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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
Response 2 Cytokines secretion
-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
Cytokines chemokine
-an attractant controls migration of cells to site of infection
27
Cytokines Colony stimulating factor (CSF)
stimulates the differentiation of neutrophils and monocytes/macrophages
28
Cytokines growth factor
has an effect on a variety of immune cells
29
Cytokines interferon
viral replication inhibition and IFNgamma immunoregulatory roles
30
Cytokines interleukin
secreted by many different cells and have many different roles
31
Cytokines tumour necrosis factor
-activates macrophages and endothelium secreted by monocytes
32
the inflammatory response
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
lymphocytes
-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
APCs are essential components of the immune response
-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
The lymphatic system
-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
primary lymph tissue
-B/T cell differetiation
37
Secondary/ peripheral lymph tissue
immune response
38
why do we need the adaptive response?
-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
Pathogens have evolved ways to subvert our surveillance strategies for example
-Production of a sugar (polysaccharide) coat -surface molecules very similar to host -target macrophages
40
Immunoglobulin (Ig) heavy and light chains
-Both chains have a constant and variable domains with a characterstic folded structure -7-10 Beta strands lubked via disulphide bonds (immunoglobulin fold)
41
Ig hypervariable regions
-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
The B cell receptor (BCR)
-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
immunoglobulin or antibody
Ig has glycoproteins that highlight teh structure
44
SImilarities between TCR and BCR
-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
TCR is a
heterodimeric membrane bound receptor -hypervariable regioms allow antigen to bind to T cell receptor -Alpha and Beta chain attached to membrane
46
TCR can only see its cognate antigen if
it is presented by a specific MHC molecule
47
MHC class 1
-made of 2 chains alpha and beta -one chain bound to membrane -major histo compatibility
48
MHC class 2
-2 chains bound to membrane -alpha and beta chains
49
T cells will express either CD4
or CD8 surface antigens -these proteins stabilise the binding of TCR to the MHC: peptide complex
50
CD4
a single polypeptide with 4 domains and binds to MHC2
51
CD8
either a heterodimer or homodimer MHC1
52
Binding sites for CD4 and CD8 on MHC II and MHC I respectively are on the
immunoglobulin domains
53
role of CD4/8 and MHC
-bind to MHC -increase stability -signalling role (intracellular)
54
MHC binds peptides tightly within the cleft
-MHC class I are held tightly at each end -MHC class 2 extend beyond the groove
55
peptides are bound to MHC class 1 molecules by their ends
-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
peptides are bound to MHC class II molecules along their length
-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
peptides which bind MHC class II molecules also have anchor residues along their length but
the length is more variable
58
BCR/Ab diversity -the diversity is the repertoire of BCR/immunoglobulin is generated by four main processes
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
number of functional gene segments in human immunoglobulin loci
very variable in variable region some in diiversity and joining region
60

microbial pathogens (3 decks)

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