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Immunology > Hypersensitivity disorders II > Flashcards

Hypersensitivity disorders II Flashcards

1
Q

which of the following symptoms of anaphylaxis is the most life threatening?

A

vascular permeability (drops blood pressure, and organs don’t receive oxygenated blood)

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2
Q

Hygiene hypothesis

A

explains why western nations have such a high rate of hypersensitivity
- too clean
- reduces exposure to pathogens (from animals and such)
- vaccination
- overreliance on antibiotics (reduced the educaiton of the immune system)

outcome:
- development of the immune system is held bacl
- develops an immune system that is incapable of fighting off “real world infections”.

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3
Q

basophils

A
  • key cell initiating Th2 response
  • make IL4 and IL13 , at the start of the immune response
  • can drive isotype switching to IgE and IgG4 through interaction with B cells through their CD40L

They can kind of act like a T cell in this way

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4
Q

lipid mediators

A

prostaglandins and leukotrienes

These are targeted in treatment of allergies and inflammation

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5
Q

Type II Allergic Rxn

A

Antibody induced

  • cell or matrix associated antigen
  • complement, FcR+ cells (phagocytes, NK cells)
  • Some drug allergies (ex: penicillin)

IgG driven

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6
Q

Type III

A

Antibody induced
IgG driven
- soluble antigen
- complement phagocytes
- serum sickness, Arthus reaction

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7
Q

Type IV hypersensitivity

A

Th1 driven, T cell induced
- soluble antigen
- macrophage activation
- contact dermatitis, tuberculin reaction

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8
Q

Type II mechanism

A

existing structures, generating an anitbody response

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9
Q

Type III mechanism

A

serum coming from another individual, forms immune complexes.

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10
Q

Type IV mechanism

A
  • T cell expansion and Th1 response with macrophages and T cells. Causes rash or swelling around the nickel containing jewelery
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11
Q

Type II

A

Small molecules that bind to cell surface molecules, changing their structure. Perceived by the immune system as foreign.
- antibody response develops, IgG
- Upon Ab binding altered molecules on cells, leads to their destruction by complement and phagocytosis
- Penicillin is one molecule that can induce this activity

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12
Q

Penicllin structure

A

Has a reactive bond, that is able to focus on a bacterial transpeptidase or localize on an erythrocyte.

  • Binds to bacterial transpeptidase and inactivates it OR
  • Penicillin modifies proteins on human erythrocytes to create foreign epitopes.
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13
Q

Penicillin - Protein conjugates

A

stimulate the production of anti-penicillin antibodies
- complement coated penicillin modifed erythrocytes are phagocytosed by macrophages
- Macrophages present peptides from penicillin-protein conjugate and activate specific CD4 T cells to become Th2 cells.
- B cells are activated by antigen and by help from activated Th2 cells
- plasma cells secrete penicillin specific IgE which arms mast cells. IgG is also produced
- Penicillin modified erythrocytes activate armed mast cells causing anaphylaxis.

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14
Q

Blood group antigens and transfusions

A
  • Transfusion can give rise to a life threatening Type II hypersensititvity response
  • the major immunogenetic barrier to transfusion is the structural polymorphisms of the carbohydrates decorating the erythrocyte surface
  • The antigenic difference in these molecules are reffered to as the ABO system of blood group antigens.
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15
Q

A antigen

A

has a GalNAc on its terminal residue

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16
Q

B antigen has

A

terminal residue of Gal (galactose)

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17
Q

O antigen

A

absence of terminal residue

18
Q

why do we produce antibodies against other people’s blood group antigens?

A

because blood group antigens are very similar to those expressed by many bacteria and we only develop tolerance to those our RBCs express

19
Q

which blood type is the universal donor?

A

Blood group O

19
Q

which blood type is the universal donor?

A

Blood group O

20
Q

what blood group can recieve blood from any group?

A

AB

21
Q

AB blood can only be transfused safely into another

A

AB patient

22
Q

Type III hypersensitivity

A

Initiated by immune complexes (antigen-antibody complexes) depositing on the walls of small blood vessels or alveoli
- immune complexes activate complement
- inflammation and tissue damage follow complement deposition
- can be a side effect of therapeutic treatment with Ab or other proteins from non-human animal species

  • Arthus reaction or serum sickness
23
Q

Mediated tissue injury - immune complex

A

site of immune complexes -> complement and Fc receptor - mediated recruitment and activation of inflammatory cells

leads to recruitment of neutrophils and lysosomal enzymes and ROS

all leads to

Vasculitis (inflammation of vasculature)
- shows up as hemmorrhage in the skin and uricarial rash (both result from serum sickness)

24
Q

vasculitis

A

blood vessel walls

25
Q

nephritis

A

renal glomeruli

26
Q

arthitis

A

joint spaces

27
Q

Arthus reaction

A

perivascular area

28
Q

Farmer’s lung

A

Alveolar/capillary interface

29
Q

immune complexes

A
  • can be small or large
  • their size, depends on the concentration of antigen and antibodies
30
Q

small complex

A

little antibody, excess antigens

Early response

31
Q

large immune complexes

A

equal amount of antigens and antibodies

potenitally very damaging

Middle of immune response

32
Q

medium sized immune complex

A

excess antibody, little antigen

late in immune response

33
Q

type IV hypersensitivity

A

caused by the products of antigen specific T cells
- CD4+ Th1 mediate the majority of these responses, reactions to insect bites, tuberculin skin test
- reffered to as delay type hypersensitivity (DTH) because it takes several days for symptoms to develop

34
Q

DTH

proteins and local skin swelling

A

proteins
- insect venom
- mycobacterial proteins (tuberculin, lepromin)

skin swelling
- erythema
- induration
- cellular infiltrate
- dermatitis

35
Q

contact hypersensitvity (type IV)

A

Haptens:
- Pentadecacatechol (poison ivy)
- DNFB

Small metal ions
- Nickel
- Chromate

Local epidermal reaction
- Erythema
- cellular infiltrate
- Vesicles
- intraepidermal abscesses

36
Q

Gluten sensitive enteropathy (celiac disease)

A

Antigen - Gliadin

Villous atrophy in small bowel - malabsorption

36
Q

Gluten sensitive enteropathy (celiac disease)

A

Antigen - Gliadin

Villous atrophy in small bowel - malabsorption

37
Q

DTH reactions on the cellular level

A

Mediated by antigen-specific effector T cells
Manifested as local irritation that occurs 24-72 hours after exposure

  • Antigen is injected into subcutaneous tissue and processed by local antigen presenting cells
  • Th1 effector cell recognizes antigen and releases cytokines which act on vascular endothelium
  • Recruitment of phagocytes and plasma to site of antigen injection causes visible lesion
38
Q

granulomas

A

chronic DTH response

Occurs in lungs and lymph nodes of those infected with mycobacterium. Provides a mechansm for walling off the infection from the rest of the bosy. Sometimes have a caseous or necrotic center.

activated macrophages and T cells. walled off by fibroblasts - contains the infection. kept in a latent state until there is some sort of stress or activation.

39
Q

Th1 is the driving factor of a Type IV rxn

A

produces IFNy
- activates macrophages, increasing release of inflammatory mediators

40
Q

the pathogenesis of celiac disease

A

inflammation of the small intestine is caused by CD4+T cells, responding to peptides derived from gluten.

  1. gluten degraded in the gut lumen to give resistant fragment
  2. gluten fragment enters gut tissue and is deaminated by transglutaminase
  3. Naive CD4 T cell responds to deaminated peptides presented by HLA-DQ
  4. Inflammatory effector T cells cause villous atrophy

Immunology (18 decks)

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