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Immunology Flashcards

1
Q

Immunity

A

state of being insusceptible or resistant to a noxious agent or process, especially a pathogen or infectious disease

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2
Q

What is the first line of defence?

A

physical and chemical barriers that are always ready and prepared to defend the body from infection

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3
Q

Skin

A

barrier function
has its own microbiome

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4
Q

Tears, mucus and saliva

A

openings are potential entry points so are protected by secretions
may contain anti-microbial peptides or enzymes
pathogens

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5
Q

Cilia

A

very fine hairs lining our windpipe that move mucus and trapped particles away from the lungs
can be bacteria or material like smoke/dust

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6
Q

Stomach acid

A

HCl secreted by parietal cells lowers the pH
activates proteases such as pepsin in the stomach and kills pathogens

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7
Q

Urine flow

A

regularly pushes out pathogens from the bladder adn urethra

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8
Q

Friendly bacteria

A

naturally occuring and form microbiome in gut, skin, mouth and vagina
acts as competition to reduce pathogens ability to colonise/grow
can be disrupted by antibiotics/antibacterials

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9
Q

Pathogen associated molecular patterns

A

how the body distinguishes between pathogen and self cells
the things that are different between them

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10
Q

Damage associated molecular patterns

A

similar to PAMPs
used to identify damaged self cells

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11
Q

Toll like receptors

A

largest family of receptors that detect PAMPs
highly expressed in macrophages, dendritic cells and neutrophils

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12
Q

How do TLRs exert their effect?

A

molecular signalling cascade through downstream effectors like Jun/Fos TFs and NFkB
changes gene expression

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13
Q

Myeloid white blood cells

A

provide innate immune protection
macrophages, neutrophils and dendritic cells

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14
Q

Lymphoid white blood cells

A

generate adaptive immunity

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15
Q

What does activation of the innate immune system lead to?

A

blood vessels become dilates and permeable to facilitate wbc access
pro-inflammatory cytokines released
fever inhibits pathogen proliferation and catalyses chemical reactions of immune system

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16
Q

How can a local immune response be dangerous systemically?

A

loss of plasma volume
crash of blood pressure
cytokine storm

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17
Q

Neutrophils

A

short lived phagocytic abundant in blood but not tissues, respond and migrate to sites of infection (make up most of puss)

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18
Q

Macrophages

A

long lived professional phasgocytes abundant in areas likely to be exposed to pathogens like airways and the gut

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19
Q

Eosinophils

A

specialists in attacking objects too large to engulf

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20
Q

Adaptive immunity

A

can generate highly specific responses to specific pathogens
can indentify, target and destroy vast range of pathogens and toxins

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21
Q

When can adaptive immunity become lethal?

A

if directed towards host molecules/proteins
if directed towards harmless foreign molecules

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22
Q

What are the 2 primary lymphoid organs?

A

thymus- T cells
bone marrow- B cells

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23
Q

Lymphatic system

A

lymphocytes develop in primary organs and then migrate to secondary oragns where they are exposed to foreign antigens
lymph drains into bloodstream and cells circulate

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24
Q

Natural killer cells

A

take part in early defence against foreign cells and autologous cells undergoing stress
are lymphoid cells by considered part of innate immune response

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25
Antibody responses
secreted soluble immunoglobins of various types tht bind to antigens, produced by B-lymphocytes and ultimately secreted by the plasma cells
26
What are the 3 subtypes of T cells ?
cytotoxic T cells helper t cells regulatory t cells
27
Cytotoxic t cells
directly kill infected host cells
28
Helper t cells
activate macrophages, dendritic cells, B-cells and cytotoxic T-cells by secreting a variety of cytokines and displaying a variety of co-stimulatory proteins on their surface
29
Regulatory t cells
use similar strategies to inhibit function of helper T cells, cytotoxic T cells and dendritic cells
30
How is the adaptive immune system activated?
binding of an antigen to activated cells leads to their proliferation and clonal expansion triggers differentiation into effector cells
31
Dendritic cells
specialist phagocytic cells derived from monocytes express a large variety of recognition receptors phagocytose pathogens, cleave them into peptides to bind to MHC migrate to lymphoid tissues to stimulate T cells
32
What are the 5 classes of antibodies?
IgG IgM IgD IgE IgA
33
IgG
msot common antibody found in the body made up of 2 copies of 2 proteins linked by covalent disulphide bonds
34
What are the 2 parts of antibodies?
constant domains- interact with other parts of the immune system and is always the same variable domains- make up antigen binding sites and differ
35
Junctional diversification
gain or loss of nucleotides during recombination
36
Allelic exclusion
choice of one allele during recombination
37
Somatic hypermutation
process in which point mutations accumulate in the antibody V-regions of both the heavy and light chains, at rates that are about 10 6-fold higher than the background mutation rates observed in other genes
38
BCL-6
transcriptional repressor expressed in germinal centres binds to sites in the p53 promoter switches off expression leaving them without watch keeper oversight
39
P53 pathway
pathway that acts as a watch keeper for cells experiencing double stranded breaks and high levels of DNA damage will cause them to undergo apoptosis
40
What are the 2 ways antigen presenting dendritic cells can respond to T cells?
activate or tolerise
41
What are t cells activated by?
partially degraded antigens displayed on the surface of antigen presenting cells MHC proteins on these cells bind to peptide fragments and carry them to cell surface
42
What proteins do activating dendritic cells present?
MHC with foreign antigens stimulating ligands cell-cell adhesion molecules
43
What do tolerising antigens present?
self antigens on their MHCs but without the co-stimulatory activator protein
44
T cell receptors
how t cells bind to MHCs like immunoglobins, contain variable domains and hyper variable loops
45
Candida albicans
yeast that usually lives on/in our bodies without issues but can become pathogenic if it is transformed into its pseudohyphal filamentous form
46
What can induce candida to turn into its hyphal form?
phagocytosis by macrophages
47
Staphylococcus aureus
gram positive spherical bacterium frequently found in the upper respiratory tract and on the skin produces protein A
48
Protein A
a cell wall protein that binds to the constant domain of IgGs which means they are covered with self proteins so no longer recognised by innate immune system
49
HIV
RNA lentivirus that specifically infects t helper cells, dendritic cells and macrophages expressing NK, CD4 + CD8 infected cells no longer function and t cells target the adaptive immune system immune deficiency leads to infections and cancers
50
What cancer is only usually seen in HIV patients?
kaposi's sarcoma
51
Type I diabetes
immune system develops t killer cells that attack insulin producing beta cells within islets or langerhans
52
Multiple scerosis
immune system responds to proteins within the myelin sheath of neurons within the CNS can be ultimately fatal
53
Autoimmune inflammatory diseases
rheumatoid arthritis psoriasis crohns disease IBD ulcerative colitis
54
What cancers are HIV/ immunocompromised patients more susceptible to?
kaposi's sarcoma basal cell carcinoma hepatocellular carcinoma
55
Immunosenescence
immune competence decreasing with age suggests decreased immunosurveillance against cancer contributes to increased disease in the elderly
56
What proves the existance of tumour-specific antigens that can be recognised as non-self
tumours rejected when transplanted into syngeric hosts transplantation of normal tissues is accepted
57
What are the 3 phases of cancer immunoediting?
elimination phase- tumour cells killed equilibrium between immune and tumour cells tumour cells escape as immune system is unable to destroy them, becomes clinically detectable
58
What kills tumour cells in the elimination phase?
NK CD4+ CD8+
59
Why are there limits on the immune systems ability to fight cancer on its own?
does not see cancer as foreign recognises cancer cells but response isn't strong enough cancer cells release chemicals that stop the immunse system finding them
60
What mechanisms lead to the extreme diversity of anitbodies?
somatic hypermutation allelic exclusion junctional diversification
61
What processes lead to somatic hypermutation?
activation of b lymphocytes by t cells causes them to proliferate in lymphatic follicles which creates germinal centres in germinal centres expression of AID and repression of P53 drives mutations
62
Affinity maturation
mutations may cause antibodies to improve which will be the ones that survive and are cloned, antibodies with mutations that reduce their efficacy are got rid of means that after initial immunisation there is a progressive increase in affinity
63
AID
activation induced deaminase enzyme that drives mutations in germinal centres
64
What types of cancer immunotherapies are there?
immunomodulators checkpoint inhibitors cytokines cancer vaccines monoclonal antibodies oncolytic viruses CART cell therapy
65
(CAR) T cell therapy
chimeric antigen receptor T cell therapy patients T cells and infected with a recombinant virus that causes the expression of a TCR TCR has an antigen binding domain to a specific tumour antigen generates t cells which can attack tumour cells, transfused back into patient
66
Oncolytic viruses
viruses that have been modified in a lab to infect and kill certain tumour cells
67
Cancer vaccines
vaccines that direct an immune response designed to prevent a specific cancer epitope or cancer causing pathogen (eg. HPV)

Molecular and cell biology (8 decks)

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