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Molecular and cell biology > Immunology > Flashcards

Immunology Flashcards

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AP® Biology flashcards Biology 101 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
Q

Antibody responses

A

secreted soluble immunoglobins of various types tht bind to antigens, produced by B-lymphocytes and ultimately secreted by the plasma cells

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26
Q

What are the 3 subtypes of T cells ?

A

cytotoxic T cells
helper t cells
regulatory t cells

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27
Q

Cytotoxic t cells

A

directly kill infected host cells

28
Q

Helper t cells

A

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
Q

Regulatory t cells

A

use similar strategies to inhibit function of helper T cells, cytotoxic T cells and dendritic cells

30
Q

How is the adaptive immune system activated?

A

binding of an antigen to activated cells leads to their proliferation and clonal expansion
triggers differentiation into effector cells

31
Q

Dendritic cells

A

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
Q

What are the 5 classes of antibodies?

A

IgG
IgM
IgD
IgE
IgA

33
Q

IgG

A

msot common antibody found in the body
made up of 2 copies of 2 proteins linked by covalent disulphide bonds

34
Q

What are the 2 parts of antibodies?

A

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
Q

Junctional diversification

A

gain or loss of nucleotides during recombination

36
Q

Allelic exclusion

A

choice of one allele during recombination

37
Q

Somatic hypermutation

A

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
Q

BCL-6

A

transcriptional repressor expressed in germinal centres
binds to sites in the p53 promoter
switches off expression leaving them without watch keeper oversight

39
Q

P53 pathway

A

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
Q

What are the 2 ways antigen presenting dendritic cells can respond to T cells?

A

activate or tolerise

41
Q

What are t cells activated by?

A

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
Q

What proteins do activating dendritic cells present?

A

MHC with foreign antigens
stimulating ligands
cell-cell adhesion molecules

43
Q

What do tolerising antigens present?

A

self antigens on their MHCs but without the co-stimulatory activator protein

44
Q

T cell receptors

A

how t cells bind to MHCs
like immunoglobins, contain variable domains and hyper variable loops

45
Q

Candida albicans

A

yeast that usually lives on/in our bodies without issues but can become pathogenic if it is transformed into its pseudohyphal filamentous form

46
Q

What can induce candida to turn into its hyphal form?

A

phagocytosis by macrophages

47
Q

Staphylococcus aureus

A

gram positive spherical bacterium frequently found in the upper respiratory tract and on the skin
produces protein A

48
Q

Protein A

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
Q

HIV

A

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
Q

What cancer is only usually seen in HIV patients?

A

kaposi’s sarcoma

51
Q

Type I diabetes

A

immune system develops t killer cells that attack insulin producing beta cells within islets or langerhans

52
Q

Multiple scerosis

A

immune system responds to proteins within the myelin sheath of neurons within the CNS
can be ultimately fatal

53
Q

Autoimmune inflammatory diseases

A

rheumatoid arthritis
psoriasis
crohns disease
IBD
ulcerative colitis

54
Q

What cancers are HIV/ immunocompromised patients more susceptible to?

A

kaposi’s sarcoma
basal cell carcinoma
hepatocellular carcinoma

55
Q

Immunosenescence

A

immune competence decreasing with age
suggests decreased immunosurveillance against cancer contributes to increased disease in the elderly

56
Q

What proves the existance of tumour-specific antigens that can be recognised as non-self

A

tumours rejected when transplanted into syngeric hosts
transplantation of normal tissues is accepted

57
Q

What are the 3 phases of cancer immunoediting?

A

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
Q

What kills tumour cells in the elimination phase?

A

NK
CD4+
CD8+

59
Q

Why are there limits on the immune systems ability to fight cancer on its own?

A

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
Q

What mechanisms lead to the extreme diversity of anitbodies?

A

somatic hypermutation
allelic exclusion
junctional diversification

61
Q

What processes lead to somatic hypermutation?

A

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
Q

Affinity maturation

A

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
Q

AID

A

activation induced deaminase
enzyme that drives mutations in germinal centres

64
Q

What types of cancer immunotherapies are there?

A

immunomodulators
checkpoint inhibitors
cytokines
cancer vaccines
monoclonal antibodies
oncolytic viruses
CART cell therapy

65
Q

(CAR) T cell therapy

A

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
Q

Oncolytic viruses

A

viruses that have been modified in a lab to infect and kill certain tumour cells

67
Q

Cancer vaccines

A

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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