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immuno Flashcards

1
Q

common techniques used in immunology

A

ELISA : enzyme-linked immunosorbent assay -> measures antibodies, antigens, proteins and glycoproteins in samples
eg anti- AChR ELISA test: myasthenia gravis diagnosis

flow cytometry: analyse cells in blood

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2
Q

hematopoiesis

A

formation of blood cellular components

  • hematopoietic stem cells are pluripotent and give rise to 2 cell lines

lymphoid: T cell, B cell, NK cell
myeloid: monocyte (fight pathogens), macrophage, basophil , neutrophil, eosinophil

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3
Q

lymphoid organs

A

primary: bone marrow and thymus (sites of B and T cell maturation)

secondary: spleen, lymph nodes, peyer’s patches in small intestine and mucosa-associated lymphoid tissue (MALT) in submucosal membrane sites

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4
Q

neutrophil

A

most abundant WBC, first to reach site of infection, high count indicates bacterial infection

express TLR 1,2,4,5

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5
Q

basophil

A

increase histamine release as part of inflammatory response

basophil circulating in blood while mast cells at tissues

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6
Q

eosinophil

A

increase allergy reaction and anti-parasitic activity

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7
Q

monocytes

A

in blood: blood monocyte
in tissue: tissue macrophage

  • produce cytokines to initiate and regulate inflammation
  • phagocytosis
  • clear dead tissue
  • tissue repair
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8
Q

natural killer cell

A

anti-viral defence -> contain granules with perforin, granzymes and granulysin

non specific cytotoxic killing of pathogens
- to protect healthy cells, NK cell shuts off when inhibitory receptors on NK encounter self MHC

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9
Q

NK cell + macrophage

A

macrophage ingest microbe + secrete IL-12 -> NK cell activated by IL-12 -> NK secrete IFN-gamma -> macrophagte activated to become more effective at killing -> cytokines IL-12, 15, IFN-gamma secreted by macrophage and DC enhance effects of NK cell

(similar process as T cell and macrophage)

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10
Q

surface barriers

A

physcial: skin, mucosa, bronchial cilia

physiological: diarrhoea, cough, sneeze, etc

chemical: low pH (prevent pathogen growth) eg skin, gastric acid, vagina
innate antimicrobial molecules eg IgA, defensins, complements

biological: normal flora

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11
Q

innate immunity

A

provides a rapid, non-specific response against pathogens but does not confer long-lasting immunity

triggered by PAMPs and DAMPs

3 main innate immune cells: dendritic cell, macrophage, neutrophils

key molecules involved in innate immunity: complement proteins, lysosomes, type 1 interferons, defensins

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12
Q

PAMPs and DAMPs

A

recognised by toll-like receptors expressed by innate immune cells

binding to TLR induces signal transduction pathway and triggers pro-inflammation cascade with cytokine production and proliferation (TNF and IL1) which bring leukocytes and plasma proteins to site of infection by binding them to endothelial adhesion molecules

PAMPs: conserved molecular patterns shared by broad classes of pathogens

detected by:
bacteria -> TLR 2,4,5
RNA -> TLR 3,7,8
DNA -> TLR 3,9

DAMPs: originate from host and signals released from damaged tissues

detected by: TLR 4

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13
Q

key molecules in innate immunity

A

defensins: antibiotic peptides found in tears, sweat and saliva and adheres to bacterial surface to induce osmotic lysis through pore formation

type 1 interferons: produced in response to viral infections and interferes with viral replication, activate NK cell and increase MHC I expression
IFN-a: dc, macrophage
IFN-b: fibroblast

lysosymes: digestive enzymes secreted in tears and saliva that digest cell wall

complement system

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13
Q

complement system

A

complement proteins mainly synthesised by liver and found circulating in blood

classical activation pathway: binding of IgM/G with antigen to C1

  1. C3 splits into C3a, C3b and C5
  2. C3a cause mast cells to release histamine for inflammation to bring leukocytes to site of complement activation
  3. C3b binds to extracellular microbe, resulting in opsonisation (opsonised with complement proteins)
  4. C3b splits C5 into C5a and C5b
  5. C5a cause mast cells to release histamine for inflammation to recruit immune cells with opsosin receptor to recognise opsosin in microbe
  6. C5b binds to C6-9 to form membrane attack complex which causes inflow of extracellular fluid and cause microbe to lyse
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14
Q

Major histocompatibility complex (MHC)

A

MHC I (intracelluar + all nucleated cells)
1. ubiquitin bind to misfolded host and viral proteins and protease cleave to peptides
2. MHC complex formed in ER
3. TAP transporter complex pumps peptide into ER to form peptide:MHC complex via chaperone
4. peptide:MHC complex transported to golgi apparatus and expressed on cell surface membrane

interact with cytotocis CD8 T cell

MHC II (extracellular + professional APC -> monocyte, macrophage, DC, B cells)
1. MHC class II form in ER and folds around chaperone, invariant chain Li to prevent peptides in the ER from binding to MHC
2. phagosome fuse with lysosome to form phagolysosome and microbe is cleaved
3. invariant chain-MHC class II transported to endocytic pathway and invariant chain processed into CLIP peptide
3. peptide with higher binding affinity to MHC class II will replace CLIP to form stable peptide MHC complex

interact with CD4 helper T cell

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15
Q

naive T cell migration to lymph node

A

APC express CCR7 which causes it to be drawn to the lymph node T cell zone for presentation to the T cell. Binding of CCR7 to CCL 19 and 2 at lymph node induced chemotaxis (directed movement of cells along a chemical gradient) -> naive T cells sense chemokine gradient and migrate towards source of CCL 19 and 21

in presence of APC, L selectin on T cell binds to L selectin receptor on high endothelial venule (weak binding). CCR7 sends downstream expression LFA receptor which binds to ICAM on APC and HEV (weak binding)

Upon binding of TCR to peptide:MHC complex, conformational change of LFA-1 to bind with greater affinity to ICAM-1.

There is simultaneous suppression of S1P receptor to keep T cell within lymph node

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16
Q

activated T cell migration to site of injury

A

within low S1P environment in the lymph node, T cell express more S1P receptors to push the T cell out of the S1P poor lymph node to the blood which is S1P rich and to the site of infection

activated T cell express E/P selectin ligand which binds to the E-/P- selectin receptor at the infection site

activated T cell express receptor LFA-1/VLA-4 which binds to ICAM-1/VCAM-1

17
Q

T cell activation

A

requires 2 signals

1st signal: initial interaction
TCR binding to peptide:MHC complex which is mediated by LFA-1

2nd signal: co-stimulation
CD28 on T cell binds to B7-1/B7-2 proteins on APC (microbes stimulate expression of B7 on APC -> ensuring T cells are only activated by foreign antigens

18
Q

T cell differentiation

A

activated T cells synthesise IL-2 and high affinity IL-2 receptor. IL-2 binding to receptor serves as signal for T cell to enter cell cycle and triggers T cell clonal expansion.

resting T cells: only moderate affinity IL-2R ( 2 subunits: by)
activated T cells: high affinity IL-2R, IL-2 (3 subunits: aby)

19
Q

immune tolerance

A

immunity: triggered during infection in response to antigens derived from pathogens

tolerance: tolerance to self antigens to prevent autoimmune conditions

immune tolerance divided into
- central tolerance: immature lymphocytes undergo selection in primary lymphoid organs (early development of B and T cell maturation)

  • peripheral tolerance: mature lymphocytes undergo selection in periphery after leaving primary lymphoid organs (deletion of autoreactive B and T cells to prevent autoimmunity)
20
Q

central tolerance (T cells)

A
  1. positive selection
    location: cortex of thymus
    ensure production of functional T cells
  • test if TCR bind appropriately to MHC, just enough to elicit immune response (if bind too strongly/weakly, apoptosis)
  1. negative selection
    location: medulla of thymus
    ensure no self-reacting T cells
  • test if TCR bind to tissue-restricted self antigens presented on MHC by thymic medullary cells
  • T cells that dont bind receive survival signals while those that bind undergo apoptosis except regulatory T cells
  • mediated by autoimmune regulator protein (AIRE)
21
Q

4 mechanisms of peripheral tolerance

A
  1. ignorance -> interaction between TCR and self-peptide MHC too weal so antigen recognition
  2. anergy -> no costimulatory signal -> inactivation of T cell
    cause:
    - immature DC =>express low levels of costimulatory molecules
    - non-APC => present peptide MHC I complex but does not express/express low levels of costimulatory molecules
  3. deletion -> mature T cells that recognise self antigens undergo apoptosis
    major pathways
    - mitochondrial pathway => regulated by members of bcl-2 family
    - death receptor pathway => mediated by Fas-Fas ligand signalling
  4. regulation -> Tregs inhibit immune response
    mechanism: posses TCR that recognise self peptide-self MHC strongly and act on self-reactive immune cells to suppress activity

eg CD4 + CD25+ T cells express transcription factor Foxp3 (constitutive expression of CTLA4, secreting inhibitory cytokines)

22
Q

T cell immune checkpoints

A

serve as immune checkpoint by
1. limit T cell mediated tissue damage during chronic infection
2. inhibit autoreactive T cell

CTLA-4
mechansim: cross linking of CD28 to B7-1/B7-2 -> upregulate CTLA-4 expression-> CTLA-4 bind with greater affinity to B7 -> transduction of negative signal -> T cell inactivation

ensure T cell not activated all the time
also constitutively expressed by Tregs

Programmed cell death protein 1 (PD-1)
- expressed by T cells and bind to PD-L1 on APC to inhibit T cell proliferation
- negatively regulates T cell function during chronic antigen stimulation

23
Q

CD4 T cell subsets

A

Th1: CD40 ligand and IFN-y activate M1 macrophages
- CD 40 ligand binds to CD 40 receptor on macrophage and activated macrophage becomes highly microbicidal
- CD 40 ligand binds to CD 40 receptor on B cell to stimulate CD 8 T cells
- secrete IFN-y to inhibit Th2 growth

Th2: IL-4,5,13
- 4,13: act on B cells to stimulate M2 (tissue repair, fibrosis) and stimulate IgE production
- 5: act on eosinophil to kill helmiths
- secrete TGF-b and IL-10 to inhibit Th1 growth

Th17
- IL-17: inflammatory cytokines for chemokine production -> recruit neutrophils to site of inflammation
- IL-22: main GIT barrier integrity

Tfh (T follicular helper cells)
- produce Th2 cytokines for B cell activation and maturation

24
Q

cytotoxic T cells

A

effector molecules in granules
- perforin: form pore in cell membrane of infected cell
- granzymes: a type of serine protease which activates apoptosis
- granulysin: induce apoptosis

  • binding of FasL on CTL to FAS on target triggers apoptosis

process
- presentation of antigen to CD8 T cell -> migration of specific cytotoxic T cell to site which carries out killing

25
Q

types of cytokines

A

IL-1: fever, inflammation
2: IFN-gamma production, Th1 differentiation
IFN-gamma: activation of macrophage
10: inhibition of IL-12 production (reduce expression of costimulators and MHC II)

26
Q

memory T cells

A

allow for faster and more potent response upon repeat encounter

central memory T cell: stay in lymphoid tissue

effector memory T cell: migrate to peripheral tissue

27
Q

macrophage activation

A

M0 (undifferentiated macrophages) require
- cytokines produced by Th1 to become M1 (pro-inflammator -> phagocytosis)
- cytokines produced by Th2 to become M2 (anti-inflammatory -> wound repair, fibrosis)

28
Q

early B cell development

A
  • maturation of B cell in bone marrow (but not activated)
  • involves production and expression of pre-BCR
  1. positive selection -> select for functional VDJ heavy chain (pre BCR)
    - see if it reacts to bad things
    - failure to express pre BCR = death
  2. negative selection -> autoreactivity (see if it reacts to self)
    - if BCR binds to self antigen on stromal cell in bone marrow, death

final stage of B cell development -> secondary lymphoid organ (spleen and lymph node)

29
Q

B cell activation

A

B cell activation can be:

T cell dependent -> CD4 helper T cell
T cell independent -> immediate response to non-protein antigens

30
Q

types of antibodies

A

IgM-> first produced ad is evidence of acute infection

structure: pentamieric (5 subunits) and decavalent (10 binding sites)
low affinity antibodies so compensate by having many binding domains

Ig G -> neutralise pathogen (block binding between pathogen and receptor on host cell) + complement activation

structure: tetrameric (4 subunits) and divalent (2 binding sites)
only antibody that can cross the blood-placental barrier -> passive immunity from mother to foetus

IgA -> at mucosal sites

IgE -> mast cell degranulation + defence against parasites (Fc region binds to specific receptors on mast cells at tissues and basophils in plasma, providing immunity agaisnt large parasites

31
Q

affinity vs avidity

A

affinity: strength of monovalent binding

avidity: combined strength of simultaneous binding involving more than 1 binding site

32
Q

isotype swtiching

A

change in constant region of antibodies -> irreversible process

33
Q

affintiy maturation

A

B cells interact with Th cells within germinal centre of lymph nodes to secrete immunoglobins with high affinity for specific antigens

repeated exposure to antigen results in the production of antibodies with increasing affinity

as immune response to atigen develops, amt of antibody produced increase so amt of available antigen decreases. B cells selected must be able to bind to antigen low conc so higher affinity BCR selected

34
Q

late B cells development in lymph node

A

somatic hypermutation and affinity maturation

dark zone:
rapidly proliferating b cells (centroblasts) undergoing somatic hypermutation (rapid point mutations in VDJ region which is driven by activation induced deaminase (AID) _> cytosine to uracil

light zone:
centrocytes compete to bind to iccosomes from follicular dendritic cells

mantle zone:
if can bind to antigen, present peptide:MHC complex to helper T cell. if TCR binds to peptide, B cell receive survival and differentiation signal

AFTER: isotype switching trigged by binding of CD40 on B cell and CD40L on T cell

istotype swtiching of B cells at the periphery results in the production of short-lived plasma B cells, some of which would migrate to the germinal centre of lymph node for affinity maturation

35
Q

antibody functions

A

agglutination: antibody have multiple binding sites -> form large complex -> easier for phagocytes to destroy pathogen

complement activation: complement bind to Fc region of antibody to initiate complement cascade, resulting in formation of MAC

opsonisation: antibodies bind to pathogen -> Fc region on antibody binds to Fc receptor on phagocyte and phagocyte destorys microbe

neutralisation: antibodies bind to surface of pathogen to block their binding to receptors on host cells

antibody dependent cellular toxicity: antibodu binds to pathogen -> Fc region on antibody to Fc receptor on NK cell -> cross linking trigger degranulation

PANIC (precipitation, agglutination, neutralisation, inflammation, complement)

36
Q

process for bacteria

A

bacteria induce APC to secrete IL-12 and native T cell activated. T cell secrete IL-2 and express more IL-2 receptor, Binding triggers release of IFN-gamma to activate M1 macrophage and differentiate into Th1 cell

T cell express CD40 ligand to bind to bind to CD40 receptor on macrophage and activated macrophage become highly microbicidal

37
Q

process for helmiths

A

worms induce APC to secrete IL-4 and naive T cell activated in presence of IL-4 to differentiate into Th2 cell. secrete IL-5 to activate eosinophil and stimulate IgE production activates m2 macrophages

38
Q

cytokines

A

interluekin -> influence function of other cells
chemokines -> recruit immune cells
interferons -> viral defence
tumour necrosis factor -> regulate inflammation

39
Q

mechanisms of microbial defence

A

virus
- innate immunity
-> soluble factors: type 1 interferon
-> cells: NK cell

  • adaptive immunity
    -> soluble factors: antibodies
    -> cells: CD8 T cells helped by CD 4 T cell

extracellular bacteria
- innate immunity
-> soluble factors: complement
-> cells: neutrophils, macrophage

  • adaptive immunity
    -> soluble factors: antibodies
    -> cells: CD4 T cell for activation of B cell

mycobacteria
- innate immunity
-> soluble factors: TNF-alpha, IL-1
-> cells: macrophage

  • adaptive immunity
    -> soluble factors: IL-12, IFN-gamma
    -> cells: CD4 T cell for activation of macrophage
40
Q
A

immunology (5 decks)

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