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Samenvatting boek Immunologie
Samenvatting van het boek 'The Immune System - 4th edition' dat wordt gebruikt bij het vak Immunologie bij de BSc Gezondheidswetenschappen op de Vrije Universiteit Amsterdam
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Voorbeeld van de inhoud
U1- ELEMENTS OF THE IMMUNE SYSTEM + THEIR ROLES IN DEFENSEMain purpose of the immunesystem: Protect the human body from infectious disease
- Body also contains commensal organisms + microbiota, these are safe
1.2. PATHOGENS ARE INFECTIOUS ORGANISMS THAT CAUSE DISEASE
Pathogen=an organism with the potential to cause disease
- Opportunistic pathogens: Cause illness if the body’s defenses are weakened/if the microbe
gets into the ‘wrong’ place.
4 kinds: Bacteria, viruses, fungi, parasites.
1.3. THE SKIN AND MUCOSAL SURFACES FORM BARRIERS AGAINST INFECTION
Skin: First defense- epithelium lines outer surface and inner cavities of the body.
Mucosal surfaces: Internal surfaces that give way to tissues that are specialized for communication
- Contains glycoproteins, proteoglycans and enzymes- protect epithelial cells from damage
o Respiratory mucose is continuously cleansed by epithelial cells beating cilia and
replenished by mucus-secreting goblet cells.
Epithelial surfaces secrete antimicrobial substances
- Antimicrobial peptides- kill bacteria, fungi and enveloped viruses- perturbs membranes
- Lysozyme- enzyme that kills bacteria by degrading their cell walls (in tears and saliva)
- Acidic environments deter micro-organisms (stomach, vagina, skin)
o When these barriers are breached- the innate system is brought into play
1.4. THE INNATE IMMUNE RESPONSE CAUSES INFLAMMATION AT SITES OF INFECTION
Innate immune response- 2 parts:
1. Recognition that a pathogen is present-
2. Recruitment of destructive effector mechanisms that kill and eliminate the pathogen
a. Effector cells provide the effector mechanisms.
i. Complement: Battery of serum proteins that help the effector cells by
marking pathogens + attack pathogens themselves.
Surface wound:
1. Cells and proteins in the damaged tissue sense the presence of bacteria and send out soluble
proteins called cytokines
2. Cytokines interact with other cells to trigger the innate immune response
3. Induced state of inflammation in the infected tissue.
4. Cytokines induce local dilation of blood capillaries- causes the skin to warm and redden
5. Vascular dilation (vasodilation) introduces gaps between endothelium cells (lines interior of
blood vessels)- endothelium becomes permeable
6. Increased leakage of blood plasma into the connective tissue- edema (swelling) + dolor
7. Cytokines change adhesive properties of vascular endothelium- invites white blood cells to
attach to it and move into the inflamed tissue (the blood cells are called inflammatory cells)
8. Infiltration of cells into inflamed tissue causes tumor and dolor
1.5. THE ADAPTIVE IMMUNE RESPONSE ADDS TO AN ONGOING INNATE IMMUNE RESPONSE
Some infections outrun the innate immuneresponse. When this occurs, the innate immune response
works to slow the spread of the infection while it calls upon white blood cells called lymphocytes
- Lymphocytes increase the power and focus of the immune response
Lymphocytes are very specific, so they proliferate and differentiate to produce large numbers of
effector cells specific for the pathogen they carry the receptor of clonal selection/expansion
- Primary immune response=First time an adaptive response is made to a given pathogen.
- Secondary immune response=Second and subsequent times (when immunological memory
applies)
,1.7. IMMUNE CELLS WITH DIFFERENT FUNCTIONS ALL DERIVE FROM HEMATOPOIETIC STEM CELLS
Hematopoiesis=Developmental process that generates blood cells- takes place in the bone marrow.
- Pluripotent hematopoietic stem cell: Progenitor- makes:
o Leukocytes- white blood cells
o Erythrocytes- red blood cells
o Megakaryocytes- source of platelets
Hematopoietic cells=These cell types + their precursor cells.
- Hematopoietic stem cells divide: Self renewal- daughter cells can become more mature stem
cells that commit to one of three cell lineages
o Erythroid
Megakaryocyte- Produce platelets
Erythroblast- red blood cell (carries oxygen
o Myeloid (=of the bone marrow)
Granulocytes- have prominent cytoplasmic granules containing reactive
substances that kill microorganisms and enhance inflammation
Neutrophil- specialized in the capture, engulfment and killing of
micro-organisms Most lethal type of phagocytes
o Effector cells of innate immunity- form pus
Eosinophil- defends against parasites
Basophil- also responds to parasites, but is very rare
Monocytes, macrophages and dendritic cells
Monocytes: Leukocytes that circulate in the blood travel to
tissues where they mature into macrophages.
Dendritic cells- act as cellular messenger sent to call up an adaptive
immune response when needed.
Mast cell- contribute to inflammation when activated at site of infection
o Lymphoid
Natural Killer cells- enter infected tissue where they prevent the spread of
infection by killing virus-infected cells + secreting cytokines innate
Small lymphocytes- responsible for the adaptive immune response
B-cells Plasma cells- adaptive
T-cells Effector T-cells- adaptive
1.8. IMMUNOGLOBULINS AND T-CELL RECEPTORS ARE THE DIVERSE LYMPHOCYTE RECEPTORS OF
ADAPTIVE IMMUNITY
B lymphocytes: Cell-surface receptors are immunoglobulins
- Effector B cells (Plasma cells)- secrete soluble forms of immunoglobulins called antibodies.
T lymphocytes: Receptors are T-cell receptors
Antigen: Contains structure recognized and bound by an immunoglobulin/T-cell receptor
- T-cell receptors + immunoglobulins are also known as antigen receptors of lymphocytes
1.9. ON ENCOUNTERING THEIR SPECIFIC ANTIGEN, B CELLS AND T CELLS DIFFERENTIATE INTO
EFFECTOR CELLS
Effector T-cell
- Cytotoxic T cells: Kill cells infected with viruses/certain bacteria
- Helper T cells: Secrete cytokines that help other cells of the immune system become fully
activated effector cells.
o Regulatory T-cells: Control activity of other T-cells- prevents unnecessary damage
,1.10. ANTIBODIES BIND TO PATHOGENS AND CAUSE THEIR INACTIVATION OR DESTRUCTION
Humoral immunity=immunity due to antibodies circulating the blood and entering infected tissues
- Neutralization: Antibodies bind tightly to a site on a pathogen to inhibit pathogen growth
- Opsonization: Coating of the entire surface of the pathogen by an antibody
o Neutrophils and macrophages have cell-surface receptors that bind to the antibody
molecule site
Thousands of the receptors on the phagocyte will bind to thousands of
antibodies on the pathogen- can’t escape a rapid engulfment and death.
1.11. MOST LYMPHOCYTES ARE PRESENT IN SPECIALIZED LYMPHOID TISSUES
Majority of lymphocytes are found in lymphoid tissue/organs
- Lymphoid organs: Bone marrow, thymus, spleen, adenoids, tonsils, appendix, lymph nodes
and Peyer’s patches
- Lymphoid tissue:
o Primary/central lymphoid tissue: Where lymphocytes develop and mature
Bone marrow + thymus
B-cells mature in bone marrow
T-cells migrate to thymus, where they mature
o Secondary/peripheral lymphoid tissues: Sites where mature lymphocytes become
stimulated to respond to invading pathogens.
Mature B and T cells move through the body in both blood and lymph
Lymphocyte recirculation=Pattern of movement between blood and lymph
1.12. ADAPTIVE IMMUNITY IS INITIATED IN SECONDARY LYMPHOID TISSUES
Draining lymph node=Lymph node receiving the fluid collected at an infected site
- Arriving lymphocytes segregate to different regions of the lymph node:
o B-cells to B-cell areas- lymphoid follicles
o T-cells to T-cell areas
- Pathogens + pathogen-laden dendritic cells from the infected tissue arrive at a lymph node in
afferent lymphatic vessels- leave as a single efferent lymphatic vessel.
o As lymph passes the node- the dendritic cells settle there and pathogens are filtered
out by macrophages prevents infectious organisms from reaching the blood.
- Germinal center: Dense spherical structure in each follicle from pathogen specific B cells that
have bound the pathogen.
1.13. THE SPLEEN PROVIDES ADAPTIVE IMMUNITY TO BLOOD INFECTIONS
Spleen=Lymphoid organ that serves as a filter for the blood. Remove damaged or senescent red cells/
acts as a secondary lymphoid organ that defends the body against blood-borne pathogens.
- Red pulp- red blood cells monitored and removed
- White pulp- white blood cells gather to provide adaptive immunity
Encapsulated bacteria: Cells surrounded by a thick polysaccharide capsule.
Immunodeficiency disease: Condition in which the inheritance of one or more mutant genes leads to
defects in one or more aspects of the immune system’s functions (f.e. asplenia- no spleen)
1.14. MOST SECONDARY LYMPHOID TISSUE IS ASSOCIATED WITH THE GUT
Gut-associated lymphoid tissue (GALT): Tonsils, adenoids, appendix, Peyer’s patches (line the small
intestine)
Bronchial-associated lymphoid tissue (BALT): Line the respiratory epithelium
Mucosa-associated lymphoid tissue (MALT): Mucosal lymphoid tissue
- Pathogens arrive at MALT by delivery across mucosa, mediated by M cells (specialized cells of
mucosal epithelium)
, U2- INNATE IMMUNITY: THE IMMEDIATE RESPONSE TO INFECTION
2.1. PHYSICAL BARRIERS COLONIZED BY COMMENSAL MICROORGANISMS PROTECT AGAINST
INFECTION BY PATHOGENS
External defense: Skin + mucosal epithelia that line digestive, respiratory and urogenital tracks
Commensal microorganisms: Colonize the skin and mucosal surfaces of healthy individuals-
pathogens have to compete with the resident commensals for nutrients and space
2.2. INTRACELLULAR AND EXTRACELLULAR PATHOGENS REQUIRE DIFFERENT TYPES OF IMMUNE
RESPONSE
Extracellular infections: Pathogens live and replicate in the spaces between human cells
- Accessible to soluble, secreted molecules of the immune system.
Intracellular infections: Pathogens replicate inside human cells
2.3. COMPLEMENT IS A SYSTEM OF PLASMA PROTEINS THAT MARK PATHOGENS FOR DESTRUCTION
Complement: Plasma proteins- soluble proteins made by liver and present in blood, lymph +
extracellular fluids
- Coats the surface of bacteria/extracellular virus particles and makes them more easily
phagocytosed- especially bacteria enclosed in thick polysaccharide capsules resist phagocyt.
Zymoges: Functionally inactive forms of proteases.
- Infections triggers complement activation: Series of enzymatic reactions in which each
protease cleaves and activates the next protease in the pathway.
o Enzymes are highly specific for complement component it cleaves
Complement Component 3 (C3) =Most important protein in the complement system
- When complement system is activated it leads to the cleavage of C3 into a small C3a and a
large C3b fragment. Some of the C3b fragments become covalently bound to the pathogens
surface Essential function of the complementsystem
o Complement fixation: C3b becomes firmly fixed to the pathogen
C3b tags the pathogen for destruction + organizes the formation of protein
complexes that damage the pathogen’s membrane
C3a acts as a chemoattractant to recruit effector cells (f.e. phagocytes)
- C3 enters circulation in an inactive form: A thioester is stabilized within the hydrophobic
interior of the protein to protect is from the hydrophilic environment.
o When C3 is cleaved: Thioesterbond is exposed (nucleophile). C3b either:
Soluble C3b: Attack by H2O- remains inactive
C3b binds to pathogen surface: Attack by OH/NH2 groups
3 pathways:
- Alternative pathway/complement activation=Pathway that works at the start of infection
- Lectin pathway of complement activation=Second pathway: induced by infection and
requires some time before it gains strength- part of innate immunity
- Classical pathway of complement activation=Third pathway: requires binding of either
antibody/ innate immune-system protein called C-reactive protein to the pathogen’s surface-
both adaptive + innate immunity
2.4. AT THE START OF AN INFECTIONS, COMPELMENT ACTIVATION PROCEEDS BY THE ALTERNATIVE
PATHWAY
Alternative pathway: C3 changes its conformation and exposes the thioester bond (no cleavage)
- Thioester bond becomes active + makes covalent bond- attaches C3 to molecule with amino/
hydroxyl group gives a form of C3 called iC3/C3(H2O)
iC3 binds to the inactive complement factor B B becomes susceptible to cleavage by protease
factor D produces Ba (small fragment) + Bb (large fragment), which binds to iC3
- iC3bBb complex cleaves C3 into C3a and C3b
C3 convertases: Proteases that cleave and activate C3 (f.e. iC3Bb)
C3bBb=Alternative C3 convertase- works at surface of pathogen- cleaves C3 into C3a and C3b
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