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Summary Immunology NinjaNerd Videos
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This document contains an English summary of all NinjaNerd videos about the subject immunology, with some additional notes.
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Immunology SummaryInnate Immune System
Inflammation: Vascular Events
Inflammation = tissue damage that initiates vascular/cellular/molecular events that clean up
any type of debris or pathogens and initiate repair
Causes: physical/chemical/infections/sunlight
Inflammation signs: (1) swelling, (2) pain, (3) heat, (4), redness, (5) joint immobility
Bacteria have antigens on their surface.
Antigen has to be:
1) Immunogenic
a. Has to be able to activate certain type of immune system cells after which
proliferation occurs
2) Reactive
a. Has to activate plasma cells to produce antibodies
Whenever a bacterium enters, many mast cells surrounding the bacterium are also present.
The endotoxins released by the bacteria can activate the receptor on the mast cell, resulting
in the mast cell producing different molecules. Most important one is histamine,
leukotrienes and pastagladins.
After a series of events in which the mast cell releases many cytokines, receptors on the
vessels sense the cytokines and P-selectins move to the cell surface. The endothelial cells
contract as a result to the cytokines, causing spaces between the endothelial cells
increase vascular permeability. Plasma leaks out the intercellular clefts, causing the
interstitial space becoming bigger, causing swelling. The interstitial space contains pain
receptors. Fluid presses on these receptors, causing pain. All cytokines released bby the
mast cell can bind receptors on smooth muscle cells, making the cell relax, expanding the
blood vessel vasodilation. Blood vessel gets bigger, so more blood flow, so more redness
and heat because blood is around 37 degrees. Because of some really bad inflammations,
joint immobility can occur due to the fluid suppressing movement.
The white blood cells, e.g. neutrophils and monocytes, interact with the p-selectins on the
endothelial cell surface. P-selectins prevent the leukocytes from flowing past the inflamed
area: margination. Due to rollingadhesion, the white blood cells interact with the P-CAMs
and the white blood cells squeeze through the endothelial cells: diapedesis. All the cytokines
released by the mast cell bind to the receptors on the cell surface of the leukocytes. These
cytokines stimulate the right site of the leukocytes, causing them to migrate to the site of
inflammation: positive chemotaxis.
The white blood cell, especially the macrophage, starts fighting the bacterium but wants to
alert other cells that there's more bacteria in this area. The macrophage, therefore, secretes
IL-1, IL-8 and TNF-alfa. IL-1 and TNF-alfa activate the endothelial cell to produce E-selectins,
, allowing monocytes and neutrophils to adhere with the E-selectins. IL-8 binds to specific
receptor on endothelial cell membrane, activating endothelial cell to synthesize ICAM and
VCAM. Neutrophils get activated, integrins on neutrophil surface becomes activated and
now interacts with VCAM and ICAM, inducing diapedesis and positive chemotaxis again.
IL-1 and TNF-alfa travel to the hypothalamus, activating the secretion of PGE2. PGE2 resets
our body temperature, initiating fever. Fever is a harsh environment for certain organisms to
survive (1)and it speeds up metabolism, beneficial for our healing process (2). IL-1 and TNF-
alfa stimulate the liver to release acute phase reactant proteins – C-reactive peptide.
Moreover, the bone marrow is stimulated to blasting out more leukocytes leukocytosis.
Inflammation: Cellular Events
The macrophage's cytoskeleton undergoes a conformational change, coming around the
bacterium. The neutrophil will do the same, phagocytosing the bacterium. Vesicle inside the
macrophage/neutrophil forms and is called the phagosome. This phagosome contains the
bacterium with the antigens still presented on the cell surface. The macrophage/neutrophil
contains lysosomes with specific types of hydrolytic enzymes. The membranes of the
lysosome and phagosome fuse together, breaking down the cell wall of the bacterium. The
vesicle that is formed right now is a phagolysosome. The bacterium is degraded but the
antigens remain. The phagolysosome now fuses with the cell membrane, releasing the
intracellular particles (antigens), a process called exocytosis. The antigens are transported to
the lymph node afterwards.
Sometimes the bacterium is very aggressive. Free radicals can destroy both the bacterium as
well as the neutrophil's membrane proteins. This is called oxidative burst. The neutrophil is
about to die because of its free radical reactions. The leukocyte releases its chromatin/DNA
during the apoptosis, binding on foreign bacteria antigens, activating other enzymes by
tagging the bacterium. This is all called neutrophil extracellular traps (NETs).
Macrophages are antigen presenting cells. Macrophages has a specific gene sequence on
chromosome 6, responsible for producing proteins, also known as MHC molecules specific to
fit the antigens. The specificity is arranged by gene recombination. MHC molecules (II) bind
to the intracellular antigens and present them on the cell membrane. This is also gonna go
into the lymph node. There's 3 types of MHC class I: A, B and C genes can shuffle and
produce different types of fragments. MHC class II has: DP, DQ and DR.
Inflammation: Complement Proteins
The liver excretes complement proteins, which also squeeze out the blood vessels through
diapedesis.
Classical Pathway
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.
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