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zFoM by me > Immune System 1-4 🗸 > Flashcards

Immune System 1-4 🗸 Flashcards

1
Q

Innate immunity

A

immunity present from birth and is generally non-specific
includes physical barrier, inflammatory mediators, complement proteins, acute phase proteins, immune cells, etc.

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2
Q

barriers to infection

A

skin, mucus, commensal bacteria

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3
Q

skin barrier

A

physical barrier - tightly packed, highly keratinised cells
low ph (5.5)
low oxygen tension
sebaceous glands- hydrophobic oils, lysosomes, ammonia

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4
Q

Mucus

A

mucous membranes line all body cavities that are in contact with the external environment
mucus traps bacteria lysosomes and defensisns that directly kill invading pathogens
Secretory IgA

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5
Q

Commensal bacteria

A

compete with pathogens for resources and produce fatty acids and bactericidins that stop pathogens growing

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6
Q

Cytokines

A

interferons released by virally infected cells to signal to neighbouring uninfected cells
destroy RNA and reduce protein synthesis
undergo apoptosis
interferons also activate immune cells e.g. NK cells

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7
Q

Macrophages

A

Phagocytose bacteria

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8
Q

Seven steps of macrophage

A
  1. PRRs on macrophages bind to PAMPs on pathogen, which signals the formation of the phagocytic cup
  2. cup extends around the pathigen and pinches off - phagosome
  3. Phagosome fuses with lysosome - phagolysosome
  4. pathogen killed and contents degraded
  5. debris released into extracellular fluid
  6. pathogen-derived peptides expressed on special cell surface receptors (MHC-II)
    7.Pro-inflammatory mediators released (TNF⍺)- acute inflammation
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9
Q

Mast cells

A

deal with pathogens too large for phagocytosis
associated with allergy

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10
Q

Two step process of mast cells

A

1.when PRRs on mast cell bind to PAMPs on pathogen, the mast cell is stimulated to release pre-formed pro-inflammatory substances such as histamine and tryptase - degranulation
2.as this happens, the mast cell also begins to produce pro-inflammatory substances ie histamine, TNF, chemokines, leukotrienes

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11
Q

Transendothelial migratiom

A

recruitment of neutrophils to the site of infection/damage during acute inflammation

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12
Q

5 steps of neutrophils

A
  1. loss of intravascular fluid in the presence of inflammation causes slower blood flow, allowing neutrophils to undergo margination (moving close to endothelial cells instead of the centre of the vessel)
  2. neutrophils can then encounter and bind to adhesion molecules expressed by the endothelial cells (selectins, ICAM-1)
  3. neutrohpils migrate across the endothelium via diapedesis
  4. Once in the tissues, the neutrophils travel to the exact site of injury via chemotaxis
  5. Neutrophils are then activated by PAMPs and pro-inflammatory mediators such as TNF⍺
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13
Q

Three killing mechanisms

A

Phagocytosis
Degranulation
NETs

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14
Q

Phagocytosis (killing mechanism)

A

phagolysosomal killing via the production of reaction oxygen species (ROS)

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15
Q

Degranulation

A

release of anti-bacterial granules

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16
Q

NETs

A

release pf a net-like structure that traps pathogens, leading to phagocytosis

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17
Q

Modes of ingestion

A

receptor mediated endocytosis
pinocytosis
phagocytosis

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18
Q

receptor mediated endocytosis

A

molecules bound to membrane receptors are internalised
(imporntant in the generation of adaptive immunity

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19
Q

pinocytosis

A

ingestion of fluid of surrounding cells

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20
Q

phagocytosis (ingestion mode)

A

bacterium engulfed by cell surface

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21
Q

NK cells

A

lymphocytes involved in the rejection of tumours and virally infected cells which respond to the reduced levels of MHC class I in cancerous and virally infected cells
kill by degranulation and release perforin
produce IFN𝛾

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22
Q

Dendritic cells

A

act as a bridge between the innate and acquired immune system
express antigens on their cell surface and present them to T cells -antigen presenting cells

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23
Q

basophils

A

granules containing histamines which act as effector cells in allergic reactions

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24
Q

Eosinophils

A

associated with allergy

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25
Q

What is the complement system

A

the activated response to inflammation which created a cascade of chemical reactions

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26
Q

What is the process of the complement system

A

C3 cleaves (splits) into C3a and C3b
C3b then cleaves C5 into C5a and C5b, it will also cause C3 to cleave more via the alternative pathway
C5b (with other things, will produce a membrane attack complex (MAC) which inserts into cell walls and destoyd the cell by allowing salt amd water in
C3a and C5a are responsible for acute inflammation (anaphylatoxins)

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27
Q

what are acute phase proteins?

A

proteins produced by the liver whose plasma concentrations increase or decrease in response to inflammation

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28
Q

three acute phase proteins

A

C3
CRP
MBL

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29
Q

C3

A

involved in complement

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30
Q

CRP

A

activates complement via classical pathway
very short half life, but numbers are very rapidly increased during inflammation

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31
Q

MBL

A

activated complement vis MBL pathway

32
Q

the classical pathway can be activated by ____ and _____

A

IgM and IgG

33
Q

what does IgG act as in the enhancement of the immune system?

A

opsonins (attach to target cells and make it more obvious for phagocytosis)

34
Q

Acquired (adaptive) immunity

A

Induced by the presence of foreign material
able to discriminate between self and non-self
includes cytokines, antibodies, B and T cells

35
Q

General features of innate immunity

A

rapid response (hours)
no memory
non-specific
basophils, eosinophils, neutrophils, mast cells, nk cells

36
Q

general features of acquired immunity

A

slower response (days)
immunological memory (subsequent responses are quicker and more powerful)
specific
B and T cells

37
Q

B cells

A

mature in the bone marrow
important in humoral immune response
normally circulate the primary lymphoid tissue in their inactive form (antigen presentation activates them in secondary lymphoid tissue)

38
Q

B cell activation

A

membrane bound antibodies on the B cells bind to target antigen IgM or IgD within the B cell zone of lymph nodes
requires 2 signals to become fully active and begin proliferation ie from TH cells, PRR and PAMPs or from multiple antigens

39
Q

generation of high affinity antibodies

A

Once active, clonally proliferate and become either plasma cell (antibodies) or a memory B cell (germinal centre response)
high affinity antibodies are generated IgM (by plasma) becomes IgG (by B cells) assisted by TH cells

40
Q

transport of lymphocytes

A

lymph and lymphocytes leave lymph node and go to the medullary sinus then to the efferent lymphatic vessels then to the blood circulation via the lymphatic ducts at the subclavian vain

41
Q

antibodies

A

made up of 2 light chains and 2 heavy chains
each has a unique variable region (antigen binding site) which is specific against one antigen

42
Q

membrane bound antibody

A

located on surface of B cell

43
Q

secreted antibody

A

secreted by plasma cells, present in serum and tissue fluids

44
Q

five types of antibody

A

IgM
IgG
IgA
IgD
IgE

45
Q

IgM

A

first antibody to be made in an infection
monomer when bound to B cell membrane but pentamer when released into plasma

46
Q

functions of IgM

A

B cell activation
agglutination (immune complex formation - enhances phagocytosis)
complement system activation through classical pathway

47
Q

IgG

A

most abundant antibody in the plasma
monomer
dominant type during secondary response

48
Q

functions of IgG

A

foetal immunity (placenta transfer)
complement activation
NK cell activation
neutralisation

49
Q

IgA

A

second most abundant antibody
monomer in serum, helps with neutralisation of pathogens (membrane bound form)
Dimer in secretory fluids (ie colostrum)

50
Q

function of IgA

A

neonatal defense
protects GI tract of neonates

51
Q

IgD

A

second least abundant antibody
monomer

52
Q

function of IgD

A

B cell activation

53
Q

IgE

A

least abundant antibody normally
monomer

54
Q

function of IgE

A

produced in allergic response

55
Q

T cells

A

mature in the thymus

56
Q

four types of T cells

A

CD4+ Helper T cells
CD8+ Killer T cells
Regulatory T cells
Memory T cells

57
Q

CD4+ Helper T cells

A

activate B cells and stimulate production of memory B cells

58
Q

CD8+ Killer T cells

A

kill infected cells via perforin/granzymes/granulysin

59
Q

regulatory T cells

A

lymphocyte suppression

60
Q

Memory T cells

A

involved in the adaptive immune response

61
Q

MHC molecules

A

T cells can only recognise peptide antigens that are presented to their TCR by MHC molecules
Class I or II

62
Q

Class I MHC

A

expressed on all nucleated cells, present peptide antigens to CD8+ Killer T cells

63
Q

Class II MHC

A

expressed only on antigen presenting cells
present peptide antigens to CD4+ Helper T Cells

64
Q

T cell activation

A

in the presence of pro-inflammatory mediators (ie TNF⍺), dendritic cells mature and increase expression of stimulatory molecules on their surface
Dendritic cells phagocytose the pathogenic antigens, break the antigens down into short peptides and load them onto MHC II molecules
these transport to the cell surface (maturing dendrites will also move to lymph nodes via afferent lymphatic system)
Co-stimulatory molecules enable T cells to respond to antigen and fully differentiate

65
Q

Two types of T cell differentiation

A

CD4+ T cells to make T helper cells
CD8+ T cells to make CTLs (TC cells)

66
Q

CD4+ T cells to make T helper cells

A

antigen activated CD4+ T cells secrete IL-2 and express IL-2 receptors (T cell growth factor)
CD4+ T cells → T helper (THO) cells → effector TH cells like TH1, TH2 and TFH cells

67
Q

TH1 cells

A

secrete pro-inflammatory cytokines (IL-2, IFN𝛾) which stimulates the production of ROS (macrophage mediated)

68
Q

TH2 cells

A

secrete mainly IL4, IL5 and IL6 which promote B cell proliferation and induces antibody production

69
Q

TFH cells

A

stimulated by the presented antigen peptides + MHC II molecules on B cells to proliferate and differentiate (plasma + memory) by secreting IL4 and IL21

70
Q

CD8+ T cells → CTLs (TC cells)

A

IL-2 (provided by TH cells) promotes differentiation and proliferation of antigen activated (via MHC I) CD8+ cells into cytotoxic T lymphocytes (CTLs)
CTLs migrate out of secondary nodes and enter site of infection (via transendothelial migration) and then kill virally infected host cells by recognising pathogenic antigens attached to MHC class I
theyre also involved in killing caner cells

71
Q

what kills bacteria?

A

phagocytes
antibody and B lymphocytes
complement system

72
Q

what kills viruses

A

T lymphocytes
antibody and B lymphocytes

73
Q

what kills fungi?

A

phagocytes
T lymphocytes
eosinophils

74
Q

what kills protozoa

A

T lymphocytes
Eosinophils

75
Q

what kills worms

A

Eosinophils
mast cells

zFoM by me (37 decks)

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