Week 5: Immunology Flashcards Preview

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

Flashcards in Week 5: Immunology Deck (39)
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What cells make up the lymphocytes?

B Cells
T Cells
Natural Killer Cells


+ve selection of T cells occurs in ______

cortex of thymus


-ve selection of T cells occurs in _______

medulla of thymus


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



3 'classical' APCs

B Cells


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

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


Define hypersensitivity

immune responses that are capable of causing tissue injury


Type I Hypersensitivity

- Immediate
- IgE and Th2 cells
- Injury caused by mast cells, eosinophils, and their mediators


Type II hypersensitivity

- 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


Type III hypersensitivity

- 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


Type IV hypersensitivity

- 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


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

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


Clinical sign vs clinical symptom

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)



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



- swelling of soft tissues
- localized to subcutaneous or submucosal tissues: face, lips, mouth, eyelids, airway, bowel
- fast onset


3 diagnostic categories for anaphylaxis

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.


How does epinephrine work for anaphylaxis?

- 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


Second line treatments for anaphylaxis

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)


How are complement proteins generated?

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.


Role of complement (4)

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


what is the primary complement mediator for all complement pathways

c3 convertase and c5 convertase


Compare the complement pathways

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


+ve selection (TCR)

Does the T cell receptor (TCR) bind MHC?


-ve selection (TCR)

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


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

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.


Somatic Hypermutation (B cell)

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


Affinity maturation

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.


primary vs secondary immunodeficiency

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


3 signals needed for adaptive immune activation

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


Response to T-independent antigen

- 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.