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Med 1 UBC Fall 2019 > Week 5: Immunology > Flashcards

Week 5: Immunology Flashcards

1
Q

What cells make up the lymphocytes?

A

B Cells
T Cells
Natural Killer Cells

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2
Q

+ve selection of T cells occurs in ______

A

cortex of thymus

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3
Q

-ve selection of T cells occurs in _______

A

medulla of thymus

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4
Q

after -ve and +ve selection of T cells, approximately what percent are still remaining?

A

5%

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5
Q

3 ‘classical’ APCs

A

B Cells
Macrophages
DCs

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6
Q

What is different about how B cells and T cells recognize antigen

A

B cells recognize the 3D shape of peptide, whereas T cells recognize the sequence

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7
Q

Define hypersensitivity

A

immune responses that are capable of causing tissue injury

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8
Q

Type I Hypersensitivity

A
  • Immediate
  • IgE and Th2 cells
  • Injury caused by mast cells, eosinophils, and their mediators
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9
Q

Type II hypersensitivity

A
  • Ig mediated
  • IgM, IgG against cell surface and EC matrix
    Causes disease by (1) damaging cells with complement activating phagocytes (via FcR) or (2) disrupting cell signalling.

ex: hemolytic anemia, drug allergies, Graves Disease, Myasthenia Gravis

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10
Q

Type III hypersensitivity

A
  • Immune complex-mediated
  • Immune complexes of circulating antigens and IgM or IgG
  • Immune complexes deposit in blood vessels, joints, and glomeruli
  • Immune complexes trigger inflammation promoting tissue damage

Ex: Lupus, serum sickness, post-streptococcal glomerular nephritis

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11
Q

Type IV hypersensitivity

A
  • T cell-mediated
    Often called ‘delayed type hypersensitivity’ as the reaction takes two to three days to develop
  • (1) CD4 T cells (Th1 and Th17); (2) CD8 CTLs
  • (1) cytokine-mediated inflammation; (2) direct target cell killing, cytokine-mediated inflammation
  • Ex: contact dermatitis, Type 1 diabetes, MS, Tuberculin test
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12
Q

Clinical features (signs and symptoms) of Type I hypersensitivity reaction

A
  • Conjunctivitis
  • Angioedema (swelling)
  • flushing
  • urticaria
  • Rhinitis
  • laryngeal edema (Upper airway obstruction, stridor)
  • voice change
  • Shock
  • Asthma (lower airway obstruction; wheezing)
  • GI (diarrhea, vomiting)
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13
Q

Clinical sign vs clinical symptom

A

Sign = indication of a medical condition that can be objectively observed (i.e., vomiting)

Symptom = manifestation of a condition that is apparent to the patient (i.e., nausea)

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14
Q

Urticaria

A

raised, arythematous, central clearing, irregular border, often migratory

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15
Q

Angioedema

A
  • swelling of soft tissues
  • localized to subcutaneous or submucosal tissues: face, lips, mouth, eyelids, airway, bowel
  • fast onset
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16
Q

3 diagnostic categories for anaphylaxis

A

simply put, it’s anaphylaxis if 2 or more body systems are involved.

1) acute onset of illness with skin/mucosal involvement and 1 of resp symptoms or reduced BP or signs of end-organ dysfunction.
2) Exposure to a likely allergen for that patient and 2 of: skin-mucosal involvement, resp compromise, reduced BP, persistent GI symptoms.
3) REduced BP after exposure to a known allergen for that patient.

17
Q

How does epinephrine work for anaphylaxis?

A
  • alpha 1 receptors - vasoconstriction and relief of airway obstruction
  • Beta1 receptors - increased contractility and HR; prevent hypotension and shock
  • Beta2 receptors - decrease mediator release from mast cells & basophils; increase bronchodilation
18
Q

Second line treatments for anaphylaxis

A

H1 antihistamines (relieve itching, lushing, urticaria, angioedema, nasal/eye symptoms)

Glucocorticoids (turn off pro-inflam genes, take several hours to work)

Inhaled B-2 agonists (salbutamol to lower respiratory tract symptoms)

19
Q

How are complement proteins generated?

A

Produced by the liver and mostly act as regulatory proteins. They are circulate as zymogens and become active when cleaved in response to contact with a pathogen or antibody.

20
Q

Role of complement (4)

A
  1. Opsonize pathogen for phagocytosis
  2. Inflammation - bind mast cells and induce degranulation
  3. Promote a stronger immune response
  4. Direct attack through Membrane Attack Complex
21
Q

what is the primary complement mediator for all complement pathways

A

c3 convertase and c5 convertase

22
Q

Compare the complement pathways

A

Classical initiated by Ag-Ig complexes.
Alternative initiated by spontaneous cleavage of C3
Lectin initiated by Mannose-Binding Lectin bound to pathogen surface.

They all ultimately lead to formation of C3 convertase and C5 convertase

23
Q

+ve selection (TCR)

A

Does the T cell receptor (TCR) bind MHC?

24
Q

-ve selection (TCR)

A

Does the cell react to cell-peptides? If it binds them too strongly, that T cell will be removed.

25
Q

Once T cells are activated, how do we control the degree and duration of response?

A

After T cell gets activated, it does its job and eventually upregulates its own inhibitory molecules, which, for example, bind to CD28’s receptor stronger than CD28 does itself.

26
Q

Somatic Hypermutation (B cell)

A

a process that introduces random mutation in the variable region of the BCR Ig heavy and light chains at a high rate during B cell proliferation

27
Q

Affinity maturation

A

the process that leads to increased affinity of Igs for a particular antigen as a T-dependent humoral response progresses and is the result of somatic hypermutations of Ig genes followed by selective survival of the B cells producing the Igs with the highest affinity.

28
Q

primary vs secondary immunodeficiency

A

Primary immunodeficiencies are the result of genetic defects, and secondary immunodeficiencies are caused by environmental factors, such as HIV/AIDS or malnutrition

29
Q

3 signals needed for adaptive immune activation

A

Innate Signal 1 (Ag presentation), Signal 2 (co-stimulation), & Signal 3 (cytokines) produced by the APC control adaptive immune activation

30
Q

Response to T-independent antigen

A
  • B cell can be activated directly by Ag that extensively crosslink BCR
  • Because there is no T cell stimulation through CD40, there will be no class switching and B cell will only make IgM
  • young children (<2) are relatively unable to produce strong T-independent immune responses.
31
Q

primary immune response

A

first time infected

32
Q

Correlates of Immunity

A

= measures that predict against infection

Ig levels in serum.

33
Q

conjugate vaccine

A

○ Link a protein to the polysaccharide (antigen) to help T cell
○ Increases responses in young children (now T-dependent)

34
Q

Adjuvants

A
  • increase the immunogenicity of vaccine; reduced dose of antigen required for effectiveness.
  • Broadens repertoire of antibody responses
  • Modulate the phenotype of T cell responses
  • Adjuvants induce signal 2 & 3 for non-live vaccines (co-stimulation & cytokines)
  • Example adjuvants:
    ○ ALUM - oldest; used in many routine vaccines
    ○ Squalene solutions (oil in water)
35
Q

natural passive immunity

A

the type passed from mother to fetus in the form of antibodies delivered from mother to fetus through placenta and breast milk. It is only in effect for a short period of time.

36
Q

artificial active immunity

A

vaccination
exposure to antigen - mimicking a primary immune response - so your immune system can generate a response and memory for reinfection - a secondary immune response.

37
Q

passive artificial immunity

A
  • administration of antibodies to fight infection immediately.
  • Only done when necessary
  • no lasting immunity.
38
Q

bioavailability

A

the amount of drug that reaches systemic circulation unchanged

39
Q

How does anaphylaxis work?

A
  • antigen binds IgE
  • Mast cells degranulate
  • Efflux of blood contents into periphery –> rapid decrease in BP and hypoxia
  • inflammation of bronchi - trouble breathing

Med 1 UBC Fall 2019 (16 decks)

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