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MOL3005 - Immunologi > Antibody and cell-mediated effector functions > Flashcards

Antibody and cell-mediated effector functions Flashcards

1
Q

CD4+ T helper (Th) cells

A

The key to adaptive immunity
- Must be activated by an antigen- presenting DC
- Activated CD4+ T cells activate many responses

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2
Q

CD8+ T cytotoxic (Tc) cells

A

Must be activated by an antigen-presenting DC
- Activated T cell KILLS the cell presenting the antigen (Ag)

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3
Q

B cells

A

Recognize antigen directly
- Need help from activated CD4+ T cell to optimize antibodies and for memory
- Activated B cells differentiates to a plasma cell that produces antibodies that recognize the same Ag as the BCR on the mother cell

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4
Q

Th cells

A

–>cytokines–>indirectly contribute to the activation of phagocytic cells, B cells and cytotoxic T cells Th1, Th2, Th17, TFH, (Treg)

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5
Q

Cytotoxic cells

A

–> directly attack infected cells and certain pathogens - CD8+ CTL
- NK cells
- NK T cells

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6
Q

Antibody-mediated immunity

A

Mediated by antibodies secreted
by plasma B cells

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7
Q

Ab

A

detect antigens from pathogens found in extracellular spaces and
clear infection by;
* Neutralization
* Agglutination
* Opsonization
* Complement activation
* Antibody-Dependent Cell-mediated Cytoxicity
* NK cells
* Antibody-mediated Degranulation and Mediator Release * Granulocytes

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8
Q

Effector T cells:

A

Activated CD4+ Th cells  Cytokines -> activate other cells Aktivert CD8+ Tc cells  Cytotoxins -> kill virus-infected cells

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9
Q

Cytokines

A

– signal proteins

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10
Q

Cytotoxins

A

– death proteins

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11
Q

Cytotoxic effector cells include three subsets

A
  1. Cytotoxic T Lymphocytes (CTL)s
  2. Natural Killer (NK) cells
  3. Natural Killer T (NKT) cells
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12
Q

apoptosis

A

is the process of programmed cell death. It is used during early development to eliminate unwanted cells; for example, those between the fingers of a developing hand. In adults, apoptosis is used to rid the body of cells that have been damaged beyond repair.

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13
Q

Precursor Cytotoxic T lymphocytes need to be activated by

A

CD4+ Th cells or licensed DC

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14
Q

Precursor (naïve) CTL

A

In order to be activated, a naive T cell must recognize a foreign peptide bound to a self MHC molecule. But this is not, on its own, sufficient for activation. That requires the simultaneous delivery of a co-stimulatory signal by a specialized antigen-presenting cell
-no high-affinity IL-2R, or IL-2 production
* No cytotoxic activity

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15
Q

Activated CTL

A

-Expres scytotoxins packaged into lytic granules
* UpregulateIL-2R
* ProduceIL-2(proliferation and differentiation)

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16
Q

Cross-presentation

A

allows presentation of exogenous antigens on MHCI and priming of CD8+ T cells

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17
Q

Dendritic cells (DC)s primary cross-presenting cell type

A

Exogenous antigens are redirected to the endogenous presentation pathway
– Allows presentation on MHC class I molecules, priming CD8+ T-cell responses
– Licensed DC are resistent to the cytotoxic effects of Tc.

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18
Q

Antigen presentation to T cells

A

All cells can present antigen from inside cytoplasm on MHCI
- Signals that the cell is infected or cancerous
- Aktivated CD8 T cells that recognize Ag will kill
cell

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19
Q

Professional antigen-presenting cells

A

Can take up Ag from outside cell and present on MHCII –Activate CD4+ Th cells
- Can activate T cells without being infected
- Dendritic cells (DCs) -naïve T cells –> activated
T cell
- Macrophage
- Bcell

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20
Q

Exception Cross-presentation

A

DCs kan present antigen from outside the cell on
MHCI to CD8 T cells without being infected and
without getting killed
-> activate CD8+ Tc cells

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21
Q

Cross presentation activates naïve CTL to become effector CTLs

A

Naïve Tc must be activated by APC to become effector Tc (CTL)
APC licensing Th1 express CD40L  binds CD40  CD80/86 up + cytokines
– CD4+ T cells are required for CD8+ T-cell memory and optimal expansion.

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22
Q

Signal 1

A

―TCR binds peptide on MHC classI on APC

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23
Q

Signal 2

A

―co-stimulatory signa lCD28-CD80/86
– APCs get help from Th1\Th17 cells to upregulate stimulation molecules

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24
Q

Signal 3

A

IL-2–>proliferation and differentiation into CTL form

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25
Q

Cross-presentation is important for CTL activation

A

Best CTL activation is achieved when the APC can present peptides on both types of MHC molecules in response to intracellular abnormality.
– Ex Ag + MHCIIActivates CD4+
– Int Ag + MHCIActivates CD8+
– Crosspresentation- presentation of Ex Ag on MHCI
* APC not necessarily infected.
* Cross-presentation allows DC to acquire antigens from non-APCs and present them on both types of MHC molecules

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26
Q

Effector CTLs recognize and kill infected or tumor cells via TCR activation

A

CTLs induce apoptosis (programmed cell death) in infected or malignant target cells by;
1. Directional release of granule contents
2. Fas-FasL interactions
– Ability to bind target cells well is critical
* Central ring of TCR surrounded by a peripheral ring of adhesion molecules
* Adhesion molecule LFA converted to a high affinity statebinds ICAM

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27
Q

Granzyme/perforin-mediated cytolysis

A

When stimulated, CTLs release granule contents
* Perforin is a 65 kDa pore-forming protein
* Granzymesareserineproteases
* Both taken up by endocytic processes,
* Perforin punch holes in the membranes and release GranzymeB
* Granzymes activates apoptotic pathways that lead to fragmention of target cell DNA
–>Induce apoptosis from the inside out

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28
Q

Granzyme/perforin-mediated cytolysis activates apoptotic pathways leading to apoptosis (Programmed cell death)

A
  • Cleaves Caspase 3–>Apoptosis
  • Proapoptotic BID–>Cytochrome c–>Caspase 9–>
    Caspase 3 –> Apoptosis
  • Need to activate both paths for optimal pro-apoptotic activity
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29
Q

Fas/FasL pathways

A
  • FasL expressed on CTLs
  • crosslinks Fas (CD95) on
    target
    FADD- delivers a death signal
    EXTRINSIC PATHWAY
    CTL
  • FADDCaspase 8 Caspase 3Apoptosis
  • BIDCytochrome c Caspase 9Caspase 3  Apoptosis
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30
Q

CTLs recognize and kill infected or tumor cells via TCR activation

A

CTLs activate dormant death pathways in target cell.
 “Persuade target cells to commit suicide”.

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31
Q

Two pathways:

A
  1. Perforin/granzyme pathways
  2. Fas/FasLpathways
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32
Q

Natural Killer (NK) cells

A

Make up 5–10% of circulating lymphocytes
– Lack specific Ag receptors (no TCR)
– Innate immune cells
– Help to regulate innate/adaptive immunity by cytokine secretion
– Recognize and destroy pathogen-infected cells and abnormal tumor cells
– Proliferate earlier in infection than CTLs

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33
Q

NK cells recognize

A

and kill infected cells and tumor cells by their absence of MHC class I

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34
Q

How NK cells recognize targets:

A

The missing self model

35
Q

Normal cells:

A

present a ligand for the activating (killing) receptor on NK cells AND
* a ligand for the inhibitory receptor (MHCI))
* MHCIexpressedon~nucleatedcells
* FailuretoexpressMHCInormallyactivatesNKcells
* Altered MHCI expression–>something is wrong with the cell–> triggers NK cells to kill the cell.
Viral infection, malignant cells

36
Q

Cell-mediated effector responses

A

How NK cells recognize target
– The balance of inhibitory vs activating signals determines whether NK is activated or not

37
Q

NK cell receptors

A
  • Inhibitory NK receptors and ligands
  • Activating NK receptors and ligands
    – Whether a cell is killed or not, depends on the BALANCE between inhibiting and activating signals the NK cell receives
38
Q

NK cells induce apoptosis of their targets

A

Once activating signal molecules are engaged, NK cells use mechanisms very similar to CTLs to induce target cell death

39
Q

NKT cells bridge innate/adaptive immune systems

A

ossess a TCR, but it is invariant (constant, doesn’t vary)
– This TCR recognizes glycolipids presented by nonpolymorphic CD1d
* Can act as helper cells (secreting cytokines) or killer cells – Killing seems dependent on Fas-FasL interactions
* Include both CD4+, CD4–. CD8+ and CD8- cell types
* Don’tformmemorycells
* Possess NK surface proteins rather than T-cell varieties

40
Q

NKT cells

A

May recognize lipid antigens specific to tumor cells
– Appear to play a role in viral immunity, although virus don’t usually express
glycolipids.
* May play an indirect role in shaping the viral immune response
* IFNg, IL-2, TNF and IL-4

41
Q

Cell-mediated immunity:

A

Comparison of ways effector cells of the immune system recognize their targets

42
Q

Antibody-mediated immunity

A

Immunity mediated by antibodies secreted by plasma B cells

43
Q

B cells

A

are part of the immune system and develop from stem cells in the bone marrow. Also called B lymphocyte. Enlarge. Blood cell development. A blood stem cell goes through several steps to become a red blood cell, platelet, or white blood cell.
B cells kan bind Ag directly, but need Th cells for memory
* B cells take opp and present Ag om MHCII to CD4+ Th cells that recognize the
same antigen in the lymphnode
* Some B cells produce IgM Ab quickly in primary foci
* Other B cells form germinal centers and go through somatic hyper mutation (SHM)
and Class switch recombination (CSR) and compete for survival signals from Th
Antigen binding site
Antibody/Immunoglobulin («soluble BCR»)
cells
* B cells that bind Ag best
–> plasma cells that produce Ab –> memory B cells

44
Q

Two types of B-cell responses elicited by distinct Ag types

A

T-dependent (TD) and T-independent (TI)

45
Q

T-dependent (TD)

A

responses require help from T cells * Are typically generated upon recognition of protein Ag

46
Q

T-independent (TI)

A

responses do not require T-cell help
* Generated upon exposure to multivalent/polymerized Ag
– TI-1 Ag bind to B cells through PRRs and mIgs
– TI-2 Ag cross-link BCRs

47
Q

Effects of antibodies

A

Antibodies promote removal and destruction of pathogens in several ways
* Effector function is determined by antibody isotype, FC receptor and which cell expressed the given FC receptor

48
Q

Neutralization:

A

protects against viral or bacteria infection or the damaging effects of toxins

49
Q

Agglutination

A

enhances neutralization and more efficient clearance of pathogens from the body

50
Q

Opsonization

A

promotes and/or enhances the engulfment of antigens by phagocytes.

51
Q

Complement Activation:

A

results in the generation of the membrane attack complex (MAC), creating pores in pathogen membranes and killing the microbe

52
Q

Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)

A

activates the killing activity of several types of cytotoxic cells, e.g., NK cells

53
Q

Antibody-Dependent Degranulation and Mediator Release:

A

triggers mediator release from granulocytes

54
Q

IgM

A

First Ab produced in a primary response
– Tend to be lower affinity
– Pentavalent (10 total Ag binding sites)
– Very good at complement fixation leading to MAC formation and target lysis
– Also efficient at forming dense Ab-pathogen complexes that are efficiently engulfed by macrophage (agglutination)

55
Q

IgGs

A

Include several subclasses, each with distinct effector
capabilities
– Human IgG1/IgG3 effective at complement fixation
– Human IgG1 (Mouse IgG2a) mediates ADCC by NK cells
* All variants bind to FC receptors, enhancing phagocytosis by macrophages (opsonization)

56
Q

IgA

A
  • Majorisotypefoundinsecretions
    – Mucus in gut
    – Milk from mammary glands – Tears
    – Saliva
  • Effective at neutralizing toxins and pathogens
  • Protects epithelial surfaces from infectious agents
  • Does not fix complement, so does not drive inflammation
  • Long half-life in secretions due to protease-resistant amino acid sequence in Fc region
  • IgA1 monomer  serum
  • IgA2 dimer  secretions
  • MediatesADCC
  • Triggers degranulation of granulocytes
57
Q

IgE

A

Best known for role in allergy and asthma
* May also play a role in protection against parasitic helminths (worms) and protozoa
* Made in very small quantities, but induce potent effects
– Degranulation of eosinophils/basophils
– Release of molecules such as histamine from mast cells to damage large pathogens

58
Q

Antibody isotypes bind different Fc receptors

A

FcγRs–>IgG
- FcαR–>IgA
- FcεR–>IgE
- pIgR –Polymeric Ig Receptor –> IgM and IgA
- FcRn –Neonatal Fc Receptor –> IgG and Albumin

59
Q

Ab-binding can activate FC receptors on effector cells

A

Fc region of Ab’s – bind Fc receptors expressed by accessory cells an trigger;
– Phagocytosis of Ab-bound extracellular pathogens (Macs, DC,Neutrophils) – Secretion of stored mediators (NK cells, Eosinophils, Basophils and Mast
cells)
–>Destruction of Ab-coated pathogens

60
Q

FcR signaling

A

Multiple FcRs need to be cross-linked to initiate a signal

61
Q

FcR signaling positive

A

enhancing effector function

62
Q

FcR signaling negative

A

inhibiting effector function

63
Q

ITAM/ITIM

A

(Immunereceptor Tyrosine-based Activating/Inhibitory Motifs)

64
Q

FcγRs –> IgG

A

Most are activating receptors (three activating, one inhibiting family)
– Will induce phagocytosis if expressed by macrophages
– Will induce degranulation if expressed by cytotoxic cells

65
Q

FcαR –> IgA

A

Expressedbymyeloidcells
– Monocytes/macrophages – Granulocytes
– Dendritic cells
* triggersphagocytosis
* MediatesADCC
*Stimulates myeloid cells to release inflammatory cytokines and generate superoxide free radicals to help kill internalized pathogens

66
Q

FcεR –> IgE

A

Expressedby
– Mast cells/basophils
– Eosinophils
* Twotypes
– High-affinity FcεRI
– Low-affinity FcεRII (on B cells and eosinophils)
* Triggers a signaling cascade that releases histamines, proteases, and other inflammatory mediators
* Most often associated with allergy symptoms
* Defendsagainstparasiticworms

67
Q

pIgR

A

Polymeric immunoglobulin receptor
* Expressedbyepithelialcells
* Initiates transport of IgA and IgM from blood to the lumen of multiple tissues
– Gastrointestinal tract
– Respiratory tract
– Reproductive tract
* Responsible for carrying Ab into tears and milk
* populates gut mucosa with IgA Ab to protect against ingested microbes and toxins

68
Q

FcRn

A
  • Neonatal Fc receptor
  • Related to MHC class I
  • Expressed on many different cell types early in an organism’s lifespan
    – Epithelial/endothelial cells
  • Helps to carry Ab ingested in milk in newborn across epithelial cells of the intestine into the bloodstream
  • In adults, can help recycle IgG taken up through endothelial cell pinocytosis processes back into blood
69
Q

High affinity IgG and IgA can inhibit the infectivity of viruses

A

Viruses infect cells by binding to a particular cell-surface receptor
- Ex Hemagglutinin of influenza virus
–> binds terminal sialic acid residues on glycoproteins on epithelial cells of the respiratory tract
–>Ab against hemagglutinin prevent infection

70
Q

adhesins

A

are virulence factors that allow bacteria to attach to host cells. Although many pathogenic bacteria express various kinds of adhesins, often they are encoded on the bacterial backbone DNA (such as S fimbriae and Type 1 fimbriae expressed by E.
Ab binding of adhesins blocks bacteria entry into the cell.

71
Q

Agglutination

A

Agglutination, which refers to the clumping of particles together, is an antigen-antibody reaction that occurs when an antigen (i.e., a molecule capable of triggering the adaptive immune response) is mixed with its corresponding antibody at a suitable pH and temperature.
enhances neutralization and more efficient clearance of pathogens from the body
Impairs uptake of antigen into cells (large complexes can’t be taken up)

72
Q

Ab-coated pathogens are recognized

A

by effector cells through Fc receptors that bind to Fc portion of Ab.

73
Q

Opsonization

A

«To prepare for eating»
- Involves the coating of the surface of a pathogen by antibody and/or
complement C3b, making it more easily ingested by phagocytes

74
Q

Fc receptors activate macrophages

A

to engulf and degrade (phagocytose) antibody-coated bacteria
- Antibodies must be aggregated on a surface to cross-link Fc receptors and activate phagocytes
- Free Ig bind Fc receptors with low affinity (control mechanism).

75
Q

Fc-dependent pathogen destruction by triggering granule release

A

Ab can target effector cells to release granule contents.
* Effector cells express Fc receptors that bind Ab  crosslinking
induces activation of effector cells.
* Fc-dependent pathways for destruction by granule release include;
* Mast cell and basophil activation
* Antibody-Dependent Cell-mediated Cytotoxity (ADCC)
* NK cells
* Eosinophils ++)

76
Q

Mast cells

A

Defend against pathogens that penetrate the epithelial barriers.
The high affinity receptor for IgE is expressed constitutively by mast cells and basophils.
Can bind free monomeric IgE

77
Q

IgE bound to the surface of mast cells is
aggregated by binding to antigen

A

histamine and many other mediators
 increased blood flow to the site of infection
 recruits Ab and effector cells
 coughing, sneezing, rhinitis, vomiting

78
Q

Fc receptors on Eosinophils bind Ab-coated parasites

A

Defence against large parasites such as helminths that are too large to be phagocytosed.
* Eosinophil binds IgE-coated parasite through Fc receptors triggers the release of secretory granules containing anti- parasitic toxins by exocytosis.

79
Q

Antibody-Dependent Cell-mediated Cytotoxicity

A

A type of immune reaction in which a target cell or microbe is coated with antibodies and killed by certain types of white blood cells. The white blood cells bind to the antibodies and release substances that kill the target cells or microbes. Also called ADCC and antibody-dependent cellular cytotoxicity.
-The killing of Ab-coated target cells by cells with Fc receptors that
recognize the constant region of the bound antibody.
* ADCC is generally mediated by NK cells
NK cells express FcγRIII/CD16 and recognize bound Ab (IgG1/IgG3) on
virus-infected host cells

80
Q

Negative regulation of B cells

A

Shutting down B cell receptor (BCR) signaling when
proliferation is no longer required

81
Q

Negative signaling through FcγRIIb receptor inhibits B-cell activation

A

– Possesses ITIMs
– Antibodies bind antigens efficiently and are normally not in high concentrations in circulation as long as Ag is present.
– When Ag is no longer presentExcess circulating IgG can bind this receptor and shut down B-cell activation
– Phosphatases are recruited to phosphorylated ITIMS, stripping phosphates from signaling molecules

82
Q

antibody isotypes

A

antibodies are classified into five main classes or isotypes – IgA, IgD, IgE, IgG and IgM. They are classed according to the heavy chain they contain – alpha, delta, epsilon, gamma or mu respectively.

83
Q

Describe two ways by which antibodies can induce effector responses that promote phagocytosis.

A

Another mechanism by which antibodies can response to pathogens is known as “opsonization.” By opsonization, antibodies enable phagocytes for ingesting and destroying the extracellular bacterium. The phagocytes recognize the Fc region of the antibodies coating the pathogen and foreign particles (Fig.

84
Q

What is antigen presentation?

A

Antigen presentation, activation of both CD4+ cells (such as TH1 and TH17s) and CD8+ T cells, increases in the inflammatory cytokines, IL-6, IL-12, TNFα, and IFNγ, and NFκB activation, in addition to decreased pro-apoptotic proteins such as caspase 8 and 10, lead to enhanced immune cell survival and activation of pro-inflammatory mechanisms

MOL3005 - Immunologi (13 decks)

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