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CMP - Immunology > L21 - Hypersensitivity: type 1 and 2 > Flashcards

L21 - Hypersensitivity: type 1 and 2 Flashcards

(50 cards)

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1
Q

what is the difference between Autoimmune response and hypersensitivity

A

Autoimmune:
response to a self/harmless antigen –> attack self

Hypersensitivity:
excessive response to a foreign antigen

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2
Q

when did Gell and coomvs propose the system for classification of hypersensitivity reactions

A

1963

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3
Q

name the 4 types aof hypersensitivity classified by Gell and Coombs and which one is T-cell mediated

A

Type 1: Immediate hypersensitivity

Type 2: Cytotoxic

Type 3: Immune complex

= these 3 are antbody mediated

Type 4: delayed-type hypersensitivity

= T cell mediated

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4
Q

what is Type 1 hypersensitivity caused by

A

allergens

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5
Q

define an allergen

A

an antigen which elicits an immediate allergic reaction

= generally means T1 hypersensitivity

= can be from nearly anything

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6
Q

why do allergic reactions happen

A

development of allergen-specific IgE

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7
Q

properties of allergens

A

very small and highly soluble proteins

diverse range of biological functions

carried by airbone particles and inhaled –> house dust

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8
Q

how mcuh of allergen protein is inhaled daily

A

5-50ng

= no diverse effects
= in sccetible indviduals = IgE iunduced

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9
Q

name the 2 receptors that bind to IgE

A
  1. FcεR1 = high affinity receptor

= found on mast and basophils

  1. FcεR2 = low affinity receptor

= founf on eosinophils andf B cells

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10
Q

which Fc receptor does IgE bind to in the absence of a bound antigen

A

FcεR1

= mast and basophils
= IgE can bind to Fc receptors in the absence of an antigen

normally antibody needs to be bound to a antigenic target eptide before fc receptors can be bound to

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11
Q

where are IgE antibodys mostly found despite them being very low in serum concentration

A

bound to FcεR1 on mast or basophil cells

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12
Q

what are IgE antibodies produced in response to

A

allergens

worms/helminths

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13
Q

where in the body are mast cells found

A

mucosal surfaces

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14
Q

step by step allergen specific IgE T1 hypersensitivity reaction

A
  1. mast cells have IgE bound on surface to FcεR1
  2. allergen antigen binds and causes cross linking

= degranulation of mast cell/basophil

  1. pre-formed chemical mediators rapidly released ANS newly synethesed mediators released more slowly in later response
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15
Q

name one toxic mediator and 1 cytokine released by activated mast cells

A

TM = Histamine = increase vascular permeability and cause smooth muscle contraction

cytokine = Type 2 cytokines such as IL-4 stimulate and aplify helper T-cell-2 response

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16
Q

what does mast cell activation cause

A

inflammataory cascade

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17
Q

describe the immediate effect of interaction with allergenic to allergic person

A

inbdivividual with IgE antbodies to bee venom allergen

stung on face –> local reaction

= immediate hypersenitivity reaction with mast cells causing inflammatory cascade

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18
Q

if the reaction is ‘generalised’/enough allergen transmitted what can happen

A

Anaphylaxis

= allergen is circulating in blood
- fall in blood pressure

bronchospasm =shutting off airways from swelling

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19
Q

describe anaphylactic shock symptoms

A

systemic ‘vasodilation’ cause sudden fall in blood pressyre

= histamine causes blood vessels to expand

tracheal swelling may cause suffocation

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20
Q

how is the IgE-mediated response crucial for parasite infection

A

mast cell activation at body surfaces rapidly recruit immune cells to remove parasites

infalmmation increases flow of lympoh fluid to lymoh nodes –> increase in T helper 2 cell activation

chemical mediators induce smooth muscle contraction –> expel parasite lung or gut

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21
Q

name one way to test an indivual for allergies

Study These Flashcards
A

skin prick test
= drop knwon panel of allergens into skin and view response

wheel and flare response –> discrete lump forms for a particular allergen

22
Q

describe how IgE antibodies are produced from Derp1 - dust mite allergen

Study These Flashcards
A
  1. derp1 enzyme cleaves tight junctrions and enters mucosa from airway
  2. dendritic cell takes up and presents to Th2 cells in lymph node
  3. Th2 cell induce ‘class switching’ in B cells to IgE
  4. IgE binds to FcεR1 receptor on mast cells

= on a secondary induction with this antobody an allergeic response will take place with the ‘poised’ IgE bound mast cells

  1. Cross-linking and degranulation –> inflammatory cascade /HS1 reaction
23
Q

name the cytokine that produces class switching to IgE and the cells that do this

Study These Flashcards
A

IL-4

Th2 cells

24
Q

name the cytokine that decides how sensitive a person si to allergic reactions and why

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A

IL-10

genes coding for ε for IgE is deirectly after y4 for Ig4 on chromosome 14 for heacu chains

= IL-10 cause preference for Ig4 = less IgE made

the higher the conc of IL-10 thes less sensitive to allergens a person will be

25
what is IgE/specific antibody syntghesis by B-cell COMPLETLEY dependant on
T cell dependant = prodduces the cytokines that acuse class switching
26
describe the immediate and late phase of igaling an antigen
immediate hypersensitivity due to mast-cell degranulation and inflammatory cascade = air flow massively restricted measured by seeing how much air can be bliwn out at one point in time in late phase basophils from blood are recruited to the site of allergen and cause degranulation again = respiraratopry flow rate ince agaibn impacted = this is NOT a HS1 reaction as its not immediate
27
describe the inflammatory response in asthamtic bronchi by 1. spasmogens 2. chemoatric factors
degranulation of Mast cells release mediators: 1. spasmogens: histamine causes bronchoconstriction and idnuce musocus production 2. chemoattic factors: IL-5 and TNF-a --> recruit lymphocytes, eosinophils,basopjils ,macrophages and neutrophils = release more cytokines and mediators result is airway remodelling (thicker walls and nowwer lumen) in addition to brocnial hyperactivity
28
what is bronchial hyperactivity in asthma
due to cycle of inflammation, epithelial damage, nerve sensitization, and muscle remodeling, which makes the airways hyper-sensitive and overreactive to even small irritants = damaged epithelium exposes Nerves which can be excited to cause smooth muscle contraction = bronchoconstrictio
29
name 2 treatments for asthma
Anti-IgE monoclonal antibody - binds to IgE preventing binding to FcεR1 receptor on mast cells β2-adrenoreceptor agaonist = relaxes the smooth muscle by binding to β receptor = opens airway
30
describe allergic de-sensitisation
exposed to very small gradually increasing amounts of allergen switch away from Th2 -> Th1 = less IL-4 and more IgG teahes your body in a safe envirnment that these allergens/antigens are not dangerous
31
what is the name for T2 hypersensitivity
cytotoxic
32
which antibopdies are T1 and T2 hypersensitivity mediated by
T1: IgE T2: IgG + IgM
33
what do the antibodies in T2HS bind to
cells/components of the extracellular matrix = antibody/cell surface antigen complex --> actiavtes complement + interacts with Fc receptors on other cells
34
name the 3 ways that T2HS causes tissue damage
1. Phagocytosis: Fc receptors on macrophages bind to antibopdy bound to a cell surface 2. classical complement cascade activated --> MAC formed
35
how do IgM and IgG actiavte complement
1. IgM or IgG coat cell surface and are bound by C1q = activates pathway eventually producing C3 convertase
36
onec produced what does the C3 convertase produced at ebnd of complement pathway do
1. C3a and C5a: peptide mediators of inflammation/anaphylotoxins 2. C3b: binds to complememnt receptors on phagocytes - CRs = for opsonisation 3. MAC: cause lysis of cells
37
what are anaphylotoxins
recruits macrophages and granulocytes = recruit inflammatory cells via C3aR and C5aR = act as chemoattractants cause vasoldialtion and swelling due to vascular permeability
38
role of CR receptors on phagocytes
grab onto cells asociated with complement = C3b and C5b on surface of microbe or infected cell
39
describe frustrated phagocytosis
cell too big to be engulfed by phagocyte 1. comnpliment and Fc receptors binbd to cell 2. exocytosis of lysosomal contents = necrosis/death of cell
40
what decides the different blood group
ABO = different carbohydrate stucture = due to genes that code for enzymes that transfert termnal sugars to carb backbone
41
which is the best blood group to be a donor
O = has 0 anti-A or anti-B antigens
42
name 1 way that could cause an extreme and intense Type 2 hyper sensitisation reaction
blood transfusions - extensive detruction of donor blood cells IgM antiantibodies cause: - agllutinatination - complememnt activation - haemolysis/red blood;ood cell destruction = low blood pressure and lower back pain somtimes fatal
43
why is incompataible blood not a problem in pregancies
IgM antibodies are too big to cross placenta = cant attack the incompatible blood cells in the fetus
44
what are Rh antigens and why are they important in pregnancies
Rhesus proteins are found on red blood cell = positive rhesus refers to people with D antigen 1st pregnancy: Rh+ foetus and Rh- mum = during delivery antigens enyer mums circulation through breaks in placenta = produces ati-Rh IgG antibdoies 2nd pregnancy: the anti-Rh IgG antibodies CAN cross the placents unlike IgM and attack foetus
45
symtpoms of foetus being attacked by Rh- antibodies
enlarged liver and spleen = macrophages attack the IgG coated fetal red blood cells by binding to Fc receptors
46
name 1 way to prevent Rhesus prophylais
anti-RhD antbodies injected into Rh- mother at week 28-34 of preganacy = destroys the foetal red blood cells in mothers blood before she becomes sensitive and makes antbodies of her own = future pregancies are safe
47
decsribe autoimmune haemolytic anaemia
antibodies against own blood antigens can arrise spontaneuosuly: = warm-reactive antibodies --> binds antigen above 37℃ = cold-reactive --> binds antigen below 37℃ Destroy own red blood cells
48
give an exmaple of a Type 2 hypersensitibity reaction disease
Goodpastures syndrome: antibodies produced to collagen type 4 --> destruction of basememnb membrane of ECM
49
describe Myasthenia gravis
Type 2 response IgG antiboes bind to acetelycholine receptors on msycle cells = block acetylcholine binding = no or weak mucle contraction IgG can cross placenta so can cause infants to be born with muscle weakness from MG+ mothers
50

CMP - Immunology (7 decks)

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