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phase 2 medicine > immunology > Flashcards

immunology Flashcards

1
Q

what is passive immunity; give examples

A

Administration of preformed immunity from one person to another

ex.:
cross-placental transfer of antibodies from mother to child (e.g. measles, pertussis)

transfusion of blood or blood products including immunoglobulin (e.g. Hep B)

injection of immunoglobulins

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2
Q

what is Human normal immunoglobulin (HNIG)

A

an injection of the pooled plasma of donors which contains antibodies to infectious agents that are currently prevalent in the general population.

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3
Q

what type of immunisation do vaccines stimulate

A

active immunisation

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4
Q

define primary and secondary vaccine failure

A

Primary vaccine failure – person doesn’t develop immunity from vaccine.

Secondary vaccine failure – initially responds but protection wanes over time

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5
Q

Define active immunization

A

administering a toxoid to stimulate the immune system to produce antibodies

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6
Q

What are the three ways of inducing active immunization

A

Using a whole virus
Using parts that trigger the immune system (antigens)
Using the genetic material of the pathogen

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7
Q

Name two classes non-living vaccines

A

Whole killed and toxoid

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8
Q

Define whole killed vaccines and explain limitations

A

Vaccines using the inactivated bacteria/viruses

Limitations:
-whole pathogens can cause excessive adverse reactions
- immune responses are not always as good as response to actual infection (no CD8 TC) responses
- usually need at least 2 doses

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9
Q

Give examples of whole killed bacterial vaccines

A

diphteria
Tetanus
Pertussis
Cholera

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10
Q

What is pertussis

A

Whooping cough

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11
Q

Give 3 examples of whole killed viral vaccines

like the actual diseases

A

Polio, influenza, hep A, rabies, sars-cov-2

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12
Q

Define live attenuated vaccines

A

The organism is cultured in such a way that it’s virulescence is “attenuated” (does not cause disease when put in humans). The organism is put in host, allowed to replicate and induce an immune response which is protective against the wild type organism

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13
Q

Which provides better protection: whole killed or live attenuated vaccines

A

Live attenuated

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14
Q

what are the advantages of live attenuated

A

immune response mimics real infection more closely
lower and fewer doses required
oral administration –> more favorable

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15
Q

what are the disadvantages of live attenuated vaccines?

A

Often impossible to balance attenuation and immunogenicity
Reversion to virulence
immunocompromised hosts might have more side effects from the vaccine

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16
Q

give bacterial examples of live attenuated vaccines

A

Mycobacterium bovis and Salmonella typhi

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17
Q

give viral examples of live attenuated vaccines

A

MMR and poliomyelitis

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18
Q

what are recombinant protein vaccines?

A

genetically engineered proteins produced from bacteria yeast or mammalian cells

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19
Q

examples of recombinant protein vaccines

A

hep B
HPV
Sars-CoV-2

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20
Q

what are synthetic peptide vaccines?

A

peptides synthesised directly using a machine

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21
Q

what are live attenuated vector vaccines?

A

These vaccines also use live attenuated viruses but are modified to carry genetic material from the disease-causing pathogen rather than using the pathogen itself.

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22
Q

example of live attenuated vector vaccine

A

Sars-CoV-2

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23
Q

what are dna vaccines and how do they work

A

a vaccine with plasmids that encode for a foreign protein of interest which is injected directly

DNA goes to the nucleus, gets transcribed, and the foreign protein gets displayed by MHC to stimulate an immune response

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24
Q

what are mRNA vaccines?

A

mRNA of foreign protein is injected into the body
cells use the instructions to make the viral protein, prompting the immune system to recognize it as foreign and generate an immune response, including the production of antibodies.
If the vaccinated person later encounters the actual virus, their immune system is primed to recognize and fight it off more effectively

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25
Q

what is the complement system?

A

a system of proteins which work together to enhance the inflammatory response

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26
Q

what are the three ways of activation of the complement system

A
  1. classical -> antibody-antigen binding
  2. alternative -> complement proteins bind to microbe
  3. lectin –> mannose binds to lectin on microbe
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27
Q

what chemokines does the complement system make and what are their roles

A

C3a + C5a –> make chemokines
C3b –> opsonisation
MAC –> membrane attack complex –> lyses microbes directly

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28
Q

what percentage of blood is plasma

A

55%

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29
Q

what percentage of blood are rbc

A

45%

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30
Q

what % of blood plasma are the leukocytes and platelets

A

less than 1%

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31
Q

what progenitor do erythrocytes originate from

A

common myeloid progenitor

32
Q

what progenitor do lymphocytes originate from

A

common lymphoid progenitor

33
Q

what do thrombocytes originate from

A

megakaryocytes

34
Q

what is the function of the thymus

A

secretes thymopoietin to make lymphocytes and it is most active during neonatal and pre-adolescent periods

35
Q

what is the function of eosinophils and what do they inhibit

A

they are leucocytes prevalent in parasitic infections; they have receptors for IgE and they inhibit HISTAMINE –> inhibit basophils and mast cells

36
Q

what makes plasma cells

A

B cells

37
Q

what cells secrete antibodies

A

plasma cells

38
Q

what is humoral immunity

A

production of antibodies by B cells

39
Q

what are CD 4 cells

A

T helper

40
Q

what are CD 8 cells

A

T cytotoxic

41
Q

what are the types of CD4 cells and what are their functions

A

Th1 - makes IFy and IL-2 and promotes T-cytotoxic reactions
Th2 - makes IL-4 and IL-5 and activates B-cells

42
Q

which are the antigen-presenting cells (APC)

A

Dendritic cells
Macrophages (reticuloendothelial system)
B-cells

B cells are antgen presenting to activate other B-cells

T cells are not antigen presnting; they interact with the antigen prsenting cells to activate B cells

43
Q

what are the types of CELL-ASSOCIATED pattern recognition receptors

A

lectin receptors –> detect bacteria carbohydrates
scavenger receptors –> identify bacteria lipids
TLRs (toll-like receptors) –> detect viruses and bacteria

44
Q

what are PAMPs and what receptors in the immune system bind to them

A

Pathogen-associated molecular patterns
found on pathogens
PRR (pathogen recognition receptors) bind to them

45
Q

what are the different sites at which lymphocytes are produced and matured

A

thymus
bone marrow
spleen

46
Q

what happens to T-cells which recognise self in the foetal thymus and why

A

they are destroyed so that your immunity does not attack its own T-cells

47
Q

what is the difference between MHC-1 and MHC-2

A

MHC-1 –> found on all nucleated cells of the body; MHC 1 detects intracellular pathogen and activates CD8 (t-cytotoxic) pathway by presenting the intracellular antigen outside to TC cells
MHC-2 –> found only on antigen-presenting cells; MHC 2 detects extracellular pathogens and activates T-helper cells to activate B-cells and form antibodies

48
Q

what is clonal expansion?

A

Clonal expansion is the rapid multiplication of immune cells in response to an antigen to amplify the immune response

49
Q

explain the function of IL-2

A

when MHC-2 from the antigen-presenting cells binds to the Th cell receptors IL-2 is secreted from the Th cell which acts in an AUTOCRINE way on the IL-2R (IL-2 receptor) on the Th cell –> results in activation

50
Q

what is the role of IL-12

A

if it is upregulated it generates Th 1 cells from Th cells

if it is downregulated it forms Th2 cells from Th cells

51
Q

what type of Th cell mediates asthma attacks

A

Th 2 because allergies are caused by an overreaction to an EXTERNAL stimulus, so the reaction is via MHC-2

52
Q

what do CD8 cells release

A

perforin and granzymes

53
Q

what happens to B cells which recognise self

A

killed in bone marrow

54
Q

structurally what determines the class of an antibody

A

the change in the constant region

55
Q

what are the different types of immunoglobulins and their functions?

A

IgM - very large (can’t migrate through tissues); found at the beginning of an infection

IgG - very specific antibody; most common and smallest –> can easily migrate to tissues

IgE - responds to parasitic threats (attracts eosinophils) and is involved in allergies (triggers mast cell and basophil degranulation)

IgA - expressed in mucosal tissue and breast milk; forms dimers; found in saliva bronchi genito-urinary secretions and protects the neonatal gut

IgD - stimulates B cells to produce antibodies; present on B-cells; activated basophils and mast cells

56
Q

what is the Gell and coombs classification?

A

classification of types of hypersensitivity reactions

57
Q

what part of the antigene does the antibody bind to

A

epitope

58
Q

what is the general role of interferons?

A

produce antiviral resistance in uninfected cells to prevent the spread of the virus

59
Q

what interferons do viral infected cells produce

A

INF alpha and beta

60
Q

what is the function of the colony-stimulating factor?

A

drives division and differentiation of bone marrow stem cells

61
Q

what is the function of TNF (tumour necrosis factor)

A

TNF –> pro-inflammatory and mediates cytotoxic reactions

62
Q

what is the function of chemokines?

A

direct leukocytes to site of infection (chemotaxis)

63
Q

explain how neutrophils undergo extravasation

A
  1. Macrophages encountering the infection release TNF
  2. TNF activates endothelial cells, leading to the expression of adhesion molecules like E-selectin
  3. Neutrophils attach to capillary endothelium via E-selectin
  4. Chemokines establish a concentration gradient between the capillary and the tissue, guiding neutrophils towards the infection site.
  5. Neutrophils bind to chemokines via chemokine receptors, triggering integrin activation.
  6. Integrins on neutrophils bind to endothelial cells, driving the rolling of neutrophils between the endothelial cells down the chemokine gradient.
  7. Neutrophils migrate out of blood vessels and into the infected tissue
64
Q

what is activated if the macrophages and neutrophils can’t handle the infection

A

the complement pathway

65
Q

how do macrophages and neutrophils kill microbes?

A

ROS, enzymes, defensins, TNF, low pH

66
Q

what are DAMPs

A

Damage Associated Molecular Patterns - molecules which are created to alert the body about injury and initiate repair

67
Q

can we recognise our own DNA?

A

no, it is hidden from our pattern-recognition receptors; our PRRs only detect the DAMPs and the PAMPs

68
Q

give examples of secreting and circulating PRRs

A

CRP (C reactive protein)
mannose-binding lectin

these are all proteins which activate the complement system

69
Q

why do steroids enhance bacterial infection?

A

Steroids suppress the immune system by inhibiting the activity of immune cells, including white blood cells like neutrophils and macrophages.

70
Q

what is atopy

A

inherited trait for type 1 hypersensitivity rxns –> tendency to develop allergic rxns

71
Q

explain sensitization of the immune system

A

exposure to allergen causes T-cell activation which leads to differentiation into Th2.

Th2 causes B-cell activation which leads to IgE production and mast cell release of histamines

72
Q

What is the H1 receptor?

A

receptor responsible for allergic reactions
found in bronchi

72
Q

what are the 2 types of tumour antigens and what is the difference between them?

A

Tumour Specific Antigens (found only on tumours)
Tumour Associated Antigens (found on both normal and tumour cells but overexpressed in tumours)
ex.: PSA (prostate-specific antigen is overexpressed in cancers)

73
Q

how do tumours evade the immune system?

A

they promote immune suppressor cells and they trick the immune system into being seen as “self-cells” instead of “non-self”

74
Q

what is the difference between active immunotherapy and passive immunotherapy?

A

active –> involves creating vaccines against the tumour and training the adaptive immune system to fight against the tumour antigens
passive –> involves giving anti-tumour antibodies

phase 2 medicine (15 decks)

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