This summary document entails all the different aspects of Immunology mainly covered within the textbook. It has been split into a table of keywords and the explanations behind it and what the keywords should make you think of. It also includes a flow diagram in which it explains how B cells are de...
Innate immunity Immediate defence against attack by a pathogen
(bacteria, fungi, viruses or parasites)
Adaptive immunity Immune response takes days to arise following
exposure to Ag (antigen)
(NOTE: Adaptive immunity is activated only in the
failure of the innate immune response to control the
infection and restore homeostasis)
3 main elements of immunity 1. Recognise invading microorganisms
2. Elicit a response aiming to clear the infection
3. Terminate the response as soon as the
threat has been eliminated
Lysozyme Secreted in tears, saliva, and fluids of the respiratory
tract, cleaves the peptidoglycan components of
bacterial cell walls (thus causing bacteria and fungi)
Lactoferrin and calprotectin Bind and sequester metal ions needed for bacterial
and fungal growth (thus inhibit growth)
Psoriasin Produced by skin and has a potent antibacterial
activity against E.coli, an enteric bacterial species
(REMEMBER: Antimicrobial proteins show some
specificity toward particular antigens e.g. Psoriasin
does NOT kill Staphylococcus aureus (a major cause
of food poisoning and skin infection))
𝛂- and 𝞫-defensins, cathelicidins, histatins Antimicrobial Peptides (AMPs)
MoA of Antimicrobial Peptides (AMPs) Interaction w/ acidic phospholipids in lipid bilayers
and disruption of cell membranes or virus
membrane envelopes. Thus once it enters into the
microbe, they have other toxic effects (DNA, RNA,
protein synthesis inhibition) -> cell death
Types of pathogens AMPs work on Bacteria, Fungi, viruses and parasites
(NOTE: part of the innate immunity)
Role of normal flora in immunity ● Form a protective layer preventing
pathogens from colonising
● Producing metabolic products (fatty acids,
bacteriocins, etc.) that inhibit growth of
many pathogens
● Depleting nutrients essential for the growth
of pathogens
● Non-specifically stimulating the immune
system that strengthens the epithelial barrier
function
Primary lymphoid organs Bone marrow and thymus = responsible for
generating all immune cell types
,Cells that make up the innate immunity Myeloid and NK cells
Cells that make up the adaptive immunity B and T cell lymphocytes
Phagocytic cells that make up the innate immunity Dendritic cells, Macrophages and neutrophils
(also monocytes in the blood)
1st dedicated immune cell type to detect the Resident macrophages
presence of pathogens within tissues
Phagocytosis The cellular uptake and destruction of particulate
materials greater than 0.5 microns (such as bacteria)
Is this statement T/F: ‘All PRRs induce phagocytosis’ False; NOT all PRRs induce phagocytosis
2 ways in which phagocytes recognise microbes 1. Some receptors (PRRs) recognise directly
specific conserved molecular components
(PAMPs) on the surface of microbes such as
cell components of bacteria and fungi
2. Via opsonin receptors; they recognise
soluble opsonins bound to microbes
PAMPs Pathogen-Associated Molecular Patterns = specific
conserved molecular components on microbes
Cell component that induce PAMPs Cell wall components (including complex
carbohydrates such as mannans and b-glucans,
lipopolysaccharides (LPS), other lipid containing
molecules, peptidoglycans and surface proteins)
‘Self-nonself’ discrimination Via PRRs recognising PAMPs
(NOTE: do NOT bind on galactose or sialic acid groups
that are mammalian surface polysaccharides but they
bind to nucleic acids from bacterial and viral genomes
(e.g. dsRNA)
How do PRRs identify the pathogen A combination of PRRs is specific for a group of
pathogen-associated molecular patterns (PAMPs) ->
thus the combination of occupied PRRs decodes the
nature of the infection
(there are other PRRs that after PAMP binding, do
NOT activate phagocytosis but trigger other types
of responses)
DAMPs Damage (Danger)-associated molecular patterns
(NOTE: it’s components of the dead/dying cells and
damaged tissues recognised by PRRs leading to cell
clearance)
CD47 ‘Eat me’ vs ‘don’t eat me’ signal; it acts as a marker
of self to innate immune cells
(NOTE: CD47 is used as a signal by cancer cells to
protect itself from phagocytic clearance)
Opsonin A molecule that binds a microbial surface marking it
, for recognition by phagocytes
Opsonisation The modification of antigens with opsonins to
enhance phagocytosis
Why are opsonins referred to as soluble PRRs Many opsonins also recognise conserved
components on microbial surfaces -> thus aka
soluble PRRs
CD91 Opsonin receptor -> thus activates phagocytosis
(NOTE: all opsonins are recognised by the same opsonin
receptor; CD91)
CR1 Complement receptors (CR1) on phagocytes
connects opsonin-tagged pathogens to phagocytes
How does phagocytosis can cause extensive tissue As reactive oxygen species and antimicrobial
damage peptides can be released extracellularly and are
toxic to host cells -> thus causing extensive tissue
damage
(NOTE: ROS = reactive oxygen species, RNS = reactive
nitrogen species)
Pt w/ increased risk of infections to catalase positive Chronic Granulomatous Disease (CGD; X-linked
bacteria and fungi recessive); this is due to defects in the NADPH
oxidase -> thus resulting in no ROS production
Why do granulomas form in CGD Due to inefficiency of phagocytes, resulting in
accumulation of immune cells with ingested
microbes but unable to eliminate them
Nitroblue tetrazolium test Test for CGD
Neutrophils are stimulated w/ nitroblue tetrazolium
(NBT) test reagents → should produce ROS as
opposed to non stimulated cells which do not
(NOTE: Normal pt = presence of ROS. CGD pt = NO
ROS formed)
DHR (dihydrorhodamine) assay for analysis of NADPH oxidase activity
Normal phagocytes upon activation → produce
superoxide radicals → thus reduce DHR to
rhodamine; fluorescent molecule
(NOTE: pt w/ CGD → fail to reduce DHR → thus remain
non-fluorescent like resting cells)
Tissue resident immune cells Macrophages, mast cells and DCs
Characteristics of an inflamed tissue Heat, redness, pain and swelling
, Heat and redness aspect of inflammation Vasodilation of blood vessels close to the site of
infection -> increased local blood flow at the site of
infection (thus heat and redness) -> thus reduced
velocity of blood flow
Extravasation of circulating leukocytes into tissues Activation of endothelial cells lining the blood vessel
-> expression of cell adhesion molecules -> binding
and extravasation of circulating leukocytes into
tissue
Oedema and pain aspect of inflammation Increased vascular permeability -> plasma (+plasma
proteins e.g. complement) invade the tissue at the
point of infection (thus swelling and pain)
Purpose of clotting in inflammation Clotting in microvessels at the site of infection
prevents the spread of pathogen
Damaged tissues and dying cells also release DAMPs
molecules capable of engaging PRRs
IFN-𝛂, 𝜷 Type I Interferons
Innate immunity protein used against viruses Type I interferons (-> bind to IFNR expressed by
most cell types -> thus downstream signalling
leading to the recruitment of JAKs that activate
STATs -> induction of gene expression of proteins
that block viral replication: Protein Kinase R (PKR))
This element is used in antiviral therapies (Hep B Type I Interferons
and C) and is also beneficial in the treatment of (NOTE: PKR aspect -> useful in antiviral therapies. They
Multiple Sclerosis also activate the NK cells and regulate the activities of
macrophages and T cells; thus also beneficial in the
treatment of MS)
IL-1, IL-6, and TNF-𝛂 Pro-inflammatory cytokines
Systemic effects of pro-inflammatory cytokines ● Feedback on BM haematopoiesis to enhance
neutrophil production
● Induction of fever by inducing production of
prostaglandin E2 which acts on the
hypothalamus
● Induce production of the acute-phase
proteins by the liver
IL-10 Anti-inflammatory cytokine
(NOTE: TLR mediated induction in macrophages and
DCs -> inhibits mf activation and pro-inflammatory
cytokine production)
Chemokine Chemoattractants = agents that induce cells to move
towards higher concentration of the agent
IL-8 (CXCL8) Chemoattractant for neutrophils (during initial
stages of infection or tissue damage)
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