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Summary Immunology
- Vak
- Immunology
- Instelling
- Vrije Universiteit Amsterdam (VU)
Immunology notes directly from the lectures and course material, integration with laboratory practicals and workgroups.
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LECTURE 1 - CH 1Immunology is the study of the physiological mechanisms that humans and other animals
use to defend their bodies from invasion by all sorts of other organisms. In spite of their
immune systems, all humans suffer from infectious diseases, especially when young. This is
because the immune system takes time to build up its strongest response to an invading
microorganism, time during which the invader can multiply and cause disease. To provide
immunity that will give future protection from the disease, the immune system must first do
battle with the microorganism. In medicine the greatest triumph of immunology has been
vaccination, or immunization, a procedure whereby severe disease is prevented by prior
exposure to the infectious agent in a form that cannot cause disease.
The first line of defense is innate immunity, which includes physical and chemical barriers to
infection, and responses that are ready and waiting to halt infections before they can barely
start. Most infections are stopped by these mechanisms, but when they fail, the more flexible
and forceful defenses of the adaptive immune response are brought into play. The adaptive
immune response is always targeted to the specific problem at hand and is made and
refined during the course of the infection. When successful, it clears the infection and
provides long-lasting immunity that prevents its recurrence.
More than 1000 different microbial species live in the healthy adult human gut and contribute
about 10 pounds (4.5 kilograms) to the body’s weight; they are called commensal species.
The community of microbial species that inhabits a particular niche in the human body—skin,
mouth, gut, or vagina—is called the microbiota. Commensal organisms enhance human
nutrition by processing digested food and making several vitamins. They also protect against
disease, because their presence helps to prevent colonization by dangerous,
disease-causing microorganisms.
Any organism with the potential to cause disease is known as a pathogen, including both
viruses and bacteria that cause diseases, but also ones that weaken the body's defenses,
opportunistic pathogens. We consider the functions of the human immune system principally
in the context of controlling infections. For some pathogens this necessitates their complete
elimination, but for others it is sufficient to limit the size and location of the pathogen
population within the human host. Most pathogenic organisms have evolved special
adaptations that enable them to invade their hosts, replicate in them, and be transmitted.
However, the rapid death of its host is rarely in a microbe’s interest, because this destroys its
home and source of food. Consequently, those organisms with the potential to cause severe
and rapidly fatal disease often evolve toward an accommodation with their hosts. In
complementary fashion, human populations evolve a degree of built-in genetic resistance to
common disease-causing organisms, as well as acquiring lifetime immunity to endemic
diseases. Endemic diseases are those, such as measles, chickenpox, and malaria, that are
ubiquitous in a given population and to which most people are exposed in childhood.
Because of the interplay between host and pathogen, the nature and severity of infectious
diseases in the human population are always changing.
,The skin is the human body’s first defense against infection. It forms a tough, impenetrable
barrier of epithelium protected by layers of keratinized cells. The skin can be breached by
physical damage, such as wounds, burns, or surgical procedures, which exposes soft
tissues and renders them vulnerable to infection. Continuous with the skin are the epithelium
lining the respiratory, gastrointestinal, and urogenital tracts. On these internal surfaces, the
impermeable skin gives way to tissues that are specialized for communication with their
environment and are more vulnerable to microbial invasion. Such surfaces are known as
mucosal surfaces, or mucosae, as they are continually bathed in the mucus they secrete. All
epithelia produce antimicrobial peptides that kill bacteria, fungi, and enveloped viruses by
perturbing their membranes. When those barriers are breached and pathogens gain entry to
the body’s soft tissues, the defenses of the innate immune system are brought into play.
With very few exceptions, infections remain highly localized and are extinguished within a
few days without illness or incapacitation. Such infections are controlled and terminated by
the innate immune response, which is ready to react quickly. This response consists of two
parts. The first is recognition that a pathogen is present. This involves soluble proteins and
cell-surface receptors that bind either to the pathogen and its products or to human cells and
serum proteins that become altered in the presence of the pathogen. The second part of the
response involves the recruitment of destructive effector mechanisms that kill and eliminate
the pathogen. The effector mechanisms are provided by effector cells of various types that
engulf bacteria, kill virus-infected cells, or attack protozoan parasites, and a battery of serum
proteins called complement that help the effector cells by marking pathogens with molecular
flags but also attack pathogens in their own right. Collectively, these defenses are called
innate immunity. Cells and proteins in the damaged tissue sense the presence of bacteria,
and the cells send out soluble proteins called cytokines that interact with other cells to
trigger the innate immune response. The overall effect of the innate immune response is to
induce a state of inflammation in the infected tissue. Cytokines induce the local dilation of
blood capillaries, which by increasing the blood flow causes the skin to warm and redden.
Vascular dilation (vasodilation) introduces gaps between the cells of the endothelium, the
thin layer of specialized epithelium that lines the interior of blood vessels. This makes the
endothelium permeable and increases the leakage of blood plasma into the connective
tissue. Expansion of the local fluid volume causes edema or swelling, putting pressure on
nerve endings and causing pain. Cytokines also change the adhesive properties of the
vascular endothelium, inviting white blood cells to attach to it and move from the blood into
the inflamed tissue. The benefit of the discomfort and disfigurement caused by inflammation
is that it enables cells and molecules of the immune system to be brought rapidly and in
large numbers into the infected tissue.
Innate: exist in one from birth, so it should be the same for all of us, they all act in the same
way and their function remain the same; granulocytes, monocytes, NK cells (lymphocyte),
complement system;
Some infections outrun the innate immune response, an event more likely in people who are
malnourished, poorly housed, deprived of sleep, or stressed in other ways. When this
occurs, the innate immune response works to slow the spread of infection while it calls upon
white blood cells called lymphocytes that increase the power and focus of the immune
response. Their contribution to defense is the adaptive immune response. It develops
against one pathogen and provides a highly specialized defense that is of little use against
infection by a different pathogen. The main difference stands in the pathogen recognition.
,The receptors of innate immunity comprise many different types. They each recognize
features shared by groups of pathogens and are not specific for a particular pathogen.
In contrast, lymphocytes recognize pathogens by using cell-surface receptors of just one
molecular type. This means that the adaptive immune response can be made specific for a
particular pathogen by using only those lymphocyte receptors that bind to the infecting
pathogen. During infection, only those lymphocytes bearing receptors that recognize the
infecting pathogen are selected to participate in the adaptive response. These processes,
which select the small subset of pathogen-specific lymphocytes for proliferation and
differentiation into effector lymphocytes, are called clonal selection and clonal expansion,
respectively. Some of the lymphocytes selected during an adaptive immune response persist
in the body and provide long-term immunological memory of the pathogen. These memory
cells allow subsequent encounters with the same pathogen to elicit a stronger and faster
adaptive immune response, which terminates infection with minimal illness. The adaptive
immunity provided by immunological memory is also called acquired immunity or
protective immunity.
Adaptive immune: able to adapt to pathogens, cancer cells, etc., and other people don’t
have to have them; B and T cells (lymphocytes), and antibodies are after the B cells.
The first time that an adaptive immune response is made to a given pathogen it is called the
primary immune response. The second and subsequent times that an adaptive immune
response is made, and when immunological memory applies, it is called a secondary
immune response.
Circulatory system: white blood cells part of our
immune system, T and B cells, no macrophages (in
tissues), platelets and red blood cells link with white but
not belong to it, antigens trigger the adaptive system
but don’t belong to it, complement system and
antibodies in the plasma also.
Hematopoiesis: where all cells come from, stem cells:
myeloid precursor and lymphoid precursor; the first one gives rise to all granulocytes and
macrophages and dendritic cells (APC), it also leads to red blood and platelets (but not
interesting now); the second one leads to T cells (all kind) and B cells. For a long time the
NK were thought to come from the myeloid but they are from the other side even though
they are innate.
The cells of the immune system are principally the white blood cells or leukocytes. Along
with the other blood cells, they are continually being generated by the body in the
developmental process known as hematopoiesis. Leukocytes derive from a common
progenitor called the pluripotent hematopoietic stem cell, which also gives rise to red
blood cells (erythrocytes) and megakaryocytes, the source of platelets. All these cell types,
together with their precursor cells, are collectively called hematopoietic cells. As the bones
develop during the fourth and fifth months of fetal growth, hematopoiesis begins to shift to
the bone marrow and by birth this is where practically all hematopoiesis takes place.
Hematopoietic stem cells can divide to give further hematopoietic stem cells, a process
called self renewal; daughter cells can alternatively become more mature stem cells that
, commit to one of three cell lineages: the erythroid, myeloid, and lymphoid lineages. The
erythroid progenitor gives rise to the erythroid lineage of blood cells—the oxygen-carrying
erythrocytes and the platelet-producing megakaryocytes. Platelets initiate and participate in
the clotting reactions that block badly damaged blood vessels to prevent blood loss.
The myeloid progenitor gives rise to the myeloid lineage of cells. One group of myeloid
cells consists of the granulocytes, which have prominent cytoplasmic granules containing
reactive substances that kill microorganisms and enhance inflammation. Most abundant of
the granulocytes, and of all white blood cells, is the neutrophil, which is specialized in the
capture, engulfment and killing of microorganisms. Cells with this function are called
phagocytes, of which neutrophils are the most numerous and most lethal. Neutrophils are
effector cells of innate immunity that are rapidly mobilized to enter sites of infection. They are
short-lived and die at the site of infection, forming pus.
The second group of myeloid cells consists of monocytes, macrophages, and dendritic cells.
Monocytes are leukocytes that circulate in the blood. They are distinguished from the
granulocytes by being bigger, by having a distinctive indented nucleus, and by all looking the
same. Monocytes are the mobile progenitors of sedentary tissue cells called macrophages.
They travel in the blood to tissues, where they mature into macrophages and take up
residence, and they are well equipped for phagocytosis. If neutrophils are the short-lived
infantry of innate immunity, then macrophages are the long-lived commanders who provide
warning to other cells and orchestrate the local response to infection. Macrophages resident
in the infected tissues are generally the first cell to sense an invading microorganism. As part
of their response to the pathogen, macrophages secrete the cytokines that recruit
neutrophils and other leukocytes into the infected area. Dendritic cells are resident in the
body’s tissues and have a distinctive star shaped morphology. Although they have many
properties in common with macrophages, their unique function is to act as cellular
messengers that are sent to call up an adaptive immune response when it is needed.
The lymphoid progenitor gives rise to the lymphoid lineage of white blood cells. Two
populations of blood lymphocytes are distinguished. The large granular lymphocytes are
effector cells of innate immunity called natural killer cells or NK cells. NK cells are important
in the defense against viral infections. They enter infected tissues, where they prevent the
spread of infection by killing virus-infected cells and secreting cytokines that impede viral
replication in infected cells. The small lymphocytes are the cells responsible for the
adaptive immune response. Recognition of a pathogen by small lymphocytes drives a
process of lymphocyte selection, growth, and differentiation that after 1–2 weeks produces a
powerful response tailored to the invading organism.
The small lymphocytes, although morphologically indistinguishable from each other,
comprise several sub-lineages that are distinguished by their cell-surface receptors and the
functions they perform.
The most important difference is between B lymphocytes and T lymphocytes, also called B
cells and T cells. For B cells, the cell-surface receptors for pathogens are immunoglobulins,
whereas those of T cells are known as T-cell receptors. Effector B cells, called plasma cells,
secrete soluble forms of these immunoglobulins, which are known as antibodies. In
contrast, T-cell receptors are only ever expressed as cell-surface receptors, never as soluble
proteins. Each B cell expresses a single type of immunoglobulin and each T cell expresses
a single type of T-cell receptor. Any molecule, macromolecule, virus particle, or cell that
contains a structure recognized and bound by an immunoglobulin or T-cell receptor is called
its corresponding antigen. Surface immunoglobulins and T-cell receptors are thus also
referred to as the antigen receptors of lymphocytes. Differences in the amino acid
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