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Samenvatting Immunology van alle hoorcolleges, practica en werkgroepen
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Celbiologie en Immunologie Samenvatting DT2
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Summary Immunology 2.0Inhoudsopgave
INNATE IMMUNITY....................................................................................................................... 2
WORKGROUP 1 INNATE IMMUNITY I ..................................................................................................... 2
WORKGROUP 2 INNATE IMMUNITY II .................................................................................................... 6
B-CELL ONTOGENY, ANTIBODY DIVERSITY, B-CELL IMMUNITY ....................................................... 9
WORKGROUP 3: STRUCTURE OF AN ANTIBODY MOLECULE; GENERATION OF ANTIBODY DIVERSITY; AND ANTIBODY-
ANTIGEN INTERACTIONS ..................................................................................................................... 9
WORKGROUP 4: B-CELL ONTOGENY, B-CELL ACTIVATION AND THE GERMINAL CENTRE REACTION....................... 16
ANTIGEN RECOGNITION BY T CELLS ............................................................................................. 19
WORKGROUP 5: ANTIGEN RECOGNITION BY T CELLS ............................................................................... 19
T CELL DEVELOPMENT, TCR DIVERSITY ........................................................................................ 23
WORKGROUP 6: T CELL DEVELOPMENT, TCR DIVERSITY .......................................................................... 23
WORKGROUP 7: T-CELL MEDIATED IMMUNITY AND T-CELL SUBSETS........................................................... 26
WORKGROUP 8: NATURAL KILLER CELLS AND IMMUNOLOGICAL MEMORY AND VACCINATION .......................... 30
A: NATURAL KILLER CELLS ........................................................................................................................... 30
B: IMMUNOLOGICAL MEMORY AND VACCINATION .......................................................................................... 33
WORKGROUP 9.............................................................................................................................. 35
WORKGROUP 9A: TRANSPLANTATION ........................................................................................................... 35
WORKGROUP 9B: IMMUNE EVASION OF PATHOGENS AND IMMUNE DEFICIENCIES ............................................... 38
WORKGROUP 10 ........................................................................................................................ 41
WORKGROUP 10A: HYPERSENSITIVITY OF THE IMMUNE SYSTEM ............................................................... 41
WORKGROUP 10B: AUTOIMMUNE DISEASE .......................................................................................... 43
WORKGROUP 10C: CANCER AND ITS INTERACTIONS WITH THE IMMUNE SYSTEM ............................................ 46
TECHNIQUES .............................................................................................................................. 48
1
,Innate Immunity
Our skin is the first line of defence limiting access of pathogens to the body. Unfortunately,
pathogens have evolved to break such barriers. Pathogens must be discriminated between
'self' and 'non-self'. Specific receptor sense the presence of invading pathogens, triggering
the innate immune reponse, limiting spread of pathogen and hopefully leading to
eradication of the pathogen. However, the pathogen is not eradicated all of the times, so the
adaptive immune response is additionally activated, eradicating the pathogen. This
response also generates memory.
Innate immune response components:
- TLR, complement factors, neutrophils, pathogens, NK-cells
Adaptive immune response components:
- b/t-cells, DC's.
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
Present at birth, instantly available and
active
Extra info:
• Neutrophils: Help protect your body from infections by killing bacteria, fungi and foreign
debris.
• Lymphocytes: Consist of T cells, natural killer cells and B cells to protect against viral
infections and produce proteins to help you fight infection (antibodies).
• Eosinophils: Identify and destroy parasites, cancer cells and assists basophils with your
allergic response.
• Basophils: Produces an allergic response like coughing, sneezing or a runny nose.
• Monocytes: Defend against infection by cleaning up damaged cells.
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.
2
, - 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. Around
4,5 kg. different niches have different microbiota. Antibiotics also kill commensal
bacteria since they take their nutrients, excrete metabolic products which inhibit their
growth or alarm the immune system to eliminate pathogens.
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). The bacterium has specific antigens. C3b is special because it
can bind directly to the antigen, straight to the pathogen surface. This is
characteristic for this pathway, there is no antibody present. Technically, factor B is
present, but it's not important. Again, all of the other c-molecules can bind.
Moreover, the MAC is formed, causing extracellular fluid to leak in. c3b is now
exposed after the MAC has formed, to which the macrophages or neutrophils can
bind with their c3b receptor.
2. Lectin pathway: mannose binding lectin binds mannose-containing carbohydrates in
pathogens including MASP that cleaves C4 >>> C3 convertase. The bacterium has
specific types of antigens, mannose, present on its surface. MBL can perfectly bind
with that antigen. C4 can bind to the MBL complex, followed by c2, c3b etc. the same
cascade of reactions occurs.
3. Classical pathway: antigen-antibody reaction leads to the activation of C1 >>> C3
convertase. Memory antibodies might also leak out which have been exposed to the
specific antigen before. These can be IgM or IgG. After binding to the antigen, the Fc
portion of the antibody is attractive to the complement proteins. The first one
binding is C1, afterwards C4 binds, then C2, then C3. C3 convertase splits c3 into c3a
c3b. C3b will then allow the binding of c5b. c6 binds, then 7 all the way to c9. C5
convertase splits c5b into c5a. the proteases, released by the mast cell, activate c3a
and c5a. when activated, these enhance inflammatory response by chemotaxis.
From c3b, molecules can break of. All of these molecules can form a membrane
attack complex (MAC). This is a pore that can attach itself on the membrane of the
bacterium. There is now an open connection between the inside of the bacterium
and the outside, after which all sorts of molecules like sodium and water flow in. The
bacterium undergoes lysis because it kept becoming bigger. C3b is an opsonin.
Macrophages posit a c3b receptor which binds to the c3b which was bound to the
bacterium via the antibody. This receptor pulls the entire bacterium including the
complement proteins into the macrophage, breaking everything down and exposing
3
, it to MHC II and phagocytosis occurs. Opsonins cause opsonization, enhancing
phagocytosis. So, the overall result is MAC formation (1), opsonization (2) and c3a +
c5a (3).
These are all proteins produced by our liver, circulating in our plasma, inactive, activated by
an inflammatory response.
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
- Opsonization: marking of pathogens facilitating uptake and killing by phagocytes via
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 containing CR1 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. Factor H binds c3b and changes its
conformation, cleaving it.
The induced response to infection
When the complement system fails to eliminate the pathogen then an induced innate immune
response is made in which there is activation of cells resident in the infected 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.
4
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