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PBL SEM 1 > CASE 5 > Flashcards

CASE 5 Flashcards

1
Q

describe B cells

A
  • form and mature in bone marrow
  • then move to lymphatic system to circulate in the body
  • pre-programmed to respond to a particular antigen
  • the antigen and cytokines (produced by T-helper cells) stimulate the B cells to divide
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2
Q

what happens when a naive B cell encounters an antigen that fits?

A

it quickly differentiates into either a memory cell or effector B cell (plasma cell)

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3
Q

what do plasma cells do?

A

secrete monoclonal antibodies

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4
Q

describe T cells

A
  • form in bone marrow and mature in the thymus
  • do not make antibodies
  • have markers on their surfaces (antigens) called CD antigens (express CD8 or CD4, not both). all have CD3
  • populate the lymph nodes, MALT and spleen
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5
Q

when do T cells start to express the CD markers?

A

during maturation in the thymus

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6
Q

T cells can only recognise antigens that are bound to MHC1 and MHC2. what are these MHC molecules?

A

they are membrane-bound surface receptors on antigen-presenting cells

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7
Q

what are the 3 types of T cell and what CD antigens do they express?

A
  1. cytotoxic T cells (killer cells) - CD8 antigens.
    - destroy their targets by releasing perforin
  2. helper T cells - CD4 antigens.
    - regulate immune responses by releasing cytokines
  3. suppressor T cells - CD8 antigens.
    - down regulate both humoral and cell-mediated immune responses
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8
Q

how does perforin, released by Tc cells, work?

A

perforin inserts into the lipid bilayer of the target cell and polymerises into a large membrane channel, permeabilising the cell — kills cell

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9
Q

name 2 primary lymphoid organs

A

bone marrow and thymus

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10
Q

what develops into a macrophage if stimulated?

A

monocytes

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11
Q

what are neutrophils?

A
  • phagocytic cell
  • most abundant and motile WBC
  • 1st to reach the site of infection, involved in inflammation
  • known as polymorphs - can have 2/3/4 lobes of genetic material
  • primary granules contain lysosomes
  • secondary granules contain lysosomes that break down bacterial cell walls and lactoferrin (iron-binding protein)
  • attracted by leukotrienes
  • less effective than other phagocytes but are produced in very large quantities
  • produce adhesion molecules in response to IL-1 and TNFa
  • secrete chemical mediators that attract macrophages before they die (die once they have phagocytosed a pathogen)
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12
Q

name 3 types of phagocytes

A

macrophage, neutrophil, dendritic cell

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13
Q

describe dendritic cells

A
  • Langerhans cells in the skin and mucosa
  • also found in lymph nodes
  • antigen-presenting cells
  • in skin-infections, the Langerhan cells engulf the pathogens, presenting the antigens on its surface
  • then travel to lymph nodes where they activate CD4 cells (T Helper cells)
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14
Q

describe natural killer cells

A
  • cytotoxic lymphocytes
  • less selective than other lymphocytes
  • produce perforins, causing interstitial fluid to enter the bacterial cell
  • produce granzymes that induce apoptosis in target cell
  • activated more quickly than T and B lymphocytes
  • activated by cytokines
  • cell itself remains unharmed so can go onto kill other cells
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15
Q

name the 5 stages of infection

A
  1. entry into body (infection)
  2. replication and spread
  3. disease
  4. exit from the body (infect others)
  5. reinfecton
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16
Q

intracellular vs extra cellular pathogens

A

intracellular = spread by cell to cell contact

extracellular = spread by lymphatics and the blood stream

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17
Q

what is the innate immune response?

A

= pre-existing immunity, doesn’t amplify with repeated attacks by the same pathogen, no memory, non-specific

  • physical barriers (skin, resp tract, GI tract, eyes)
  • antimicrobial and pro-inflammatory factors
  • phagocytes and natural killer cells
  • inflammation/fever
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18
Q

what are interferons?

A

= a cytokine

  • released by activated macrophages and lymphocytes and virally affected cells.
  • act internally in these cells and they also bind to receptors on normal cells, causing them to produce antiviral proteins. these proteins interfere with viral replication inside the cell
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19
Q

what is lactoferrin?

A

= an iron-binding protein

  • binds to iron
  • this removes essential substrate required for bacterial growth
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20
Q

what are TLRs?

A

= toll-like receptors

  • recognise pathogen associated molecules
  • around 11 found in humans
  • give recognition potential to cells of the innate immune system

eg. TLR5 binds to flagellin
TLR4 binds to lipopolysaccharide from bacterial cell wall

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21
Q

phagocytes

A
  • ‘eating cells’
  • monocytes in blood that develop into macrophages in tissue
  • neutrophils in blood — less effective but produced in v. large quantities. granules contain toxic substances. live for about 5 days in blood and get attracted to tissue where they eat a couple bacteria and turn into pus
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22
Q

what is pus?

A

= death of phagocytes

= a collection of alive/dead/dying microbes/phagocytes/local tissue cells

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23
Q

how do natural killer cells work?

A

= large, granular lymphocytes that are activated by cytokines

  1. recognise virally infected cells using various receptors
  2. kill virally infected cell by apoptosis using perforin and granzymes
  3. NK cell itself is unharmed so it can go on to kill other cells
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24
Q

what are 4 symptoms present at the site of infection?

A
  • redness
  • swelling
  • heat
  • pain
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25
Q

what are the 6 stages of inflammation?

A
  1. secretion of chemical mediators of inflammation
  2. vasodilation
  3. increased vascular permeability
  4. activation of adhesion molecules
  5. chemotaxis
  6. recruitment of macrophages
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26
Q

name the chemical mediators of inflammation (CMOI)

A
  1. prostaglandins - causes vasodilation
  2. histamine - cause vasodilation, increase vascular permeability
  3. platelet activating factor (PAF) - increase vascular permeability
  4. cytokines - secreted by certain cells of the immune system and have an effect on other cells
    - IL-1 — causes production of adhesion molecules
    - IL-1B — induces fever
    - TNFa — causes production of adhesion molecules, induces fever
    - leukotrienes — attracts neutrophils from blood stream
    - IL-8 — attracts neutrophils to site of inflammation once the neutrophils have entered the tissue from the blood stream
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27
Q

what are the stages of CMOI?

A
  1. macrophages (in dermis) secrete prostaglandins, PAF, and cytokines (IL-1, IL-8, leukotrienes, TNFa)
  2. tissue mast cells and damaged tissue cells secrete histamine, prostaglandins, PAF and cytokines (IL-1/8/1B, leukotrienes, TNFa)
  3. leukotrienes attract neutrophils to injury site
  4. the other CMOI have 5 effects:
    - vasodilation
    - increase vascular permeability
    - activation of adhesion molecules
    - chemotaxjs
    - fever
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28
Q

describe vasodilation

A
  • due to secretion of histamine and prostaglandins
  • these bind to receptors on capillaries, causing them to dilate
  • increase blood flow to site of injury — area of injury becomes red and hot
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29
Q

describe increased vascular permeability

A
  • due to secretion of histamine and PAF
  • these bind to receptors on endothelial cells of capillaries
  • causes endothelial cells to shrink — forms interendothelial gaps
  • allows protein rich fluid (exudate) to leak from capillaries to the site of injury
  • causes swelling
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30
Q

what causes erythema (redness)?

A

RBCs may also leak through

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31
Q

describe activation of adhesion molecules

A
  • due to secretion of IL-1 + TNFa
  • these have 2 effects: 1. cause production/activation of adhesion molecules on the endothelial cells so that they may attract neutrophils from the blood stream. 2. cause neutrophils in the blood stream to produce adhesion molecules so that they may ‘adhere’ to endothelial cells (which already possess adhesion molecules)
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32
Q

name 2 types of adhesion molecules

A
  1. selectins

2. integrins

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33
Q

describe selectins

A
  • develop 1st on endothelial cells
  • ‘select’ for neutrophils in the blood
  • circulating neutrophils have complementary receptors to selectins
  • neutrophil loosely binds to selectins and rolls along the endothelial lining
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34
Q

describe integrins

A
  • develop 2nd on the neutrophils
  • ‘integrate’ with the endothelial lining
  • the endothelial cells have complementary receptors to integrins
  • endothelial cells bind strongly with the neutrophils and cause the neutrophils to stop rolling
  • causes the endothelial lining to be coated with neutrophils — pavementation
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35
Q

describe chemotaxis

A
  • after pavementation, neutrophils pass through the interendothelial gaps = extravasation
  • neutrophils produce collagenases that break down the basement membrane of the capillary
  • neutrophils now enter site of injury
  • CHEMOTAXIS = THE DIRECTIONAL MOVEMENT OF WBCS DETERMINED BY THE CONCENTRATION OF CHEMOTACTIC AGENTS (IL-8)
  • the conc of IL-8 is highest at the site of the injury
  • causes WBCs to move towards the centre of the site of the injury
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36
Q

what occurs at the site of the injury?

A

neutrophils phagocytise the pathogens

  • pathogen becomes coated with the antibody IgG and eventually C3b
  • neutrophils have complementary receptors to both of these
  • pathogen phagocytosis by either direct or indirect opsonisation
  • neutrophils engulf the pathogen — forms phagosome
  • phagosome binds to lysosome — forms phagolysosome
  • the pathogen killed and its contents are secreted
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37
Q

what happens to the neutrophil once is has phagocytosis the pathogen?

A

it dies

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38
Q

describe the recruitment of macrophages

A
  • before the neutrophils die, they secrete chemical mediators that attract macrophages (stronger phagocytes) to the site of injury
  • monocytes (in bloodstream) differentiate into macrophages in tissue
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39
Q

what do macrophages secrete?

A

prostaglandins, PAF, cytokines (IL-1/8, TNFa)

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40
Q

what triggers a fever and what are its effects?

A
  • triggered by IL-1B + TNFa
  • act on hypothalamus (where thermostat is)
  • these increase body temperature — inhibits bacterial growth and speeds up certain metabolic reactions and immune system eg. phagocytosis and antibody production
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41
Q

what 3 characteristics does the adaptive immune system have that the innate system doesn’t?

A
  1. specificity
  2. memory
  3. discrimination between self and non-self
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42
Q

what is the adaptive immune system split into?

A

humoral immunity and cell-mediated immunity

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43
Q

what are the 4 stages of adaptive immunity?

A
  1. inflammation
  2. phagocytosis
  3. Th- cell activation and clonal expansion
  4. B lymphocyte activation, clonal expansion and differentiation into plasma cells
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44
Q

what is humoral immunity?

A

= antibody or immunoglobulin mediated immunity

  • MHC class 2 proteins
  • B cells differentiate into memory cells and effector cells (plasma cells)
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45
Q

A LEVEL HUMORAL RESPONSE

A
  • macrophage presents antigens to B cell
  • the surface antigens of an invading pathogen are taken up by a B cell
  • the B cell’s specific complementary receptors bind to the antigens
  • B cell engulfs and digests the antigen
  • B cell divides by mitosis — clones form (clonal expansion)
  • some of the clones differentiate into memory cells but most differentiate into plasma cells
  • plasma cells make and secrete antibodies
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46
Q

describe the structure of an antibody (regular IgG antibody)

A
  • 4 peptide chains
  • 2 heavy chains, 2 light chains
  • 1 constant region (Fc), 2 variable regions (Fab - antibody binding fragment)
  • disulphide bridges join peptide chains
  • hinge region joins L and H chains
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47
Q

what is agglutination?

A

antibodies cause microbes to stick together, making it easier for the phagocytes to idenitfy and engulf pathogens

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48
Q

different heavy chain = different functions. name 5 different heavy chains and their functions

A
  1. IgG = blood and tissue antibody, monomer, standard antibody, transplacental transfer, fixes complement, binds phagocytes, neutralises toxins
  2. IgM = blood antibody, pentimer, acts as a B cell receptor, fixes complement, produced 1st
  3. IgA = secretory antibody, 2 x IgG, protection at mucosal surfaces
  4. IgE = binds to mast cells and basophils, important in multicellular parasite infections
  5. IgD = membrane receptor
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49
Q

how do antibodies protect against infection? — 3 ways

A
  1. block binding of pathogens and toxins (antibody binds to the bacterial toxins, forming immune complexes. these complexes are ingested by phagocytes)
  2. facilitate phagocytosis
  3. kill bacteria by activating complement
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50
Q

what is opsonisation?

A

the coating of bacteria by antibody — antibodies/opsonises coat the bacteria so it is targeted for phagocytosis by macrophages and neutrophils, then destroyed inside the cell

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51
Q

what is a slime layer

A
  • bacteria capsule = a polysaccharide capsule outside cell wall
  • can be cause of various diseases, found in gram positive and negative bacteria
  • when the secretion that makes up the capsule diffuses into the surrounding medium and remains a loose, demarcated secretion = slime layer
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52
Q

what is the importance of a slime layer?

A
  • a virulent factor as it enhances ability of bacteria to cause disease eg. prevents phagocytosis and engulfment by macrophages
  • a capsule-specific antibody may be required for phagocytosis
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53
Q

what is the result of a severe block in B cell development?

A

hypogammaglobinaemia (low antibody in blood — immunodeficiency)

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54
Q

what MHC proteins are used in cell-mediated immunity?

A

MHC class 1 proteins

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55
Q

what type of cells express MHC class 1 and what cells produce MHC class 2?

A 
MHC class 1 = all nucleated cells 
MHC class 2 = antigen-presenting cells (dendritic cells, monocytes, macrophages, B cells)
56
Q

what do dendritic cells do in lymph nodes?

A

present antigens to T cells

57
Q

on what chromosome is the gene for MHC?

A

chromosome 6

58
Q

what is CD 3?

A

= T cell receptor

- all T cells express this

59
Q

role of MHC proteins

A
  • allow T cells to detect cells such as macrophages that have ingested infected organisms
  • macrophage engulfs a microorganism, then displays peptide fragments of the microbe on its surface, attached to MHC molecules
  • allows the T lymphocyte to detect to foreign fragment bound to MHC
60
Q

CD4+ vs CD8

A 
CD4+ = MHC class 2 - helper T cells 
CD8 = MHC class 1 - cytotoxic T cells and suppressor T cells
61
Q

A LEVEL CELL-MEDIATED IMMUNITY

A
  • pathogens invade body cells or are taken in by phagocytes
  • viral DNA causes host cell to express viral antigens on its surface = antigen-presenting cell
  • helper T cell attaches to viral antigen on infected cell using its receptor which perfectly fits the antigen
  • the attachment activates the T cell to divide rapidly by mitosis and form clones
  • the cloned cells: a. develop into memory cells. b. stimulate phagocytes to engulf pathogens. c. stimulate B cells to divide. d. activate Tc cells to kill infected cells by making holes in their cell-surface membrane
62
Q

how do CD4 T cells (Th cells) promote proliferation of CD8 T cells?

A
  1. antigen-specific T cells are activated by dendritic cells in lymph nodes
  2. activated CD4 T cells secrete IL-2
  3. activated T cells proliferate and become effector T cells
  4. effector T cells leave the lymph mode and migrate to site of infection
63
Q

what do TH1 cells do and how do they do this?

A

= activate macrophages to kill intracellular microorganisms

  1. infected macrophages express surface membrane MHC class 2 and pathogen peptides
  2. TCR on activated Th1 cells bind MHC class 2 and peptides
  3. Th1 cells secrete IFN-y which activates macrophages to kill the pathogen
64
Q

what does AIDS stand for and what is it?

A

acquired immunodeficiency syndrome — caused by HIV infection of the mature T lymphocyte

65
Q

symptoms of late stage HIV

A
  • unintentional wight loss > 10%
  • weakness, fever, nutritional deficiencies, diarrhoea
  • malabsorption + insufficient dietary intake
  • enteric infections eg. cyrptosporidiosis and microsporidiosis
66
Q

what is the target of HIV? what is the response?

A
  • CD4 helper cell.
  • CD8 cells recognises the HIV expressed on the surface of Th cell in the context of the MHC class 1 molecule.
  • kill Th cell by apoptosis
  • results in compromised immune function as the Th cells are essential for Tc cell activation, macrophage activation and also the production of antibody by B cells
67
Q

what cells are involved in both innate and adaptive immunity?

A

T cells and NKCs

68
Q

name key characteristics of a virus

A
  • most abundant and earliest organisms on earth
  • infect animals plants, bacteria, fungi
  • consist of a protein (+/- lipid) coat surrounding a core of genetic material
  • can only replicate inside living things - obligate intracellular parasite
  • either a DNA or RNA virus
  • either single stranded or double stranded genetic material
  • multiple ‘families’
69
Q

what are the origins of HIV? when was the peak of the epidemic?

A
  • evolved from the related simian immunodeficiency virus (SIV)
  • SIV infects wild apes in central/west African forests
  • ‘jump’ to humans around 1920s
  • rapid increase across globe in 80s
  • peak in 2004
70
Q

what are the 2 different chains of HIV?

A
  1. HIV-1 - origin = chimpanzee found to be positive for HIV-1 antibodies against SIV retrovirus. hunters ate chimpanzees affected by SIV. SIV mutated to affect humans — HIV
  2. HIV-2 - origin = sooty mangabey monkeys, rarely found outside Africa
71
Q

what is a retrovirus?

A
  • an RNA virus that inserts a DNA copy of its genome into the host cell in order to replicate
  • viral genome is in the form of RNA
  • uses reverse transcriptase
72
Q

what is the role of reverse transcriptase?

A

concerts viral RNA —> DNA

73
Q

what are the 2 forms of a retrovirus?

A
  1. endogenous — normal genetic elements in chromosomal DNA. not generally pathogenic
  2. exogenous — transmitted from human to human eg. HIV
74
Q

what is the structure of HIV?

A
  • external lipid belayer and glycoproteins envelope
  • internal protein core: surface = capsid
  • the genetic material is inside the capsid
  • Gp120 — enables protein to attach top receptors on host cell = “docking glycoprotein”
  • Gp41 — transmembrane protein. enables virus to fuse membrane and pass across membrane
  • p10 protease enzymes
  • p32 intergrase enzymes
75
Q

why does HIV have lots of variants?

A

has a very high mutation rate

76
Q

how does HIV infect target cell?

A
  • gp120 binds to CD4 receptor (any cell with a CD4 receptor can be infected)
  • once in cell, virus loses its membrane
  • genetic material now free
  • reverse transcriptase transcribes viral RNA —> DNA
  • viral DNA integrated into host DNA by HIV Intergrase (once the host cell is activated)
  • cell programmed by virus RNA to start making copies of the viral genome
  • HIV protease: genome packaged into a membrane
  • mature virus released by cell (‘budding’) into blood stream — can now infect other cells
77
Q

what do antiretroviral drugs do?

A

= block key steps in life cycle

  1. fusion/entry inhibitors. co-receptor blockers.
  2. reverse transcriptase inhibitors
  3. integrate inhibitors
  4. protease inhibitors
78
Q

what is the key to managing HIV and why?

A

use at least 3 drugs as HIV mutates a lot

79
Q

there is no cure for HIV, so what does HIV treatment aim to do?

A

treatment aims to prolong the latent stage, and thus the development of AIDS

80
Q

what is HAART?

A

highly active antiretroviral therapy

81
Q

NRTIs vs NNRTIS

A

NRTIs (nucleoside reverse transcriptase inhibitors) need intracellular phosphorylation to be activated eg. Tenofovir and Emtricitabine

NNRTIs (non nucleoside reverse transcriptase inhibitors) do not need intracellular activation - bind directly to reverse transcriptase. do mot work against HIV-2. eg. Efavirenz

82
Q

protease inhibitors

A

cause viral maturation to be impaired and immature dysfunctional viral particles are produced

83
Q

integrase inhibitors

A

acts as competitive inhibitors to integrate by binding to the enzyme

84
Q

irrespective of CD4 count, after 6 months of ART people living with HIV…..

A
  1. are not at risk of HIV-associated opportunistic infections or malignancies (such as kaposi sarcoma - cancer of GI tract)
  2. cannot transmit HIV to their sexual partners during unprotected sex: UNDETECTABLE = UNTRANSMISSIBLE
85
Q

what are the 3 stages of HIV infection?

A
  1. infection
  2. latent stage
  3. development of AIDS
86
Q

immune response of HIV

A
  1. infected cells, via the endogenous pathway, present viral proteins with MHC-1 on their surface. CD8 cells (killer T cells) kill these infected cells
  2. antibodies for gp120 envelope and p24 are produced (complement or opsonisation) - seroconversion
  3. immune response eliminates 99% of the virus
87
Q

consequences of immune response to HIV

A
  • CD4 cell count begins to decrease

- the virus enters the latent stage

88
Q

why is HIV not completely eradicated by the immune response?

A
  • very high replication rate
  • can hide as a provirus where it is not detectable by the immune system
  • very high mutation rate
89
Q

what is used to test for HIV infection?

A

the detection of antibodies for HIV

90
Q

what occurs in latency?

A
  • generally asymptomatic (a few patients have swollen lymph nodes)
  • viral DNA lies dormant as a provirus
  • CD4 cell count decreases slowly
  • individuals with a lower level or viraemia in latency develop AIDS slower
91
Q

what is the average time from infection of HIV to the development of AIDS?

A

10 years — most of this time is spent in the latent stage

92
Q

what is AIDS defined clinically as?

A

1) the appearance of major opportunistic infections

2) or by a drop in the CD4 T cell count below 200 cells/ul of blood

93
Q

what are the main causes of death in AIDS?

A

pneumonia caused by Pneumocystic jivoreci and Mycobacterium Tuberculosis

94
Q

what are the main methods of transmission of HIV?

A

blood, semen (cum), pre-seminal fluid (pre-cum), rectal fluids, vaginal fluids, breast milk (mother to baby) — these fluids must come in contact with a mucus membrane or damaged tissue or be directly injected into the bloodstream for transmission to occur

95
Q

what are 3 HIV indicator conditions?

A
  1. severe oral candidiasis
  2. cryotococcal meningitis
  3. pneumococcal pneumonia
96
Q

what is candida?

A
  • yeast
  • causes fungal infections
  • HIV: mucosal infections as a result of candida
  • oral candida is one of the most common conditions — creamy plaques in the mouth and pharynx
97
Q

‘immunity’ to HIV

A
  • CCR5 (aka CD195) is a protein on the surface of lymphocytes, co-receptor for HIV
  • mutation in CCR5 gene: delta 32 = deletion of 32 base pairs in CCR5 sequence, arose in Eastern Europe, homozygous — cannot be infected with HIV, heterozygous — delayed progression of disease
98
Q

what is the window period?

A

the time it takes someone to make antibodies — majority by 4 weeks, nearly all by 3 months

99
Q

3rd vs 4th generation testing

A

3rd generation = antibody only

4th generation = assays detect HIV 1 and 2 antibody and p24 antigen

100
Q

what is Pneumocystis Jiveroci?

A
  • a yeast-like fungus
  • causes pneumonia
  • seen among immunocomprimised hosts
  • seen when CD4 count falls below 200
  • damages alveolar epithelium, which impedes gas exchange and reduces lung compliance
101
Q

what is pneumonia and what are its symptoms?

A
  • inflammation of the lung caused by infection, in which the alveoli fill with pus and may become solid.
  • symptoms: shortness of breath, non-productive cough, fever and discomfort
102
Q

what are the paired lymphatic trunks?

A
  • jugular
  • subclavian
  • bronchomediastinal
  • lumbar
103
Q

give examples of where MALT is

A
  • Peyer’s patches
  • tonsils
  • GI tract
  • lung
  • salivary glands
  • nasopharynx
  • thyroid
  • skin
  • eye
104
Q

what are the types of tonsils and where are they?

A
  • lingual = within the mucosa of the posterior third of the tongue
  • pharyngeal = roof of nasopharynx
  • tubal = lateral wall of nasopharynx
  • palatine (‘the tonsils’) = tonsillar bed of the lateral oropharynx wall
105
Q

basophils and mast cells have high affinity receptors for the fc region of which immunoglobulin?

A

IgE

106
Q

what is opsonisation?

A

where antibodies or complement coat foreign particles to give phagocytes a place to bind to

107
Q

what is diapedisis?

A

the flattening of neutrophils to allow them to pass through capillary pores into tissues

108
Q

what is chemotaxis?

A

attraction of neutrophils to the site of injury by inflammatory chemicals

109
Q

what are the first cells activated in the inflammatory response?

A

macrophages

110
Q

Tenofovir a component of the anti HIV drug truvada works by what mechanism?

A

nucleotide reverse transcriptase inhibitor

111
Q

MHC class 1 molecules are present on what cells in the body?

A

all cells in the body except RBCs and platelets

112
Q

name the 5 stages of phagocytosis

A
  1. chemotactic attraction of phagocytes
  2. adherence to microbe
  3. ingestion to form a phagosome
  4. formation of phagolysosome
  5. destruction of microbe
113
Q

after taking a rapid HIV antibody test, how long must the patient wait for a result?

A

30 minutes

114
Q

the HIV virus uses what structure to code its genetic information?

A

+ve single strand RNA

115
Q

what is the name of the coreceptor to which HIV binds?

A

CCR5

116
Q

what is the most numerous cell involved in the innate immune response?

A

neutrophil

117
Q

which is the only antibody which can cross the placenta?

A

IgG

118
Q

which cells present antigens to B cells?

A

dendritic cells

119
Q

CD4 T cells will only recognise antigen if it is presented too them on what?

A

class 2 MHC protein

120
Q

what does triple therapy for HIV consist of?

A

2 reverse transcriptase inhibitors and a protease inhibitor

121
Q

due to the complement system, what do pathogens become coated with and why is this important?

A

become coated with IgG and C3b — neutrophils have complementary receptors for these so allow them to be phagocytosed

122
Q

describe eosinophils

A
  • bi-lobular genetic material
  • involved in type 1 hypersensitivity reactions and combating multicellular parasites with IgE
  • granules contain histamine (reduce inflammation), enzymes that destroy leukotrienes (reducing attracting of neutrophils) and enzymes (peroxidase) that combat multicellular parasites
123
Q

describe basophils

A
  • least common granulocyte
  • partially bi-lobular genetic material
  • involved in type 1 hypersensitivity
  • granules contain histamine and heparin (anti-coagulant)
  • have receptors for IgE
124
Q

major granulocytes vs non-granulocytes

A

major granulocytes = neutrophils, basophils, eosinophils

non-granulocytes = monocytes/macrophages, lymphocytes

125
Q

describe monocytes/macrophages

A
  • monocytes develop into macrophages if stimulated
  • activated by interferon-y
  • monocytes in blood, macrophages in tissue
  • macrophages are phagocytes
  • involved in inflammation
  • macrophages (in dermis) secrete prostaglandins, PAF, and cytokines (IL-1/3, TNFa)
  • attracted by neutrophils before they die
  • Th1 cells activate macrophages to kill intracellular microorganisms
126
Q

what are the two secondary lymphoid organs where T and B lymphocytes come into contact with antigen ?

A

spleen and lymph nodes

127
Q

how do viral antigens activate the immune system?

A

presentation with MHC class 1 to CD8 T lymphocytes

128
Q

what is the most efficient complement binding antibody?

A

IgM

129
Q

drug treatment for HIV is most likely to inhibit what?

A

nucleic acid synthesis

130
Q

when do T cells help B cells make antibody?

A

after recognising antigen plus MHC class 2 on the B cell surface

131
Q

the rate at which new cases of a disease arise in a population during a specified time is known as what?

A

incidence

132
Q

in comparison with a primary antibody response, a secondary response…

A

is dominated by IgG production

133
Q

the only antigen-presenting cell that can present antigen in a primary immune response is what?

A

dendritic cell

134
Q

what is the most important phagocytic cell in clearing bacterial infections?

A

neutrophil

135
Q

what is the macrophage activation factor critical for immunity against intracellular pathogens such as mycobacteria?

A

interferon-gamma

136
Q

what is the factor most important in immunity against multicellular parasites?

A

IgE

PBL SEM 1 (9 decks)

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