Immunology Lectures
Lecture 1 (Chapter 1,2 Parham):
Immune system is a diffuse, complex network of interacting cells, cell products and
cell-forming tissues, that protects the body from: pathogens and other foreign
substances, destroys infected and malignant cells, and removes cellular debris.
Our immune system needs to discriminate between self and non-self AND harmless
versus harmful.
There is a delicate balance in immune activation (inflammation) and immune
response (tolerance), a disbalance can cause illness.
In our blood we can find red blood cells, platelets, plasma, white blood cells,
complement proteins and antibodies.
Innate immunity: granulocyte, monocyte, lymphocyte (NK cell) and complements.
Adaptive immunity: lymphocytes (T-cell, B-cells) and antibodies.
The innate immune system is the same for every individual, while the adaptive
immune system reacts differently for every person.
Hematopoiesis: development of immune cells with two important precursors,
common lymphoid precursor and common myeloid precursors.
Immunity is subdivided into three lines of defense based on the speed of activation
upon danger.
Physical barriers form the first line of defense against pathogens, these physical
barriers are part of the innate system.
The lymphatic system is subdivided into primary and secondary lymphoid organs
with different structures.
Primary (development of adaptive immune cells): bone marrow -> B-cells and
thymus -> T-cells.
Your innate and adaptive immune system differ in speed and specificity during
immunity.
Macrophages and neutrophils are fast responders upon bacterial infection and
induce inflammation.
Cytokine: signaling molecule for activation.
Chemokine: signaling molecule for location (google maps).
Macrophages recruit neutrophils from the bone marrow to collaborate and clear
bacterial infection.
While inflammation is ongoing, dendritic cells initiate adaptive immunity in
secondary lymphoid organs.
Innate immune cells use pathogen recognition receptor to distinguish self from non
self and get activated.
Adaptive immune cells use receptors to specifically detect danger and get activated,
these can differentiate within major pathogen species.
Antigens are specific for each pathogen and contain epitopes recognized by the
receptors of your adaptive immune system.
T-and B-cells express multiple TCR or BCR, but all with one specificity per cell.
Complement factor C3 (C3a+C3b) are the most important.
, Lecture 2 (Chapter 3 Parham):
Tissue resident macrophages of the innate immune system are the first to respond
upon infection and induce inflammation.
Macrophages are the ‘’big eaters’’ of the innate immune system and clear pathogens
by phagocytosis. These macrophages are present in tissue and are alert upon tissue
damage and/or infection.
Tissue resident macrophages respond to bacteria using pathogen recognition
receptors. Binding of bacteria to phagocytic receptors on macrophages induces their
engulfment and degradation (activation) or binding of bacterial components to
signaling receptors on macrophages induces the synthesis of inflammatory cytokines
(cytokine production).
Macrophages secrete pro-inflammatory cytokines for induction of inflammation at
site of infection, there are several types of cytokines that can be released:
1. IL-1ß/TNF-a: induce blood vessels to become more permeable, enabling effector
cells and fluid containing soluble effector molecules to enter the infected tissue.
2. IL-∂: induces fat and muscle cells to metabolize, make heat and raise the
temperature in the infected tissue.
3. CXCL8: recruits neutrophils from the blood and guides them to the infected
tissue.
4. IL-12: recruits and activates natural killer (NK) cells that in turn secrete cytokines
that strengthen the macrophages’ response to infection.
Neutrophils need to enter the tissue coming from the high-speed blood circulation.
Large reserves of neutrophils are stored in the bone marrow and are released when
needed to fight infection, they travel to and enter the infected tissue where they
engulf and kill bacteria. The neutrophils die in the tissue and are engulfed by
macrophages.
Neutrophils migrate from the blood into the tissue using adhesion molecules and
chemokines. The steps of neutrophils tissue entry are:
1. Rolling and adhesion:
Selectins -> weak binding
Integrins -> moderate binding
Chemokines -> signaling
Integrins -> tight binding
2. Diapedesis: migration across venular blood vessel walls to enter the infected
tissue
3. Migration: by a chemokine gradient.
Neutrophils express receptors for phagocytosis and toxic granules for killing.
Neutrophils have a signature multi-lobular nucleus, are recruited to infection site
and are efficient killers with a short life span.
Neutrophils efficiently kill bacteria following phagocytosis, die and are cleared by
macrophages.
Complement factor C3 is cleaved into C3a and C3b by C3 convertase activation via
three pathways.
Macrophages induce the acute phase response, initiating production of MBL and CRP
by the liver. Bacteria induce macrophages to produce IL-∂, which acts on
hepatocytes to induce synthesis of acute phase proteins. C-reactive protein binds
Lecture 1 (Chapter 1,2 Parham):
Immune system is a diffuse, complex network of interacting cells, cell products and
cell-forming tissues, that protects the body from: pathogens and other foreign
substances, destroys infected and malignant cells, and removes cellular debris.
Our immune system needs to discriminate between self and non-self AND harmless
versus harmful.
There is a delicate balance in immune activation (inflammation) and immune
response (tolerance), a disbalance can cause illness.
In our blood we can find red blood cells, platelets, plasma, white blood cells,
complement proteins and antibodies.
Innate immunity: granulocyte, monocyte, lymphocyte (NK cell) and complements.
Adaptive immunity: lymphocytes (T-cell, B-cells) and antibodies.
The innate immune system is the same for every individual, while the adaptive
immune system reacts differently for every person.
Hematopoiesis: development of immune cells with two important precursors,
common lymphoid precursor and common myeloid precursors.
Immunity is subdivided into three lines of defense based on the speed of activation
upon danger.
Physical barriers form the first line of defense against pathogens, these physical
barriers are part of the innate system.
The lymphatic system is subdivided into primary and secondary lymphoid organs
with different structures.
Primary (development of adaptive immune cells): bone marrow -> B-cells and
thymus -> T-cells.
Your innate and adaptive immune system differ in speed and specificity during
immunity.
Macrophages and neutrophils are fast responders upon bacterial infection and
induce inflammation.
Cytokine: signaling molecule for activation.
Chemokine: signaling molecule for location (google maps).
Macrophages recruit neutrophils from the bone marrow to collaborate and clear
bacterial infection.
While inflammation is ongoing, dendritic cells initiate adaptive immunity in
secondary lymphoid organs.
Innate immune cells use pathogen recognition receptor to distinguish self from non
self and get activated.
Adaptive immune cells use receptors to specifically detect danger and get activated,
these can differentiate within major pathogen species.
Antigens are specific for each pathogen and contain epitopes recognized by the
receptors of your adaptive immune system.
T-and B-cells express multiple TCR or BCR, but all with one specificity per cell.
Complement factor C3 (C3a+C3b) are the most important.
, Lecture 2 (Chapter 3 Parham):
Tissue resident macrophages of the innate immune system are the first to respond
upon infection and induce inflammation.
Macrophages are the ‘’big eaters’’ of the innate immune system and clear pathogens
by phagocytosis. These macrophages are present in tissue and are alert upon tissue
damage and/or infection.
Tissue resident macrophages respond to bacteria using pathogen recognition
receptors. Binding of bacteria to phagocytic receptors on macrophages induces their
engulfment and degradation (activation) or binding of bacterial components to
signaling receptors on macrophages induces the synthesis of inflammatory cytokines
(cytokine production).
Macrophages secrete pro-inflammatory cytokines for induction of inflammation at
site of infection, there are several types of cytokines that can be released:
1. IL-1ß/TNF-a: induce blood vessels to become more permeable, enabling effector
cells and fluid containing soluble effector molecules to enter the infected tissue.
2. IL-∂: induces fat and muscle cells to metabolize, make heat and raise the
temperature in the infected tissue.
3. CXCL8: recruits neutrophils from the blood and guides them to the infected
tissue.
4. IL-12: recruits and activates natural killer (NK) cells that in turn secrete cytokines
that strengthen the macrophages’ response to infection.
Neutrophils need to enter the tissue coming from the high-speed blood circulation.
Large reserves of neutrophils are stored in the bone marrow and are released when
needed to fight infection, they travel to and enter the infected tissue where they
engulf and kill bacteria. The neutrophils die in the tissue and are engulfed by
macrophages.
Neutrophils migrate from the blood into the tissue using adhesion molecules and
chemokines. The steps of neutrophils tissue entry are:
1. Rolling and adhesion:
Selectins -> weak binding
Integrins -> moderate binding
Chemokines -> signaling
Integrins -> tight binding
2. Diapedesis: migration across venular blood vessel walls to enter the infected
tissue
3. Migration: by a chemokine gradient.
Neutrophils express receptors for phagocytosis and toxic granules for killing.
Neutrophils have a signature multi-lobular nucleus, are recruited to infection site
and are efficient killers with a short life span.
Neutrophils efficiently kill bacteria following phagocytosis, die and are cleared by
macrophages.
Complement factor C3 is cleaved into C3a and C3b by C3 convertase activation via
three pathways.
Macrophages induce the acute phase response, initiating production of MBL and CRP
by the liver. Bacteria induce macrophages to produce IL-∂, which acts on
hepatocytes to induce synthesis of acute phase proteins. C-reactive protein binds
