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Biological Sciences > Immunology Lectures 1-7 > Flashcards

Immunology Lectures 1-7 Flashcards

1
Q

Components of innate immunity

A

structural - e.g. epithelia
Soluble - e.g. complement
Cellular - phagocytes

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2
Q

Haematopoiesis

A

the generation of leukocytes and erythrocytes.

  • HSCs sustain blood cell throughout life
  • capable of self renewal
  • multipotent
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3
Q

Myeloid cells

A

phagocytes all able to recognise microbes though specific receptors

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4
Q

Neutrophil

A
  • short lived normually found in blood
  • migrates during inflammation
  • highly phagocytic granulocyte
  • produces vast repertoire of antimicrobial factors
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5
Q

Dendritic cells

A
  • found throughout the body, sentinels of the immune system
  • phagocytic
  • crucial link between innate and adaptive immune response, via secretion of soluble factors that affect cell function (cytokines) and antigen presentation (to T cells)
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6
Q

Macrophage

A
  • Found in most, if not all tissues
  • highly phagocytic and antimicrobial
  • directs both innate and adaptive through secretion of cytokines and antigen presentation
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7
Q

Eosinophil

A
  • found in blood, gut lungs and urogenital tract
  • important in helminth infection
  • involved in allergy and asthma
    contains toxic granules and inflammatory mediators
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8
Q

Mast cell

A
  • found in tissues

- involved in allergy and histamine release (increase vessel permeability)

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9
Q

Lymphoid

A
  • targeted secretory cells
  • found in blood and tissues
  • cells are crucial for recognising changes in tumour cells and virally infected cells. target and kill these cells
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10
Q

The steady state - immediate response

A

structural barriers e.g. skin, barriers, mucosal pH

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11
Q

Soluble molecules in immediate response

A

Defensins = antimicrobial peptides, secreted by epithelial cells
Lysozyme = secreted by macrophages
The complement system

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12
Q

Cells in immediate response

A
  • the tissues phagocytes: macrophages, dendritic cells

- natural killer cells, mast cells

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13
Q

Pathogen Associated Molecular Patterns PAMPs

A
  • Bacteria PAMPs - cell wall components
  • Microbe Associated Molecular patterns bacterial DNA
  • certain bacterial proteins
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14
Q

Viral PAMPS

A
  • ssRNA, dsRNA, sugars, MAMPs
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15
Q

Yeast

A
  • sugars (β-glucans)
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16
Q

Helminths

A
  • sugars (chitin)
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17
Q

How are PAMPs/MAMPs recognised?

A
  • PAMPs are recognised specifically by pattern recognition receptors (PRRs)
  • found in all multicellular organisms
  • germline genes encoded - evolved to recognise PAMPs
  • ‘know’ the difference between harmful and non-harmful entities
  • found mainly on phagocytes (macrophages, neutrophils, dendritic cells)
  • survey all physiologically environments
  • soluble, plasma membrane (cell surface), cytoplasm in vacuoles
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18
Q

strategy for discovering immune genes

A
  • loss of function

- gain of function

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19
Q

Surface pattern recognition receptors

A
  • recognise various PAMPs
  • major classes - toll receptors, carbohydrate binding lectins
  • able to signal to produce appropriate responses and production of various cytokines and immune regulators
20
Q

PRRs survey all cellular environments

A
  • soluble
  • intracellular
  • vascular sensors
21
Q

Damaged associate molecular patterns DAMPs

A
  • molecules from dying/ damaged cells enhance the immune response
  • potential molecules released from damaged tissues and dying cells
  • HSPs, ATP, nuclear proteins (HMGB-1), extracellular matrix components (hyaluronic acid)
  • not normally released when cells undergo suicide ion a cont5rolled fashion (apoptosis)
  • these help distinguish between ‘naturally’ dying cells and damaged/killed cells
22
Q

Steps of Phagocytosis

A

Step 1: recognition - direct binding vis phagocytic receptors, indirect pathogen binding via Fc receptor, complement receptor - opsonised
Step 2: uptake, signalling and actin driven cytoskeletal remodelling
Step 3: appropriate processing - microbe killing or non-inflammatory removal of dead/apoptotic cells
- production of inflammatory signals to alert cytokines and recruit chemoattractants and other cells, macrophages.

23
Q

Uptake and degradation in macrophages and dendritic cells

A
  • activates degrading enzymes
  • low pH aids killing of microbes
  • increasing acidity
  • proteinases, lipases, hydrolytic enzymes - lysozyme
24
Q

killing mechanisms of macrophages and dendritic cells

A
  • proteolytic and hydrolytic enzymes
  • Reactive oxygen species/reactive nitrogen species
  • antimicrobial peptides
  • nutrient deprivation
25
Q

outcome of phagocytosis by macrophages and dendritic cells

A
  • killing
  • presentation (activation of T cells)
  • removal of apoptotic cells
  • production of cytokines and inflammatory molecules critical for inflammation
26
Q

Inflammation

A

the general term for the accumulation of fluid, plasma proteins and leukocytes that is initiated by physical trauma, infection or local immune response

27
Q

Three stages of inflammation

A
  • initiation
  • recruitment of effector cells (mainly neutrophils)
    resolution (switching off and removal of cells)
28
Q

Importance of neutrophils

A
  • severe congenital neutropenia (born with low numbers of neutrophils) usually die in infancy of severe infections
  • chemotherapy induced neutropenia - can lead to infection/death
  • Acute Myeloid Leukaemia - immunocompromised due to immature myeloid cells
29
Q

initiation of inflammation

A
  • damaged cells, bacterial uptake by macrophages and mast cells degranulation all lead to increase in vessel permeability
  • increased permeability leads to increase in soluble components from blood, antibodies and complement
  • chemokines and bacterial products facilitate chemotaxis ( movement up a chemical gradient)
  • inflammatory cytokines up regulate adhesion molecules on the endothelium and neutrophils allowing the recruitment of cells form the blood
30
Q

stages of leukocyte recruitment

A
  • rolling
  • activation (by chemokines)
  • firm adhesion
  • extravasation (diapedesis)
31
Q

Leukocyte migration and recruitment (postcode model)

A
  • leukocyte adhesion and migration mediated via cell surface adhesion receptors and chemokines receptors found on leukocytes and endothelia cells
  • the temporal-spatial expression as well as there activation state of adhesion and chemokine receptors and there ligands acts as a ‘postcode’ for leukocyte migration.
  • not just important in neutrophil migration but also lymphocyte recirculation NK cell and dendritic cell migration mhe10
32
Q

neutrophil killing

A

once at the site of inflammation the normally tightly regulated neutrophils are activated by PAMPs and proinflammatory cytokines

33
Q

Neutrophils deliver multiple anti-microbial molecules

A

neutrophils first activated - by PAMPs and TNF-a
Oxidative burst NADPH - oxygen free radicals, hydrogen peroxides
Nitric oxide synthetase - reactive nitrogen species
Myeloperoxidase - formation of bleach

34
Q

Neutrophils deliver multiple antimicrobial molecules

A
  • primary granules
  • secondary granules
  • tertiary granules
  • cytoplasm
  • host tissue damage
35
Q

Natural Killer NK cells

A
  • specialised granular lymphocytes
  • crucial for defence against tumour and virally infected cells
  • do not tend to recognise pathogens directly, detect affects of the pathogen on the host cell
  • either detect the lack of host proteins of the induction of stress proteins
36
Q

how do NK cells kill?

A
  • granules contain perforin and granzyme B
  • perforin forms pores to allow entry on granzyme B and other granzymes
  • granzymes B trigger apoptosis of target cells
37
Q

4 phases of Adaptive immune response

A
  1. establishment of infection
  2. induction of adaptive response
  3. adaptive immune response
  4. immunological memory
38
Q

Function of B-lymphocytes

A
  • produce antibodies
  • 10-15% of lymphocytes
  • triggered by antigen to differentiate into plasma cells and B memory cells
  • combat bacterial and some viral infections
39
Q

Function of T-lymphocytes

A
  • cell mediated immunity
  • 75-80% of lymphocytes
  • combat viruses, fungi, intracellular bacteria and cancerous cells
40
Q

How does immunological memory confer long lasting protection?

A
  • more responder cells available
  • more efficient antigen recognition/activation - may not require costimulatory signals for activation.
  • rapid and effective migration to tissues and lymph nodes - express different homing/ chemokine receptors that naïve T cells
  • produce more cytokines or antibodies
  • long lasting, memory cells can persist for years
41
Q

Primary lymphoid organs

A
  • bone marrow
  • thymus
  • initial sites for production of lymphocytes
  • lymphocytes 1st express antigen receptors
42
Q

Secondary Lymphoid organs

A
  • lymph nodes
  • spleen
  • mucosal associated lymphoid tissue
  • sites where lymphocytes first encounter antigens
43
Q

where does antigen independent differentiation occur?

A
  • In the primary lymphoid organs
  • Bone marrow B cells
  • Thymus T cells
44
Q

Where does antigen dependent differentiation occur?

A
  • In the secondary lymphoid organs
45
Q

Lymph Nodes

A
  • provides site for resting B cells and T cells
  • filter lymph cells and foreign material
  • where B cells and T cells first recognise and respond to antigen
  • antigen recognition can drive antigen dependent differentiation
  • where products of adaptive immune response are generated

Biological Sciences (4 decks)

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