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PoM > Immunology - Immune Response to Infection > Flashcards

Immunology - Immune Response to Infection Flashcards

1
Q

Phagocytes

A

Internalize pathogens and degrade them

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2
Q

Lymphocytes (B and T cells)

A

Have receptors that recognize specific molecular components of pathogens and have specialized functions

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3
Q

B cells

A

make antibodies (effective against extracellular pathogens)

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4
Q

Cytotoxic T lymphocytes (CTLs)

A

kill virally infected cells

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5
Q

Helper T cells

A

coordinate the immune response by direct cell-cell interactions and the release of cytokines

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6
Q

Cell + soluble mediator - leukocytes (lymphocytes)

A

B cell -> antibodies

T-cell + large granular lymphocyte (LGL) -> cytokines

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7
Q

Cell + soluble mediator - leukocytes (phagocytes)

A

mononuclear phagocyte -> complement and cytokines
neutrophil
eosinophil

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8
Q

Cell + soluble mediator - leukocytes (auxiliary cells)

A

basophil -> inflammatory mediators

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9
Q

Cell + soluble mediator - auxiliary cells

A

mast cells + platelets -> inflammatory mediators

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10
Q

Cell + soluble mediator - other cells

A

tissue cells -> interferons + cytokines

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11
Q

Specificity and memory

A

Essential feature of adaptive immune responses, B&T lymphocytes mount a more effective response on second and subsequent encounters with a particular antigen, non-adaptive (innate) immune responses (mediated for example by complement, phagocytes, and NK cells) do not alter on repeated exposure to infectious agent

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12
Q

Antigens

A

molecules that are recognized by receptors on lymphocytes

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13
Q

B cells antigen recognition

A

usually intact antigen molecules

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14
Q

T cells antigen recognition

A

antigen fragments displayed on the surface of dendritic cells

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15
Q

Immune response 2 phases

A

antigen recognition and antigen eradication

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16
Q

Antigen recognition

A

clonal selection involves recognition of antigen by particular clones of lymphocytes leading to clonal expansion of specific clones of T and B cells and differentiation to effector and memory cells

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17
Q

Antigen eradication

A

effector phase, specific T and B cells coordinate an immune response which eliminates the antigen source

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18
Q

Pathogen niches during infection

A

extracellular (ie staphylococccus, streptococcus, candida, microbiota, worms), intracellular vacuolar (ie salmonella, chlamydia, legionella, coxiella, plasmodium), surface adherent (ie enteropathogenic and enterohaemorrhagic E. coli), intracellular cytosolic (ie viruses, listeria, burkholderia, mycobacterium)

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19
Q

How does an immune response to infection start?

A

tissue damage (ie injury), molecular detection of microbes, inter-cellular communication (ie interleukins), priming the adaptive immune response

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20
Q

How does an immune response to an infection end?

A

Clearing infection, stopping inflammatory cytokine production, repairing tissue damage, immune memory

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21
Q

Innate immunity - general

A

Fast acting, first line of defence, germline encoded receptors

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22
Q

Innate immunity - physical barriers

A

Skin, mucous, epithelial cells

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23
Q

Innate immunity - humoral

A

complement, lectins (collectins, ficolins, detect carbohydrates), pentraxins, antimicrobial peptides

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24
Q

Innate immunity - cellular

A

neutrophils, macrophages, dendritic cells, NK cells

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25
Q

Adaptive immunity - general

A

slower but long-lasting, variable receptors that mature over time (DNA recombination)

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26
Q

Adaptive immunity - humoral

A

antibodies (immunoglobulins of various types), complement

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27
Q

Adaptive immunity - cellular

A

cytotoxic T-cells, T helper cells, T regulatory cells, B lymphocytes and plasma cells

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28
Q

Specificity - Innate vs Adaptive Immunity

A

INNATE: for structures shared by classes of microbes (Pathogen Associated Molecular Patterns), identical toll-like receptors
ADAPTIVE: for structural detail of microbial molecules (antigens), may recognize non-microbial antigens, distinct antigen-specific antibodies

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29
Q

Number of microbial molecules recognized - Innate vs Adaptive Immunity

A

INNATE: about 1000 PAMPs (Pathogen Associated Molecular Patterns)
ADAPTIVE: > 10^7 antigens

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30
Q

Receptors - Innate vs Adaptive Immunity

A

INNATE: encoded in germline = limited diversity (pattern recognition receptors; toll-like receptors, N-Formyl methionyl receptor, mannose receptor, scavenger receptor)
ADAPTIVE: encoded by genes produced by somatic recombination of gene segments = greater diversity (Ig (immunoglobulin), TCR (T-cell receptor))

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31
Q

Number and types of receptors - Innate vs Adaptive Immunity

A

INNATE: <100 different types of invariant receptor
ADAPTIVE: only 2 types of receptors (Ig and TCR) with millions of variants of each

32
Q

Distribution of receptors - Innate vs Adaptive Immunity

A

INNATE: nonclonal (identical receptors on all cells of same lineage)
ADAPTIVE: clonal (clones of lymphocytes with distinct specificities express different receptors)

33
Q

General differences - Innate vs Adaptive Immunity

A

response timing, cell types, receptors and ligands, cytokines and chemokines, molecular effector machineries

34
Q

Common aspects - Innate vs Adaptive Immunity

A

Together provide sterilizing immunity and long-term immunity

35
Q

Immune response mechanism

A
  • Microbial molecules — detection by ligands or activities—> naïve host cells (T-cells, undergo fine-tuning by dendritic cells (DC) into CD4/CD8) —gene expression changes—> antimicrobial molecules communication signals (interleukins, chemokines, interferons…) —signal transduction—> activated host cells (fight and tell others)
  • general principle: sequence of molecular and cellular events and crosstalk
36
Q

First responders: neutrophils

A

Short-lived (~6hrs), followed by macrophages, naïve cells become activated upon interaction with microbes

37
Q

First responders: phagocytes

A

Control infection and limit/repair tissue damage, uncontrolled activity = granulomas, excessive inflammation and inappropriate adaptive immunity, tissue damage

38
Q

Pathogen-specific phagocyte responses: bacteria

A

PHAGOCYTOSIS OF LIVE BACTERIA: bacterial mRNA released resulting in immune response (inflammatory cytokines, mature IL-1ß released, antimicrobial genes, metabolic genes, immunomodulatory genes)
PHAGOCYTOSIS OF DEAD BACTERIA: no bacterial mRNA released, so no immune response and resolution of inflammation

39
Q

Pathogen-specific phagocyte responses: fungi

A

Clustering of dentin 1, exclusion of phosphatases, phagocytosis and production of pro-inflammatory cytokines and reactive oxygen species, antimicrobial + metabolic + immunomodulatory genes

40
Q

Pathogen-specific phagocyte responses: viruses

A

Entry, uncoating, reverse transcription (RNA, ssDNA, dsDNA), interferon production, pro inflammatory citokines, antiviral genes, immunomodulatory genes

41
Q

Phagocyte activation and pathogen killing

A

Macrophages are tissue resident or circulatory (recruited from the bone-marrow), macrophage activation = expression of new genes induced by microbes and cytokines, activated macrophages exhibit enhanced phagocytosis and migration + cytokine/chemokine production + expression of cell surface molexules + antimicrobial activity + antigen presentation and T cell activation

42
Q

Crosstalk between macrophages and lymphocytes during infection by intracellular pathogens

A

FROM MACROPHAGES TO LYMPHOCYTES: IL -12 + -18 + -1 + -6 and TNF (tumor necrosis factor)
OTHER WAY: interferon IFN-γ
RESULT: killing of phagocytosed microbes

43
Q

Interferons - general

A

special cytokines that promote antiviral defence, antiviral genes include nucleases + inhibitors of virus entry and exit & viral uncoating and replication & protein translation, immunomodulatory roles enhanced T-cell responses + anti-inflammatory actions + tissue repair

44
Q

Interferons - mode of action

A

Detection of viruses/gram negative bacteria -> interferon (IFN) production and transcription of antimicrobial genes
IFN-γ -> antibacterial, antiprotozoal and antiviral host defence programmes (Signal transducer and activator of transcription 1 & 2 bind to GMP-AMP synthase on DNA)
IFN-α/ß -> antibacterial and antiviral host defence programmes (Signal transducer and activator of transcription 1 & 2 bind to Interferon regulatory factor 9 which binds to interferon stimulated response element on DNA)

45
Q

Death of infected cells

A

virus infected cells are killed by the action of cytotoxic T lymphocytes, cell death removes viral replicative niches, CTLs (cytotoxic T lymphocytes) and NK cells directly kill infected cells (contact-dependent), host cells infected with intracellular bacterial pathogens also undergo forms of cell death (contact-dependent)

46
Q

Humoral innate immunity and cell activation - soluble effector mechanisms

A

Complement mediated bacterial destruction, lectin-binding to neutralize cell attachment or entry, iron chelation (siderophores) to prevent replication, antibiotic-like peptides

47
Q

Humoral innate immunity and cell activation - cellular effector mechanisms

A

reactive oxygen and nitrogen radicals, acidification and digestion within phagosomes

48
Q

Humoral innate immunity and cell activation - microbe

A

Toll-like receptor -> cytokines (TNF, IL-1, IL-6, IL-12) -> inflammation, enhanced adaptive immunity

49
Q

Humoral innate immunity and cell activation - cytokine

A

Cytokine receptor -> phagocyte oxidase -> reactive oxygen species (ROS) -> killing of microbes

50
Q

Humoral innate immunity and cell activation - complement fragment

A

Complement receptor then:

  • > Inducible nitric oxide synthase -> nitric oxide -> killing of microbes
  • > phagocytosis of microbe into phagosome -> killing of microbes
51
Q

DCs and macrophages can activate T cells

A

activated macrophages and DCs present antigens in combination with major histocompatibility complex MHC-I or MHC-II to T cells, cytokines produced by antigen-presenting cells produce a suitable milieu for T-cell activation (ie IL-12 promotes T-cell replication, TNF), T cells provide cytokines that activate phagocytes (ie IFN-γ upregulates MHC-II expression for antigen presentation, IL-17), responses are specific to general class of pathogens

52
Q

T cells help B cells produce antibodies

A

Antigen presenting cells (ie DCs and macrophages) are activated by infection and cytokines, helper T cells are activated by cognate MHC and foreign peptide recognition, B cells become licensed for antibody production against antigen being presented on the B cell receptor (BCR) with T cell help, antibody-mediated enhanced antimicrobial response (phagocytosis (opsonization), complement activation)

53
Q

Timing of cellular immune response

A

Innate immunity (epithelial barriers, mast cells, phagocytes, dendritic cells, complement, NK cells and innate lymphoid cells; 0-12 hrs after infection) -> adaptive immunity (B-lymphocytes-> plasma cells producing antibodies, T-lymphocytes -> effector T cells; hr 12 - day 5)

54
Q

Timing of antibody response

A

primary -> less strong, slower; naive b-cells -> plasma cells -> memory B cells

55
Q

Thymic output as age increases

A

Decreases; more memory T cells than naive T cells after 30

56
Q

Innate and adaptive immune responses are specific to…

A

the broad classes of pathogens and their virulence strategies

57
Q

Viruses (Type 1 immunity)

A

Sensor: Batf3-dependent CD141+ (cluster of differentiation antigens) -> PRR (pattern recognition receptors): RLR, TLR3, CDS, NLR, AIM2 -> cytokines: type I, IL-6, IL-1ß -> lymphocyte differentiation: cytotoxic T lymphocyte (CTL)

58
Q

Bacteria and protozoa (type 1 immunity)

A

Sensor: Batf3-dependent CD207+ CD103+ DCs -> (pattern recognition receptors): TLR, NLR -> cytokines: IL-12, IL-6, IL-1ß -> lymphocyte differentiation: T_H_1 cell

59
Q

Bacteria and Fungi (type 1 immunity)

A

Sensor: CD1c+ CD11b+ -> PRR (pattern recognition receptors): Dectins, TLR, NLR -> cytokines: IL-23, IL-6, IL-1ß, TGF-ß -> lymphocyte differentiation: T_H_17 cell

60
Q

Helminth, allergens and venoms (type 2 immunity)

A

Sensor: langerhans cells -> lymphocyte differentiation: T_H_2 cell

61
Q

Genetic immunodeficiency - complement defect (1), leukocyte adhesion (2), chronic granulomatous disease (3)

A

(1): various complement genes involved, (2): genes involved in migration and adhesion, (3): loss of reactive oxygen species production

62
Q

Genetic immunodeficiency - Chédiak-Higashi syndrome (1), cytokine genes and their receptors (2), severe combined immunodeficiency (SCID, 3), X-linked agammaglobulinaemia (4)

A

(1): compromised lysosomes, (2): loss of cell-to-cell communication, (3): severe reduction of function of T and B cells, (4): decreased serum IgG of all types

63
Q

Acquired immunodeficiency - HIV (1), irradiation and chemotherapy (cancer treatment, 2), immunosuppression (graft rejection/chronic disease 3)

A

(1): reduced CD4T helper cells, (2): loss of bone marrow precursors, (3): depletion or impairment of lymphocytes

64
Q

First cell types that arrive at infection site

A

neutrophils and macrophages

65
Q

C5 complement cascade

A

C3b-Bb-C3b complex, C5 convertase acts on C5 on it, release of C5a = inflammation, C5b remains on complex, C6 and C7 bind to C5b, C8 binds to C6 and C7, C9 binds forming poly-C9 = cell lysis

66
Q

Against which class of pathogens are interferons active

A

Viruses and intracellular bacterial pathogens

67
Q

How do cytotoxic T-cells promote immunity against viruses?

A

killing virus infected cells

68
Q

Macrophage activation

A

expression of host-defence genes after detecting microbes and cytokines

69
Q

Main characteristic of macrophages

A

Capable of ingesting and killing pathogens

70
Q

Principal function of the immune system

A

Defence against microbial infections

71
Q

Cytokine - type of response

A

IFNg - Th1 immunity
IL-4/-5/-13 - Th2 immunity
IL-17/-22 - Th17 immunity

72
Q

T cell mechanisms

A
  • Th1 cell (CD4T cell) binds to antibody presenting cell (APC) with intracellular bacteria, releasing cytokines and causing inflammation + phagocytosis + killing of microbes
  • Cytotoxic T cell (CD8T cell) binds to antibody presenting cell (APC) with intracellular virus causing the killing of infected cell
73
Q

Broad classification of T cell functions

A

Phagocyte activation (enhanced killing of pathogens, inflammation), direct killing of infected cells (removal of replicative niches), B cell activation (antibody production and affinity maturation), innate lymphoid cells/γδ T cells (early responders, MHC independent actions)

74
Q

Microbe-specific phagocyte responses induce the appropriate lymphocyte phase

A
  • Effector T cells: Th1, defining cytokines: IFN-γ, principal target cells: macrophages, major immune reactions: macrophage activation, host defense: intracellular pathogens, role in disease: autoimmunity + chronic inflammation
  • Effector T cells: Th2, defining cytokines: IL-4/-5/-13, principal target cells: eosinophils, major immune reactions: eosinophil and mast cell activation + alternative macrophage activation, host defense: helminths, role in disease: allergy
  • Effector T cells: Th17, defining cytokines: IL-17/-22, principal target cells: neutrophils, major immune reactions: neutrophil recruitment and activation, host defense: extracellular bacteria and fungi, role in disease: autoimmunity + inflammation
75
Q

Sequence of the immune response

A

sequential change from resting/naive to activated state through antigen recognition + proliferation + differentiation, driven by gene expression changes driven by specific cytokine combinations (naive to activated macrophage), differentiation of precursor cells into specific cell lineages

PoM (33 decks)

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