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Year 2 PODT > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the two primary lymph tissues

A

Thymus

Bone marrow

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2
Q

What’s the difference between primary lymph tissues and secondary lymph tissues

A 
Primary = cells originate or mature
Secondary = cells reside and traffic
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3
Q

what are the two cells that are only involved in adaptive immunity and not innate

A

B cells and T cells

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4
Q

what are the two cells involved in both innate and adaptive immunity

A

Natural killer T cell

yG T cell

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5
Q

what are the steps of phagocytosis

A
  1. Chemotaxis and adherence of microbe to phagocyte

2 ingestion of microbe by phagocyte

3 formation of a phagosome

4 fusion of the phagosome with a lysosome to form a phagolysosome

5 digestion of ingested microbe by enzymes

6 formation of residual body containing indigestible material

7 discharge of waste materials

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6
Q

what do activated macrophages secrete

A

cytokines and chemokines

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7
Q

which MHC classes do CD4 and CD8 interact with

A

CD4 = MHC class II

CD8 = MHC class I

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8
Q

What are the markers of a B cell

A

CD19 and CD20

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9
Q

What are the markers of Th cells

A

CD3 and CD4

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10
Q

What are the markers of Tc cells

A

CD3 and CD8

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11
Q

What is the marker on all T cells

A

CD3

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12
Q

what is the marker on NK cells

A

CD16/56

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13
Q

describe the signs of Specific IgA deficiency (sIgAD)

A

IgA protects against infections of the mucous membranes of the GI tract and airways

many asymptomatic

but sometimes associated with infections or autoimmune/allergic disease

next to no IgA

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14
Q

describe the signs of X linked agammaglobulinaemia (XLA)

A

Mutations in the BTK gene; X linked
• Causes arrest of B cell development between pro B to B cell stage
• No peripheral B cells in blood
• Failure of immunoglobulin production

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15
Q

describe type I hypersensitivity

A

IgE- mediated hypersensitivity

ALLERGEN induces a humeral response

  • Secretes IgE antibody in response to activation of allergen-specific TH2 cells
  • normally this happens when there’s a parasitic infection but if you have this then you have IgE regulatory defects (atopy) and that means there’s abnormal production of IgE in response to nonparasitic antigens
  • Ag indices cross-linking of IgE (which is bound to mast cells, eosinophils and basophils) to allergen
  • degranulation occurs
  • leads to local or systemic inflammation
  • IgE Abs bind with High Affinity to Fc eRI receptor on Mast Cells

Three Phases:

  1. Sensitisation phase:
    • Exposure to allergen
    - activates TH2 cells
    - stimulate B cells to form IgE producing plasma cells
    • IgE produced in response to antigenic stimulus and binds to FC- receptors on mast cells and basophils
  2. Activation Phase:
    •Re-exposure to antigen triggers mast cells and basophils to respond by release of their granules
  3. Effector Phase:
    • Complex response occurs as a result of histamine and other pharmacologically active agents released by mast cells and basophils
  • can be systemic (anaphylactic shock) or localised (atopy)
  • Allergic Reactions can have both an immediate phase but also a late-phase response

typically manifests as systemic and localised anaphylaxis such as hay fever, asthma, hives, food allergies and eczema

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16
Q

describe type II hypersensitivity

A
  • Involves antibody-mediated destruction of cells
  • cell destruction happens via Antibody-Dependent Cell mediated Cytotoxicity (ADCC)
  • mediated by IgG and IgM
3 types:
- blood transfusions - when incorrect blood type administered body has an immune response to the foreign blood
- haemolytic disease of the newborn 
- drug- induced haemolytic anaemia
(all of these cause haemolysis)

see hypersensitivity lecture for diagram on mode of action of ADCC

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17
Q

describe type III hypersensitivity

A
  • immune complex-mediated hypersensitivity
  • Reaction of Ab’s with antigen generates immune complexes
    facilitating the clearance by phagocytic cells and mast cell activation
  • In some cases, large amounts of immune complexes can lead to
    tissue damaging type III hypersensitivity reactions
  • Magnitude of the reactions depends on the amount of immune complexes
  • Can be localized and occurs wherever immune complexes are deposited
  • Common sites are blood vessel walls, synovial membrane of joints, glomerular basement membrane of the kidney
  • Deposition of complexes results in the recruitment of neutrophils to the site (granular release)
  • Lytic enzymes causes tissue damage

Examples:

  • Farmer’s lung
  • Pigeon fancier’s disease
  • Serum Sickness (generalised) - when foreign antibodies are injected into human (eg from a mouse or something) - this is why in treatment we need to develop human antibodies treatment and not from animals
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18
Q

describe type IV hypersensitivity

A

Delayed-Type Hypersensitivity (DTH)

– Localized inflammatory response induced by T H
cells
– Characterized by large influx of inflammatory cells
and macrophages
– Delayed: 24-72 hours
– DTH is often helpful and plays important role in
intracellular pathogens and contact antigens
– DTH can cause tissue damage and be pathological if the pathogen and contact antigen persists - then DTH just keeps going and causes damage

Main examples:

  • TB
  • herpes
  • measles
  • contact antigens - jewellery, hair dyes etc

sensitisation and effector phase

  • Influx and Activation of macrophages in the DTH response important in host defence against parasites and bacteria that live within cells
  • ie. areas where Ab cannot reach them
  • Normally the intracellular pathogen/infected cell is quickly cleared with little tissue damage, BUT if antigen not easily cleared a prolonged DTH response can occur

Prolonged DTH Response can lead to Granulomas:
- Continuous activation of macrophages:
1. Macrophages adhere to each other
2. Fuse to form multinucleated giant cells
3. Form palpable nodules
4. Release lytic enzymes
5. Tissue Damage
Eg. Mycobacterium tuberculosis in the lung

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19
Q

describe the autoimmune cause of Grave’s disease

A

– antibodies against hormone receptor
– activate the receptor
– Uncontrolled hormone production
- enlarged thyroid

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20
Q

describe the autoimmune cause of Myasthenia gravis

A

– Antibodies against acetylcholine receptor
– Act as an antagonist
– Block binding to receptor
– Severe muscle weakness
– Difficulties chewing, swallowing, breathing
– genetic component HLA-DR3 alleles

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21
Q

describe the cause and features of Systemic Lupus Erythematosus (SLE) - LUPUS

A

• Chronic, multiorgan disease
• Affects predominantly women
• Characterised by production of autoantibodies
against self DNA/RNA complexes
• Symptoms a result of DNA/ or RNA/Ab complexes
forming and triggering acute inflammation: type III
hypersensitivity

Features:

  • Fever, weakness, arthritis, skin rashes, pleurisy, kidney dysfunction, etc.
  • Autoantibodies to DNA, histones, RBCs, platelets, leukocytes and clotting factors
  • RBCs & platelet autoantibodies lead to complement- mediated lysis of cells causing anaemia and thrombocytopenia
  • Accumulation of immune complexes can be deposited along walls of small blood vessels which leads to type III hypersensitivity reaction
  • why you see a rash forming
  • Activates complement system - leads to tissue damage
22
Q

describe Multiple Sclerosis (MS)

how is it linked to hypersensitivity and autoimmunity

A

Cell-mediated autoimmunity (Type IV hypersensitivity)

• Cell mediated immune attack in Central Nervous
System (CNS)
• Destruction of myelin and axons
• Central role for CD4+ helper T cells
• Self antigen = peptides of myelin - that’s the thing the cells attack
• Targets: myelin, oligodendrocytes, axons
• Numerous cells cause actual damage; prominent
role for macrophages, cytotoxic T cells
- not really known what started it ie why the body starts destroying its myelin and axons

23
Q

what treatments are available for autoimmune diseases

A

no cure

  • Immunosuppression - dampen type 2/3 hypersensitivity
  • Immunomodulation - dampen type 2/3 hypersensitivity
  • Plasmapheresis - clear blood of autoantibodies if there’s an exasberation
  • IVIg - artificially introducing antibodies to individuals
  • Protection of target - if its bound to a particular cell
  • Autologous stem cell transplantation - clear body of T cells and give them new immune system - in extreme cases and need correct donor
  • Tolerance induction / T cell vaccination (in trial) - more experimental
24
Q

what treatments are available for autoimmune diseases

A

no cure

  • Immunosuppression - dampen type 2/3 hypersensitivity
  • Immunomodulation - dampen type 2/3 hypersensitivity
  • Plasmapheresis - clear blood of autoantibodies if there’s an exasberation
  • IVIg - artificially introducing antibodies to individuals
  • Protection of target - if its bound to a particular cell
  • Autologous stem cell transplantation - clear body of T cells and give them new immune system - in extreme cases and need correct donor
  • Tolerance induction / T cell vaccination (in trial) - more experimental

can also treat the symptoms in organ-specific disorders

25
Q

Explain the five cardinal signs of inflammation

A
  • rubor (redness) - due to increased vascularity
  • tumor (swelling) - exudation of fluid
  • calor (heat) - increased blood flow and release of inflammatory mediators
  • dolor (pain) - stretching of pain receptors and nerves by inflammatory exudates and by the release of chemical mediators
  • functio laesa (loss of function) - combination of all of the above
26
Q

Describe the events that occur during acute inflammation

A
  • Local cells move towards site - mast cells and macrophages
  • these release chemical signals
  • causes things like increased blood flow
  • phagocytic cells move in from capillaries to site
  • phagocytosis occurs
27
Q

Discuss possible outcomes of acute inflammation

A

Acute inflammation: relatively short duration (hours to
days): exudation of fluid and plasma protein, neutrophil
and monoctye infiltration

can result in good things:

  • Complete resolution ( back to normal)
  • Healing ( fibrosis)

but also sometimes bad things:

  • Abscess formation
  • Progressing to chronic inflammation
28
Q

describe the three manners in which cytokines can work

A

Autocrine: Cytokine binds
to receptor on cell that
secreted it

Paracrine: Cytokine binds to
receptors on nearby cells

Endocrine: Cytokine binds
cells in distant parts of the
body

29
Q

Give examples of cytokines which are Pro-inflammatory

A 
IL- 1
TNF alpha
IL-6
IL-8
IL-12
30
Q

Give examples of cytokines which are Anti-viral

A

interferon α/B

31
Q

what is the difference between the innate response and adaptive response of the immune system

A

Innate:

  • rapid
  • non-specific
  • first line of defence
  • not enhanced by repeated exposure

Adaptive:

  • slow
  • specific
  • second line of defence
  • enhanced by repeated exposure
32
Q

describe the two types od adaptive immunity

A

• Humoral immunity
– Immunity that is mediated by antibodies
– Can be transferred by to a non-immune recipient by serum

• Cell Mediated Immunity
– Immune response in which antigen specific T cells dominate

33
Q

describe Common Variable Immune Deficiency (CVID)

A 
– Primary Immune Deficiency 
– Can occur at any age
• Reduction in IgG, IgA and/or IgM
• poor response to vaccines
• defined causes of hypogammaglobulinaemia have been excluded

• CVID is an umbrella term for patients with
antibody deficiency in whom:
– no other primary cause is identified
– no secondary cause for the antibody deficiency has been identified

34
Q

describe treatment of antibody deficiency

A 
• sIgA deficiency often needs no treatment 
• Immunoglobulin replacement therapy (IRT) 
• Chest management 
• Prophylactic antibiotics 
• Disease specific complications
– Autoimmune complications may require
immunosuppressive therapy e.g haemolytic
anaemia in CVID
35
Q

describe SCID presentation, laboratory abnormalities, management

A 
clinical presentation:
• Infancy 
• Infections
– Bacterial 
– Viral 
– Fungal
• Failure to thrive

Laboratory abnormalities :
• lymphopaenia
• +/- hypogammaglobulinaemia
• Absent T cells or non functioning T cells (depending on the type, they may have absent B and or NK cells)

Management:
• Isolation 
• Antimicrobial therapy 
• Immunoglobulin replacement 
• Talk to the transplant centre: BMT/stem cell therapy for definitive management
36
Q

what are the functions of the complement system

A
  • makes bacteria more susceptible to phagocytosis
  • directly lyses some bacteria and foreign cells
  • produces chemotactic substances - mediates inflammation
  • increases vascular permeability
  • causes smooth muscle contraction - promotes mast cell degranulation
37
Q

describe the pathology of RSV bronchiolitis and pneumonia

A 
• Pathology
– Necrosis and sloughing of small airway epithelium
– Oedema
– Increased mucus secretion
• Obstructs airflow in small airways 
– Interstitial infiltration 
– Alveolar filling

• Clinical
– Hyperinflation
– Atelectasis (collapsed lung)
– Wheezing

38
Q

describe RSV pathogenesis

A

• Virus replication triggers immune response in
lungs

– Cytokine/chemokine release

– Infiltration of …
• neutrophils
• lymphocytes
• eosinophils

– Perivascular and peribronchiolar cuffing

– Trapping of air in lower lungs
• lung hyperinflation

• Once the immune response is triggered,
removal of RSV will not stop the pathogenesis

39
Q

What is sepsis and septic shock?

A

• Sepsis
– The presence of SIRS associated with a confirmed infectious process.

• Severe sepsis
– Sepsis with either hypotension or systemic
manifestations of hypoperfusion
• Lactic acidosis, oliguria, altered mental status

• Septic shock
– Sepsis with hypotension despite adequate fluid
resuscitation, associated with hypoperfusion abnormalities

40
Q

describe Systemic inflammatory response syndrome (SIRS)

A

2 or more of following symptoms:
• Temperature >38ºC or <36ºC
• Heart rate >90 beats/min
• Respiratory rate >20 breaths/min or PaCO2 of <32 mmHg
• White blood cell count >12,000 cells/mm3, <4000
cells/mm3, or >10% immature forms

41
Q

what treatments are available for type 1 hypersensitivity reactions

A

Environmental – Avoid “it”

Pharmacologic:

  • Anti-histamines – Blocks H1 and H2 receptors
  • Cromolyn Chloride – Blocks mast cell degranulation if taken before allergen exposure (Nasodex)
  • Corticosteroids – Blocks biosynthesis of histamines and arachidonic acid (leukotrienes and prostaglandins)
  • Theophylline – Blocks degranulation through cAMP prolongation
  • Epinephrine – Counteracts the effects of anaphylaxis shock

Immunological:

  • Hypo or desensitization – Inject with increasing doses of antigen over time; induces IgG Abs to clear antigen prior to IgE binding
  • Humanized Anti-IgE Antibodies – Binds to IgE in serum and used for asthma treatment (Xolair) – £6-18k per year
42
Q

give some examples of organ-specific autoimmune diseases

A

type 1 diabetes

goodpasture’s syndrome

multiple sclerosis

  • graves’ disease
  • Hashimoto’s thyroiditis
  • autoimmune pernicious anemia
  • autoimmune Addison’s disease
  • vitiligo
  • myasthenia gravis
43
Q

give some examples of systemic autoimmune diseases

A

rheumatoid arthritis

scleroderma

  • systemic lupus erythematosus
  • primary sjögren’s syndrome
  • polymyositis
44
Q

what are cytokines

A

Cytokines are small peptides that are usually
produced and secreted by the cells of the immune
system

Monokines: produced by mononuclear phagocytes:
monocytes
Lymphokines: produced by lymphocytes
Lymphokines and monokines – collectively
CYTOKINES

Cytokines act as a messenger between cells
many cytokines are known as interleukins:
cytokines made by one leukocyte and acting on other leukocytes.

45
Q

what is the function of interleukin-2

A

Interleukin-2 (IL-2) is produced following T cell activation by antigen presenting cells. This cytokine acts in an autocrine loop to induce T cell proliferation

The major autocrine growth factor for T cells.
IL-2 (and IL-15) stimulates NK cell cytolytic function.
Acts on B cells as a growth factor.
Induces the death of activated T cells
IL-2 receptor has 3 chains IL-2Rαβγ. The α chain is the
cytokine specific chain and the γ chain is shared by a
number of cytokine receptors

46
Q

what is the function of Interleukin-4

A

Interleukin-4 (IL-4) is a Th2 derived cytokine that stimulates B cell proliferation

47
Q

what is the function of interleukin-17

A

Interleukin-17 (IL-17) is produced by activated T Helper 17 (Th17) cells

Is a major pro-inflammatory cytokine

48
Q

what is the function of Tumour Necrosis Factor-α (TNF-α)

A

Principle mediator of the anti-bacterial response

49
Q

what is the function of Transforming Growth Factor ( TGF)-β

A

TGF-β generally suppresses lymphocyte function

50
Q

what is the function of interleukin-10

A

IL-10 generally suppresses the immune system

51
Q

what is the major function of chemokine

A

act as a chemoattractant to guide the migration of cells

52
Q

what is chemotaxis

A

Migration of cells along a chemical gradient

Year 2 PODT (14 decks)

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