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PBL SEM 1 > CASE 6 > Flashcards

CASE 6 Flashcards

1
Q

what are the effects of mast cells and basophils in the innate immune system?

A

vascular leak, bronchoconstriction, intestinal hyper mobility, inflammation

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2
Q

what is the effect of eosinophils in the innate immune response?

A

granules contain cytotxic cationic granule proteins (capable of producing tissue damage) and histamine

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3
Q

mast cells vs basophils

A

mast cells — present in relatively high numbers in skin and mucosa, can survive for months or years in situ

basophils — minority population, can only survive a few days in the blood

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4
Q

mast cell responses in the skin

A

increased blood flow and increased permeability — vasoconstriction, endothelial cell activation, cellular recruitment (neutrophils and eosinophils)

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5
Q

mast cells responses in airways

A

decreased diameter and increased mucus — coughing (expulsion), immobilisation of pathogen by mucus and cytoprotection

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6
Q

mast cell responses in GI tract

A

increased fluid secretion and increased peristalsis — expulsion of GIT contents (parasites), immobilisation of pathogen by mucus and cytoprotection

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7
Q

mast cell responses in blood vessels

A

increased blood flow and increased permeability — increased tissue fluid, lymph flow to lymph nodes, cells/protein in tissues

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8
Q

name 2 functions of eosinophils

A
  1. attack multicellular parasites

2. tissue remodelling

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9
Q

what antibody is mainly responsible for the initial immune response after a 1st vaccination?

A

IgM

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10
Q

what antibody is mainly responsible for the initial immune response after the 2nd vaccination?

A

IgG

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11
Q

name 5 actions of T lymphocytes in cell-mediated immunity

A
  1. kill virus-infected cells
  2. resistance against intracellular pathogens
  3. activate macrophages
  4. help antibody respones
  5. immunoregulatory function
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12
Q

T cells cannot see antigen in isolation. what do they need to see it with?

A

need to see antigen in the context of an antigen-presenting cell (eg. dendritic cell) and in the context of MHC

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13
Q

MHC class 1 vs class 2

A 
CD8 lymphocytes (cytotoxic T cells and suppressor T cells) — MHC class 1
CD4 (T Helper cells) — MHC class 2
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14
Q

endogenous pathway vs exogenous pathway

A

endogenous pathway (intracellular antigens) — MHC class 1 on outside, viral or intracellular bacteria are fragmented then cross cell membrane by transporter protein. CD8 T cells

exogenous pathway (extracellular antigens) — MHC class 2, endocytosis. CD4 T Helper cells

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15
Q

what is CD3?

A

= part of T cell receptor complex

- all T cells express this

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16
Q

what is CD4+?

A
  • T helper cells
  • MHC Class 2 restricted
  • helps activate Tc cells, activates macrophages (Th1) and helps antibody responses (Th2)
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17
Q

what is CD8+?

A
  • Tc cells

- kill virus infected cells

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18
Q

by what mechanism do T and B cell antigen receptors form?

A

random recombination events and gene rearrangement

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19
Q

how do self-reactive antigen receptors arise and why do we limit the production of them?

A

= random selection of gene segments from a large gene pool generates >10^7 antigen specificities and therefore can generate self-reactive antigen receptors due to the wide range of possibilities.
— we limit the production of self reactive T and B cells to prevent the immune system from making tissue damaging reactions against self proteins

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20
Q

how many rounds of selection to T cells undergo to get rid of unwanted self-reactive T cells and what are the rounds?

A

2 rounds of selection =

  1. positive selection — for host MHC class 1 or 2. at this stage the cells are double positive. if T cell fails to recognise host MHC and self-peptide it is deleted — apoptosis
  2. negative selection — to remove self-reactive T cells. occurs when double positive T cells bind to bone marrow derived antigen presenting cells, macrophages and dendritic cells, expressing class 1 or 2 MHC with self peptides (low affinity cells escape)
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21
Q

what is a double positive T cell?

A

expresses both CD4 and CD8 molecules

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22
Q

what are the 2 populations of T reg cells?

A
  1. natural T regs = produced in thymus

2. inducible T regs = produced in periphery, usually mucosa

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23
Q

what do T reg cells do?

A

produce anti-inflammatory cytokines (inhibit proliferation of nearby cells), IL-10 + TGF-B (control/dampen down immune system responses — prevent allergy and autoimmunity)

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24
Q

what is an autoimmune disease?

A

a disease that develops when a specific immune response develops to self-antigen

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25
what is allergy?
inappropriate or excessive immune responses to allergens
26
what is an allergen?
an antigen that triggers allergic respones
27
what are induction and elicitation?
- induction = 1st exposure — individual is ‘primed’ | - elicitation = subsequent exposure to same allergen — sensitised individual shows clinical manifestations
28
describe the different types of hypersensitivity
- type 1 = immediate hypersensitivity - type 2 = cytotoxic reactions - type 3 = immune complex disorders - type 4 = delayed hypersensitivity
29
describe type 1 hypersensitivity
= acute/immediate — occurs within minutes - IgE mediated - most allergic reactions (food allergy, asthma, rhinitis, atopic eczema)
30
how does anaphylactic shock come about after a large load of allergen?
large load of allergen —> increases vascular permeability and airway constriction —> can’t supply vital organs and fall in blood pressure —> anaphylactic shock
31
what is the sensitisation phase of type 1 hypersensitivity?
- the Fc part of IgE binds to mast cells/basophils, exposing its variable region - mast cells/basophils are ready to work the next time the pollen appears - when the antigen reappears, they will come into contact with sensitised (IgE-loaded) mast cells and stimulate it and cause an initial phase reaction and secondary reaction
32
how long does IgE loading take?
10-15 days
33
what is the initial phase reaction in type 1 hypersensitivity?
upon stimulation, the mast cells undergo degranulation, secreting preformed products (primary mediators)
34
what are the preformed products (primary mediators)
include histamine and proteases
35
what are the effects of proteases?
proteases do further tissue damage, causing the release of more inflammation mediators
36
what are the effects of histamine?
- vasoconstriction - increased vascular permeability leading to partial oedema in the area - spasmatogenic: histamine receptor are found on smooth muscle lining of the various tracts. histamine causes them to contract - increases glandular secretions = luminal obstruction - causes narrowing of the lumen of the tract
37
what is the secondary reaction of type 1 hypersensitivity?
upon stimulation, the mast cells secrete cytokines
38
what cytokines are secreted by the stimulated mast cells?
IL-3, IL-5 and leukotrienes
39
why are the cytokines termed secondary mediators?
because they are not pre-formed
40
what are IL-3 and IL-5?
cytokines — they are chemotactic agents for eosinophils
41
what do eosinophils do in the secondary reaction?
eosinophils secrete their glandular contents: histaminases (reduce inflammation) and enzymes that destroy leukotrienes (reducing attraction of neutrophils)
42
what is the role of the leukotrienes?
attract neutrophils (phagocytic cell)
43
type 1 hypersensitivity reactions effect on the skin
increased blood flow and permeability — increased fluid, redness, swelling, rashes
44
type 1 hypersensitivity reactions effect on airways
decreased diameter and increased mucus — congestion/blockage of airways (wheezing, coughing, phlegm, swelling/mucus secretion)
45
type 1 hypersensitivity reactions effect on the GI tract
increased fluid secretion and peristalsis — expulsion of GI tract contents (diarrhoea, vomiting)
46
type 1 hypersensitivity reactions effect on blood vessels
increased blood flow and permeability — increased tissue fluid, lymph flow to lymph nodes, cells/protein in tissues
47
treatment of type 1 hypersensitivity reactions and diagnosis
DIAGNOSIS = detection of IgE 1. antihistamines 2. mast cell stabilising compounds 3. topical and systemic corticosteroids 4. for systemic anaphylaxis: adrenaline (EpiPen)
48
describe a type 2 hypersensitivity reaction
= cytotoxic hypersensitivity - occurs when IgG or IgM attack intrinsic antigens bound to cell surfaces - IgG antibodies against cell/matrix associate antigens causing cell lysis or phagocytosis - eg. some drug allergies
49
what is the antigen in a type 2 hypersensitivity reaction?
cell/matrix
50
penicillin allergy is a type of what hypersensitivity reaction?
type 2
51
describe type 3 hypersensitivity
= immune complex hypersensitivity - specific immune responses to innocuous antigens resulting in pathology - occurs when IgG forms free antigen-antibody complexes i tissue fluids or in circulation that are deposited in different tissues - at the sites of deposition, these complexes activate complement and trigger intense inflammation — tissue destruction - occurs 9-10 hours after exposure to antigen - eg. serum sickness, autoimmune diseases such as acute glomerulonephritis
52
describe type 4 hypersensitivity
- mediated by Th1 cells/ Tc cells - signs appear 12-72 hours after exposure - antigen presented with MHC2 to a Th1 cell - if Th1 cell is primed it will become activated — releases chemokines to recruit macrophages and cytokines (eg. interferon-y) to activate them - CD4 cells also secrete IL-2 which activated Tc cells - eg. Crohn’s Disease, multiple sclerosis, type 1 diabetes melitus, contact dermatitis
53
what do the activated macrophages do in a type 4 hypersensitivity reaction?
release pro-inflammatory factors, leading to local swelling, oedema, warmth and redness
54
diagnosis and treatment of type 4 hypersensitivity reactions
DIAGNOSIS — patch testing treatment: identification of allergen = avoidance, mid to high potency topical corticosteroids, extensive (>20% systemic steroids)
55
what does breastfeeding provide?
1. natural nutrition to newborn and infant 2. IgG antibodies 3. secretory IgA antibodies 4. lysosomes
56
what is the possible consequence of prematurely discontinuing breastfeeding?
may facilitate pathogenesis of many chronic diseases later in life eg. autoimmune disorders
57
what is staphylococcus aureus?
= gram-positive bacteria - round-shaped (cocci-shaped) - frequently found in the upper respiratory tract and on the skin - common cause of skin infection by breaching the barrier (eg. in dry skin)
58
how do disease associated strains of S. aureus often promote infection?
by producing potent protein toxins and expressing cell-surface proteins that bind and inactivate antibodies
59
what is MRSA?
methicillin-resistant staphylococcus aureus
60
treatment of a staph infection? problem?
penicillin — however penicillin resistance is very common
61
what is eczema?
= a chronic inflammation of the skin (“boil over”) | - also referred to as atopic dermatitis (inflammation of the skin)
62
what are the common symptoms of eczema?
- redness - skin oedema (swelling) - itching and dryness - crusting - flaking - blistering - cracking - oozing - bleeding
63
what are the 2 types of eczema?
1. atopic dermatitis (atopic eczema = type 1 HS) | 2. contact dermatitis (type 4 HS)
64
what are the 2 different causes of atopic dermatitis?
1. genetics — inherited mutated gene of filaggrin (ichthyosis vulgaris) 2. environment — defective barrier function — insufficient filaggrin and immune dysregulation (increases serum IgE 80%)
65
what is filaggrin?
involved in keratinocyte adhesion. important in the skin barrier’s function
66
what are the 2 different types of contact dermatitis?
1. allergic: type IV hypersensitivity reaction (delayed) | 2. irritant: direct reaction to irritant
67
how can more potent drugs lead to deformation of the skin?
a drug of higher potency can have detrimental side effects because steroids work by affecting protein synthesis in the skin and so using a drug of increased potency (or using a drug in the long term) can lead to deformation of the skin
68
what cytokine is responsible for the sensation of an itch?
IL-31
69
what are corticosteroids?
steroid hormones, either produced by the body or man-made
70
name 2 naturally occurring steroids and where they are produced
cortisone and hydrocortisone — produced by the outer portion of the adrenal gland — the cortex
71
name the 2 different types of corticosteroids and what they do
1. GLUCOCORTICOIDS (anti-inflammatory) — suppress inflammation and immunity, and assist the breakdown of fats, carbs, and proteins. increase blood sugar when in stress and inhibit transcription of chemokines (to suppress the immune system) 2. MINERALOCORTICOIDS (salt-retaining) — regulate the balance of water and salt in the body. promote sodium retention in the kidney
72
in the bloodstream, corticosteroids are bound to transport proteins. what is the name of the proteins?
transcortins
73
how to corticosteroids exert their effects?
exert their effects by determining which genes are transcribed in the nuclei of their target cells, and at what rates
74
what is the adrenal (suprarenal) gland divided into?
divided into 2 parts with separate endocrine functions. 1. superficial suprarenal cortex 2. inner suprarenal medulla
75
what is the superficial suprarenal cortex divided into and what are its functions?
divided into 3 zones: 1. outer zona glonerulosa — produces mineralocorticoids (aldosterone) 2. middle zona fasciculata — produces glucocorticoids (hydrocortisone/cortisol) 3. inner zona reticularis — produces small quantities of androgens (testosterone)
76
what is the role of the suprarenal medulla?
produces epinephrine (andrenaline) and norepinephrine (noradrenaline)
77
what are fever a result of?
pyrogens
78
how do viral antigens activate the immune response?
presentation with MHC class 1 to CD8 T lymphocytes
79
the clinical manifestations of an immediate hypersensitivity response are triggered when what?
mast cells release histamine, serotonin and heparin
80
what is the main function of emollients in the treatment of eczema?
to prevent flare ups by preventing the skin from becoming dry
81
what is a characteristic of a gram positive bacteria?
airborne mode of spread
82
give a few features of staphylococcus aureus
- gram positive - coagulase positive - cocci (round) shaped
83
what do aminoglycosides, tetracyclines and macrolides all inhibit in bacteria?
protein synthesis
84
how long is the latent stage of HIV?
10 yeats
85
T cells which survive selection in the thymus have TCRs specific for which antigens and MHCs?
foreign antigenic peptide and self-MHC
86
by the time a keratinocyte reaches the stratum corneum it has been alive for approx how long?
35-45 days
87
what primarily causes the swelling in inflammation?
increased vasopermeability leads to build-up of fluid in interstitial space
88
what do myeloid precursor cells give rise to?
RBCs/erythrocytes, platelets, mast cells, osteoclasts, dendritic cells, monocytes, granulocytes
89
mast cells are the effector cells in which sort of hypersensitivity?
type 1
90
which antibiotic is suitable to treat staphylococcus aureus?
flucloxacillin (not penicillin, methicillin, amoxicillin)
91
which class of immunoglobulin attaches as an individual molecule to exposed surfaces of basophils and mast cells?
IgE
92
what is opsonisation?
a coating of antibodies and complement proteins increases the effectiveness of phagocytosis
93
what is the job of Langerhans cells?
stimulate an immune response
94
what does the eczema type 1 hypersensitivity reaction involve?
IgE cross linking receptors on mast cells causing release of histamine
95
what do natural killer cells do in the innate immune system?
recognise abnormalities in cells, such as lack of MHC proteins, and bind to them causing apoptosis

PBL SEM 1 (9 decks)

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