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microbial pathogens > Immunology > Flashcards

Immunology Flashcards

1
Q

immune cells develop in the

A

bone marrow

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2
Q

commensal bacteria

A

-healthy bacteria in the gut microbiome

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3
Q

Pathogens the famous five

A

-viruses
-bacteria
-Fungi
-Protozoan parasites
-Helminths (worms)

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4
Q

defence mechanisms can be non beneficial sometimes when …

A

-rejection of organ transplantation
-hypersensitive response to innocuous particles (pollen, gluten dust mite faeces
-breaking of self-tolerance = auto immune disease

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5
Q

immune cells recognise foreign cells by

A

receptor mediated recognition
-leading to inflammatory response

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6
Q

physical barriers summarised

A

-skin, epidermis needs to piecered or ruptured
-ciliated mucosal surfaces removal and expulsion of debris and organisms
-all mucosal surfaces - sticky mucous glycoproteins inhibits movement

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7
Q

chemical barriers
lysozyme

A

-in sweat and tears breaks down peptidoglycan in bacterial cell wall

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8
Q

chemical barriers
fatty acids

A

-secreted by sebaceous gland and have antimicrobial properties

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9
Q

chemical barriers
defensins

A

-have small charged membranes that act on membranes without cholesterol
-found in mucus and skin secretions are antimicrobial

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10
Q

chemical barriers
collectins

A

-in lung surfactants and serum bind sugar molecules on bacterial surfaces promoting elimination

literally means collagen containng electin = protein that binds sugar

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11
Q

chemical barriers
acid

A

-proprionic and lactic acid produced by commensal bacteria in the vagina that lowers pH
-HCL- secreted in the stomach that is lethal to many bacteria

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12
Q

chemical barriers
cathelicidins

A

-antimicrobial proteins found in mucosal scretions

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13
Q

routes of entry

A

-respiratory
-open wounds
-burns
-needle
-animal bite
-hookworm
-Urogenital tract
-insect bite

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14
Q

site of infection and multiplication

A

-typically infections develop at the site of entry (can become systemic)
-extra/intracellular multiplication of single celled organisms
-both intra and extraceullar depending on life cycle
-parasitic worms may not replicate but can lay eggs

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15
Q

vasculature

A

blood and lymph

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16
Q

exotoxin secretion

A

-inhibit protein synthesis (cell death)
-increased cAMP
-neurotoxins
-enzymatic action on cell membranes
-superantigen (toxic shock syndrome)

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17
Q

endotoxins

A

-components of the organism = promote the host to produce factors that lead to certain symptoms = cytokines and chemokines

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18
Q

pathogens can cause blockages

A

= physical presence (blocking of lymphatic vessels

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19
Q

coevolution of pathogens

A

-means that pathogens can evade and counter the effects of our immune systems

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20
Q

innate immune system

A

-pre-existing defence mechanism preventing infection
-physical and chemical barriers
-specific cells and proteins to defend against pathogens

IMPORTANCE = recognition of foreign entry and triggering a specialised cellular response

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21
Q

Pattern recognition receptors (PRRs)

A

-macrophages, neutrophils and dendritic cells use PRRs to discriminate between self and non-self by recognising pathogen associated molecular patterns (PAMPs)

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22
Q

some epithelial cells also have PRRs

A

-PRRs are membrane bound and cytoplasmic

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23
Q

invarient PRRs play a few roles

A

-recognise abundant conserved surface ligands = PAMPs
-recognise dead/damaged cells via DAMP(damage associated molecular patterns
-must not recognise and phagocytose healthy cells

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24
Q

Response 1Phagocytosis

A

-Attachment via PRR
-ingestion by wrapping cell membrane around object via pseudopodia
-formation of phagosome and fusion with lysosome
-enzymatic destruction of the ingested particle
-presentation of parts of the object

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25
Q

Response 2 Cytokines secretion

A

-released in paracrine fashion
-proteins secreted locally in response to pathogens
-can help kill or destroy invading micro-organisms directly or indirectly
-recruit more cells to the site of infection
-have a very localised effect on tissues

26
Q

Cytokines
chemokine

A

-an attractant controls migration of cells to site of infection

27
Q

Cytokines
Colony stimulating factor (CSF)

A

stimulates the differentiation of neutrophils and monocytes/macrophages

28
Q

Cytokines
growth factor

A

has an effect on a variety of immune cells

29
Q

Cytokines
interferon

A

viral replication inhibition and IFNgamma immunoregulatory roles

30
Q

Cytokines
interleukin

A

secreted by many different cells and have many different roles

31
Q

Cytokines
tumour necrosis factor

A

-activates macrophages and endothelium secreted by monocytes

32
Q

the inflammatory response

A

1)defence is breached recognised as foreign cells and chemokines released
2) inflammation -> vasodilation (increased vascular permeability) heat and swelling by oedema which drains to lymphatics
-more inflammatory cells migrate in and release mediators

33
Q

lymphocytes

A

-about 5 x 10^11 in total
-20% are B cells and 80% are T
-49% in tissues and 49% in lymph nodes and spleen
-only 2% circulates in the blood 10^10 10% B cells
-only inactivate cells circulate
-activated cells home to lymphatic tissues

34
Q

APCs are essential components of the immune response

A

-immature dendritic cells reside in peripheral tissues
-dendritic cells migrate via lymphatic vessels to regional lymph nopdes
-mature dendritic cells activate naive T cells in lymphoid organs such as lymph nodes

35
Q

The lymphatic system

A

-tissue fluid drains into the lymphatics and returns to the blood circulation via the right subclavian vein of the heart
-Constant traffic of tissue fluid (and APC) to and through lymph nodes
-this is where B and T lymphocytes are found

36
Q

primary lymph tissue

A

-B/T cell differetiation

37
Q

Secondary/ peripheral lymph tissue

A

immune response

38
Q

why do we need the adaptive response?

A

-First encounter thanks to immediate innate response - very often inflammation and elimination of the pathogen
-this is dependent on our phagocytes (macrophages and dendritic cells) being able to recognise the pathogen with limited PRRs
-Pathogens have evolved ways to subvert our surveillance strategies = no or limited inflammatory response

39
Q

Pathogens have evolved ways to subvert our surveillance strategies for example

A

-Production of a sugar (polysaccharide) coat
-surface molecules very similar to host
-target macrophages

40
Q

Immunoglobulin (Ig) heavy and light chains

A

-Both chains have a constant and variable domains with a characterstic folded structure
-7-10 Beta strands lubked via disulphide bonds (immunoglobulin fold)

41
Q

Ig hypervariable regions

A

-these regions of hypervariability lie in discrete loops of the variable domains within the Ab structure
-these loops are also called the complementarity determining regions (CDRs) from sntigen binding site
-three CDRs in the heavy chain and 3 CDRs in the light give variation to the Ag binding site

42
Q

The B cell receptor (BCR)

A

-the BCR has to fit the shape of the antigen exactly
-Ag can bind in pockets, grooves or extended surfaces in the binding site of the BCR (and antibodies) but recognition is always of 3D shape

43
Q

immunoglobulin or antibody

A

Ig has glycoproteins that highlight teh structure

44
Q

SImilarities between TCR and BCR

A

-T cell receptor resembles a membrane bound Fab fragment, also has regions of hypervariability (CDRs)
-but is encoded by a completely different set of gene segments

45
Q

TCR is a

A

heterodimeric membrane bound receptor

-hypervariable regioms allow antigen to bind to T cell receptor

-Alpha and Beta chain attached to membrane

46
Q

TCR can only see its cognate antigen if

A

it is presented by a specific MHC molecule

47
Q

MHC class 1

A

-made of 2 chains alpha and beta
-one chain bound to membrane
-major histo compatibility

48
Q

MHC class 2

A

-2 chains bound to membrane
-alpha and beta chains

49
Q

T cells will express either CD4

A

or CD8 surface antigens
-these proteins stabilise the binding of TCR to the MHC: peptide complex

50
Q

CD4

A

a single polypeptide with 4 domains and binds to MHC2

51
Q

CD8

A

either a heterodimer or homodimer
MHC1

52
Q

Binding sites for CD4 and CD8 on MHC II and MHC I respectively are on the

A

immunoglobulin domains

53
Q

role of CD4/8 and MHC

A

-bind to MHC
-increase stability
-signalling role (intracellular)

54
Q

MHC binds peptides tightly within the cleft

A

-MHC class I are held tightly at each end
-MHC class 2 extend beyond the groove

55
Q

peptides are bound to MHC class 1 molecules by their ends

A

-H bonds ionic interactions hold in cleft
-MHC molcule interacts with the peptide backbone via hydrogen bonds and ionic interactions
-peptide 8-10 aa in length

56
Q

peptides are bound to MHC class II molecules along their length

A

-not restricted at ends
-MHC molecule interacts with the peptide backbone via hydorgen bonds and ionic interactions
-peptide sixe is less constrained around 13-17 aa in length

57
Q

peptides which bind MHC class II molecules also have anchor residues along their length but

A

the length is more variable

58
Q

BCR/Ab diversity
-the diversity is the repertoire of BCR/immunoglobulin is generated by four main processes

A

1)combinatorial diversity during segment recombination
2)junctional diversity during segment joining
3) combinational diversity driven by different combinations of heavy and light chain
4)somatic hypermutation

59
Q

number of functional gene segments in human immunoglobulin loci

A

very variable in variable region
some in diiversity and joining region

60
Q
A

microbial pathogens (3 decks)

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