacteria, viruses etc.

43
Q

IgM Antibodies

A

Form pentomers –> 10 binding sites > Affinity, < Avidity

First class to be made

44
Q

IgE Antibodies

A

low concentration

Involved in parasitic response and allergies

45
Q

IgD Antibodies

A

expressed on B-cell surfaces

46
Q

Effects of Antibody binding

A

Neutralisation

Agglutination

Opsonisation

Complememtn activation

ADCC (antibody-dependent cell-mediated cytotoxicity)

47
Q

antibody-dependent cell-mediated cytotoxicity

A

ADCC, Antibodies bind to Antigen on cell and mark it

FC receptors of other immune cells bind to it, kill cell

48
Q

B-lymphocites origin and Maturation

A

Origin: Hematopoietic stemm cells

Maturation: in Bone Marrow

Gene recombination for diversity, dow selection of antibodies which are not harmful (don’t detect “self”)

49
Q

B cell activation

A

Always need secound stroke to get activated (not just antigen alone)

  1. Thymus independant

–> Antigen binding (e.g. bacterial polysaccharides) + binding of e.g. LPS (produced by bacteria)

  1. Thymus dependant

T- helper cells activate B cells –> secrete cytokines, bind to B-cells

50
Q

T cells origin + maturation

A

Origin from bone marrow, mature in thymus

–> recognize processed antigen fragement on MHC molcule

double negative –> pre TCR–> double positivem+ TCR–> selection (CD4 or CD8)

51
Q

CD Markers of T-Cells

A

All: CD3 (part of TCR)

CD4: “helper cells” (MHC class 1) –> activation of B Cells, pruduce cytokines

CD8: MHC class 2 –> cytokines, apostosis, cytotxic!

52
Q

MHC (human name, basic facts)

A

Human: HLA

Major Histocompatibility comples

idicatio of healthy self + presenting antigens to t cells

Class 1 and 2

53
Q

MHC class 1:

A
  • transplantation antigens ( CD8)

1 heavy chain inkl. 1 transmembrane region + 1 light chain

ca. 8-10 AA/ peptide

all nucleated cells

(endogenous Antigen)

54
Q

MHC class 2

A

present Atigen to T helper CD4+

two equally big heavy chains inkl. two transmembrane reigions

anitigen presenting cells

>13 AA polypeptieds

(exogenous antigen presentation)

55
Q

Endogenous AG

A

Antigen made in cell (e.g. virus infected cell)

Present to CD8+ on MHC class 1

56
Q

Exogenous AG

A

Cought from outside

Present to CD4+ on MHC 2

57
Q

Antigen presenting Cells

A

Dendritic Cells

B-lymphocytes

Macrophages

58
Q

T cell activation (by Dendritic cell)

A

Induction –> DC catches AG + presentation on suface, moves to lymph nodes

Effector –> AG recognition by T-cell –> Naïve T-cell becomes Effector

Effector kills cells

Memory

59
Q

3 Signal model

A

3 signals required for T-cell activation:

  1. Antigen recogniton
  2. Co-stimmulatin (other receptors, suface-surace interaction)
  3. Cytokine response (produced by APC)
60
Q

CD8 effector cell

A

induce apostosis

–Y when recgnize antigens –> polarisation and ganuloes released, induced through perforin pore

–> one T cell kills several infected cells

61
Q

CD4 effector T cells

A

differentiation into different subsets, defined by different produced cytokines

Th1, Th2, Th17, Treg, Tfh

Funtion:

  1. Macrophage activation
62
Q

Three functions of CD4 eiffector cells

A
  1. Macrophage Activation
  2. Delayed Type Hypersensivity
  3. B-cell activation
63
Q

T cell exhaustion

A

when t cells see antigen too often –> get shut down, exhausted (e.g. in cancer)

64
Q

Why is immune regulation important?

A

Prevent response against self

avoid excessive lymphocyte activation

avoid tissue damage

65
Q

Distinguish between active and passive immune regulation

A

Passive: removing the pathogen –> no initiation of response

Active –> tolerance

66
Q

List and explain different principles of immunonological tolerance

A

Anergy : co-stimmulation missing

Ignorance: Antigen concentratin too low, no APC im tissue (e.g. eye)

Antigen induced cell death: Antigen causes T cell apostosis

Regulation: regulatory T cells (Treg) produce IL10 (cytokine) which inhibits other immune cells

67
Q
A