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Immunology [AB_1244] Lecture Notes
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Complete summary of the lectures from the course Immunology [AB_1244] lectures of the Bsc. Biomedical Sciences at the Vrije Universiteit.
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Immunology [AB_1144]Bsc. Biomedical Sciences 2024
CH1/2 Complement
Blood consists of
● Red blood cells
● Platelets
● Plasma (complement and antibodies)
● White blood cells, consisting of
○ Granulocytes (neutrophils, basophils, eosinophils & mast cells)
○ Lymphocytes (NK cells, T and B cells)
○ Monocytes (macrophages and dendritic cells)
Hematopoiesis: The development of immune cells with two important precursors. For
example, a common myeloid cell precursor can become a monocyte, which can become a
macrophage or a dendritic cell. A common lymphoid cell precursor cell can eventually
become a B or T cell.
Three lines of defense
1. Epithelial barriers like skin, gut, lungs and eyes/nose/oral cavity form the first line of
defense by mechanical, chemical or microbiological ways.
2. The second line of defense are quick-reacting cells from the innate immune system
like neutrophils, macrophages, NK-cells and complement.
3. The third line of defense is the adaptive immune system, with T-cells, B-cells and
antibodies.
The lymphatic system is divided into primary and secondary lymphoid organs
Primary lymphoid organs
, ● develop adaptive immune cells.
● B-cells come from bone marrow
● T-cells come from the thymus
Secondary lymphoid organs activate adaptive immune cells
● Lymph nodes
● Spleen
● Gut Associated Lymphoid Tissues (GALT)
Innate immunity
● Immediate & fast
● Equal in all of us
Adaptive immunity
● Adapted & slow
● Highly specific for each type of danger
Macrophages and neutrophils are fast responders upon bacterial infection and induce
inflammation. A bacterial infection activates effector cells (macrophages or T/B-cell) who will
then secrete cytokines (signaling molecules for activation) that
can be recognized by other cells, causing vasodilation.
Macrophages recruit neutrophils from the bone marrow to help
them clear the bacterial infection.
During inflammation, dendritic cells initiate adaptive immunity in the
secondary lymphoid organs. Dendritic cells take up antigen and
present it to T-cells to activate them.
Innate immune cell receptors are used for activation and
pathogen uptake. They have an equal expression per cell subset
and can differentiate between major pathogen species using
molecular patterns for pathogens (PAMPS) or danger (DAMPS).
Adaptive immune cells use receptors to specifically detect danger and get activated. The B
cell-receptor (BCR) becomes soluble (antibody). A T-cell has a T-cell receptor. Adaptive
immune cell receptors can differentiate within major pathogen species using antigens, which
are highly specific for each pathogen.
Antigens are specific for each pathogen and contain epitopes, which are recognized by the
receptors of the adaptive immune system. An epitope is the minimal portion of an antigen to
get bound by antibodies, BCR or TCR.
T- and B-cells express multiple receptors, all with one specificity per cell. Cells with a
receptor specific for ongoing infections will be activated in the secondary lymphoid organs.
They will then proliferate and become a clone of cells with the same receptor specific for one
epitope.
T-cell receptors can bind processed antigen and can activate other cells who present
epitopes by the cellular response.
,B-cell receptors can only bind intact antigen. B-cells can differentiate into plasma cells and
can produce antibodies (humoral response).
Antibodies are produced during the humoral response and have a
broad range specific for the same pathogen. They can recognize
different epitopes between antibodies, but recognize one epitope
per antibody. They can also neutralize, opsonize or activate the
complement system. Moreover, they can activate innate cells via
antibody-receptor (Fc-FcR) interaction to enhance phagocytosis and
activate granulocytes and NK cells.
The complement system complements ongoing inflammation and
consists of plasma proteins with enzymatic activity. C3 gets cleaved
by C3 convertase into C3a and C3b. C3a is an anaphylatoxin and
recruits immune cells to enhance inflammation within minutes. C3b
is complement fixation (opsonin) and binds pathogens for enhanced
phagocytosis and lysis. Three pathways get activated sequentially:
The alternative pathway activates soluble (detachable) C3-
convertase via hydrolysis. Additional complement factors are bound and cleaved for
activation, forming a soluble C3-convertase. This C3-convertase binds C3, cleaving it into
C3a and C3b. Opsonized C3b is used to form membrane-bound C3-convertase to amplify
C3 cleavage.
The lectin pathway activates membrane-bound C3-convertase by binding mannose-binding
lectin (MBL) to the pathogen surface and cleaving two complement factors (C4 and C2). C4b
and C2a form the active C3-convertase.
The classical pathway activates membrane-bound C3-convertase by binding C-Reactive
Protein (CRP) or antibodies to the pathogen surface, to which complement factor C1 can
then bind. C1 cleaves two complement factors C2 and C4. C4b and C2a form the active
C3-convertase
, C3b is also important for formation of the membrane attack complex (MAC) and pathogen
lysis. C3b can also bind C3-convertase on the pathogen surface, forming a new convertase
which cleaves C5 into C5a and C5b. C5a is also an anaphylatoxin (like C3a) that increases
vascular permeability by vasodilation. C5b initiates formation of the MAC for bacterial
perforation (lysis).
CH3 Innate cells
Lecture note: names of chemokines and receptors are not important, just their general
function.
Macrophages and neutrophils
Macrophages in the tissue are the first to respond upon infection and induce inflammation.
They clear pathogens by phagocytosis, after which lysosomes inside the macrophage
degrade phagosomes that are taken up. Macrophages respond to bacteria using pattern
recognition receptors (PRR) on their cell surface, which activates their transcription so they
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