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Summary Immunology
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summary Immunology, all reading material, working groups and lectures. Practicals included
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Summary ImmunologyInhoudsopgave
Innate Immunity ............................................................................................................................................. 2
Workgroup 1 Innate immunity I ......................................................................................................................... 2
Workgroup 2 Innate immunity II ........................................................................................................................ 4
B cell ontogeny, antibody diversity, B cell immunity ..................................................................................... 4
Workgroup 3 structure of an antibody molecule; generation of antibody diversity; and antibody antigen
interactions ......................................................................................................................................................... 5
Workgroup 4: B-cell ontogeny, B-cell activation, and the germinal center reaction ......................................... 8
Antigen recognition by T-cells ...................................................................................................................... 10
Workgroup 5: Antigen recognition by T-cells .................................................................................................. 10
T cell development, TCR diversity ............................................................................................................... 13
Workgroup 6: T cell development, TCR diversity ............................................................................................ 13
Workgroup 7: T-cell mediated immunity and T-cell subsets ............................................................................ 15
Workgroup 8: Natural killer cells and immunological memory and vaccination ............................................ 18
A: Natural killer cells .................................................................................................................................. 18
B: Immunological memory and vaccination ................................................................................................ 20
Workgroup 9..................................................................................................................................................... 22
A: Transplantation ....................................................................................................................................... 22
B: Immune evasion of pathogens and immune deficiencies ........................................................................ 25
Workgroup 10................................................................................................................................................... 27
A: Hypersensitivity of the immune system.................................................................................................. 27
B: Autoimmune disease ............................................................................................................................... 28
C: Cancer and its interactions with the immune system .............................................................................. 30
Techniques .................................................................................................................................................... 33
Antibodies ................................................................................................................................................... 33
Flow Cymetry .............................................................................................................................................. 34
Anatomy of the lymphoid organs ................................................................................................................ 34
1
,Summary Immunology
Innate Immunity
Innate immunity Adaptive immunity
Rapid response within hours Slow response in days to weeks (activation
of specific correct receptor and clonal
expansion of particular receptor takes time)
Limited number of specificities (is receptor- Numerous highly selective specificities due
mediated on the other hand) to specific receptors (specific to particular
pathogen)
Constant during the course of response The ability to improve during the course of
response (establishment of immunological
memory after exposure)
Does not entirely clear the infection Does entirely clear the infection
Workgroup 1 Innate immunity I
Physical barriers to infection
The innate immune system consists of different elements that play different, but often
complementary functions in the innate response:
- Mechanical (1st line of defense): physical barrier function of the epithelia, fluids such
as tears and mucosa along with physiological functions such as cilial action, motility,
peristaltic action and mucus secretion.
- Humoral/chemical (1st line of defense): soluble (enzymatic) proteins or small peptides
that hydrolyze microorganisms or affect their reproduction, and small messenger
molecules (cytokines and chemokines) that orchestrate the course of the innate
immune response.
- Cellular (2nd line of defense): all cells of the immune system that may function in
innate defenses. These are epithelial cells, endothelial cells, mast cells, dendritic cells,
natural killer (NK)-cells and phagocytes, i.e. monocytes/macrophages and neutrophilic
granulocytes
- Microbiological: Commensal microbiota that pathogens have to compete with.
Second line of defense (innate immunity)
The immediate response to infection
The complement system facilitates the immediate response against an infections and has
different activation pathways that become subsequently activated in this order:
1. Alternative pathway: certain constituents of the bacterial cells surface change the
physicochemical environment leading to spontaneous hydrolysis of C3 causing the
formation of soluble C3 convertase >>> C3 convertase at pathogen surface
(expodential growth)
2. Lectin pathway: mannose binding lectin binds mannose-containing carbohydrates in
pathogens including MASP that cleaves C4 >>> C3 convertase
3. Classical pathway: antigen-antibody reaction leads to the activation of C1 >>> C3
convertase
Eventually all routes of activation lead to the convertase of C3 into C3a and C3b by C3b
being covalently bound to the pathogen surface. This has different effector mechanisms:
- Induce inflammation (anaphylatoxins such as C3a and C5a):
o Chemotaxis: recruitment of inflammatory cells
o Vascular permeability
o Degranulation of mast cells and basophils
2
,Summary Immunology
- Opsonization: marking of pathogens facilitating uptake and killing by phagocytes vua
CR1 receptor that binds C3b
- Cell lysis: perforating of pathogen cell membrane by Membrane Attack Complex
(MAC)
- Activation of B-cells (acquired immune response)
- Remove immune complex (resolution): erythrocyte carries c3b-tagged immune
complex to the liver or spleen where it is detached and taken up by a macrophage
Regulatory proteins called complement control proteins determine the extent and sit of C3b
deposition such as factor H, DAF, MCP and properdin
The induced response to infection
When the complement system fails to eliminate the pathogen then an induced innate immune
response is made in whihch there is activation of cells esident in the infectected tissue and
recruitment of effector cells leading to inflammation, fever and acute phase response.
The induced phase of innate immunity involves soluble and cellular receptors that detect the
presence of infecting organisms and recruit leukocytes to make an inflammatory response,
which induces a state of inflammation in the infected tissue.
Cell-surface receptors on innate immune cells detect the differences between self, non-self
(microbes) and altered-self (infected/cancerous cells). These cell-surface receptors are pattern
recognition receptors (PRRs) that recognize structural features common to many different
types of pathogens. These ligands can be pathogen-associated molecular patterns (PAMPs) or
damage-associated molecular pattern (DAMPs).
There are different types of receptors, which each target different ligands and therefore
different pathogens:
- Complement receptors: bind to c3b that have been deposited on pathogen surgace by
activation of the complement system and is therefore an indirect form of recognition
- Toll-like receptors (TLRs): direct form of pathogen recognition. TLRs are signaling
receptors that produce and secrete inflammatory cytokines instead of inducing
phagocytosis. TLRs can be present on the plasma membrane of leukocytes which
recognize ligands on the outer surface of pathogens. On the otherhand TLRs can be
present within the membranes of endosomal vesicles and recognize features of nucleic
acids of degraded/phagocytized pathogens (DNA/RNA).
o When toll-like receptors detect the presence of a pathogen then the cytokine
IL-1 is synthesized but kept in an pro-form. When NOD-like receptors sense a
pathogen it can form an inflammasome that transforms pro-IL-1 to the active
form. Secretion of the IL-1 is then achieved by pyroptosis (death macrophage)
- Fc-receptors:
- Scavenger receptors (SR-E2, SR-A1): Scavenger receptors trigger processes of
phagocytosis, cell adhesion, and intracellular signaling to identify microbes and
molecules that could be harmful to the host, and then cause their elimination or
degradation. They also remove cells that have died by apoptosis
- NOD-receptors: recognize products arising from the intracellular degradation of
phagocytosed bacteria eventually leading to the activation of a transcription factor that
orchestrates macrophage activation.
- RIG-I-like receptors (RLRs): detect intracellular viral RNA leading to interferon
production leading to an interferon 1 response (autocrine and paracine fashion):
3
, Summary Immunology
o Induces uninfected cells to produce enzymes that are able to degrade viral/cellular
mRNA (infected cell will die as well)
o Enhances the ability of NK cells to lyse infected cells by (1) activating NK
cells and (2) by increasing expression of ligands for receptors on NK cells
(stress signals?)
o Increases MHC-I ligand expression on APCs so that CD-8 cells can respond
(aquired IS)
➢ The overall effect of ligands binding to these receptors is the production of (pro-)
inflammatory cytokines (humoral) or facilitate phagocytosis (cellular)
Workgroup 2 Innate immunity II
There are different types of effector cells that carry out effector mechanisms guided by
complement:
1. Cells that engulf pathogens by phagocytosis: neutrophilic granulocytes, monocytes,
macrophages and dendritic cells, collectively called phagocytes
2. Cells that release inflammatory mediators (cytokines, chemokines)*: phagocytes, mast
cells and basophilic and eosinophilic granulocytes
3. Cells involved in anti-viral and anti-tumor immunity: natural killing lymphocytes (NK
cells)
Viral infections
*Cytokines and chemokines:
Inflammation
Inflammation is characterized by different characteristics:
1. Heat: cytokines induce dilation of nearby blood capillaries which increase the blood
flow causking skin to warm
2. Pain: dilation of blood vessels leads to the endothelium becoming more permeable
causing edema leading to pressure on nerve endings causing pain. Cytokines alter the
adhesive properties of endothelium permitting infiltration of inflammatory cells that
release chemicals that cause pain
3. Redness: cytokines induce dilation of nearby blood capillaries which increase the
blood flow causking skin to redden
4. Swelling: dilation of blood vessels leads to the endothelium becoming more
permeable causing edema leading to swelling. Cytokines alter the adhesive properties
of endothelium and attract inflammatory cells permitting infiltration of inflammatory
cells increase swelling
➢ The reason for inflammation is that it enables an army of immune system cells and
soluble effector molecules to be brought rapidly and in quantity to the infected tissue.
B cell ontogeny, antibody diversity, B cell immunity
4
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