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Summary Modules 0-3 - Immunotechnology (CBI30806)
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Summary Modules 0-3 - Immunotechnology (CBI30806), useful for the first multiple choice exam
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Immunotechnology summaryIntroduction to the immune system
Immunology: the study of our protection from foreign macromolecules or invading organisms and our
responses to them. These invaders include viruses, bacteria, protozoa or even larger parasites. The
immune system is composed of two major subdivisions, the innate or nonspecific immune system
and the adaptive or specific immune system. The innate immune system is our first line of defence
against invading organisms whilst the adaptive immune
system acts as a second line of defence and also affords
protection against re-exposure to the same pathogen.
Each of the major subdivisions of the immune system has
both cellular and humoral (= soluble) components by
which they carry out their protective function. Although
the innate and adaptive immune systems both function to
protect against invading organisms, they differ in a
number of ways. The adaptive immune system requires
some time to react to an invading organism, whereas the
innate immune system includes defences that, for the most part, are
constitutively present and ready to be mobilized upon infection.
Second, the adaptive immune system can react very specific and
reacts only with the organism that induced the response. In contrast,
the innate system is not antigen specific and reacts equally well to a
variety of organisms. Finally, the adaptive immune system
demonstrates immunological memory.
In addition, to these active immune responses, anatomical barriers
are very important to prevent pathogens from entering the body.
All cells of the immune system have their origin in the bone marrow
and they include myeloid (neutrophils, basophils, eosinophils,
macrophages and dendritic cells) and lymphoid (B lymphocyte, T
lymphocyte and Natural Killer) cells, which differentiate along distinct
pathways. For T-cell + development, the precursor T- cells must
migrate to the thymus, where they undergo differentiation into two
distinct types of T-cells, the CD4+ T-helper cell and the CD8+ pre-
cytotoxic T-cell.
Disease occurs only when a high number of pathogens enters the body, when the virulence of the
invading organism is great or when immunity is compromised, or due to a combination of these
factors. During inflammation, which is the response of the immune system to an invading organism,
there may be local discomfort and collateral damage to healthy tissue as a result of the toxic products
produced by the immune cells.
Anatomical barriers to infections:
Mechanical factors: epithelial surfaces form a physical barrier. The skin is thus the first line of
defence. The mucus that lines the respiratory and gastrointestinal tract prevents direct access
of pathogens to the underlying tissue.
Chemical factors: fatty acids in sweat inhibit the growth of bacteria (low pH). Lysozymes and
phospholipases found in tears, saliva and nasal secretions can breakdown the cell wall of
, bacteria and destabilize bacterial membranes. Defensins (low molecular weight proteins)
found in the lung and gastrointestinal tract have antimicrobial activity.
Biological factors: the normal flora of the skin and the gastrointestinal tract can prevent the
colonization of pathogenic bacteria by secreting substances that are toxic for other bacteria
or by competing with pathogenic bacteria for nutrients or attachment to cell surfaces.
Phagocytes: take up pathogens and other particles and digest them. They do this by engulfing the
particle, which will then become entrapped inside a phagosome. Lysosomes will fuse with the
phagosome, releasing aggressive substances, that will kill and break down the ingested microbe.
Mononuclear phagocytes/monocytes: long lived blood cells that can migrate to the tissues, where
they develop into tissue macrophages. In addition to phagocytosis and degradation of particles,
macrophages are capable of extracellular killing of infected or altered self-targeT-cells. Furthermore,
macrophages contribute to tissue repair and act as antigen-presenting cells, which are required for
the induction of specific immune responses.
Dendritic cells: can also phagocytose and are the most important antigen presenting cells. By their
receptors, they can determine what kind of microbe is entering the body and by the release of
cytokines, they will promote the induction of the proper kind of adaptive immune response.
Polymorphonuclear neutrophils: the most abundant type of leukocyte that can efficiently
phagocytose and destroy bacteria after which the neutrophils die. Neutrophils are short lived and will
die within one to several days after forming.
Polymorphonuclear eosinophils: can also ingest and kill bacteria, although much less efficient than
neutrophils. Their main function is the killing of certain parasites by releasing the aggressive content
of their granules near the parasite.
T-cells contain surface receptors specific for a certain antigen (the T-cell receptor or TCR). These
receptors do not recognize intact antigen, but small (pathogen derived) peptides bound to major
histocompatibility complex (MHC) molecules expressed on the surface of nucleated cells.
T-helper cells (or Th):
T-helper-1 (or Th1) cells provide help to the cellular part of the immune system by activating
macrophages to destroy phagocytosed pathogens or pre-cytotoxic T-lymphocytes to develop
in effective cytotoxic T-lymphocytes (CTLs)
T-helper-2 (or Th2) cells, which provide help to the humoral part of the immune system by
activating B-cells to develop into antibody secreting plasma cells.
T-helper-17 (Th17) cells, which secrete interleukin-17 (IL17) that promotes the recruitment of
neutrophils to the site of infection. Th17 cells play an important role in the control of
extracellular microbes like many bacteria and fungi. They are also involved in autoimmune
disease.
Regulatory T-cells (Tregs). These cells can suppress immune responses and are crucial to
prevent autoimmune diseases.
Cytotoxic T-lymphocytes (CTLs): destroy cells that have become infected with viruses or other
pathogens. By swiftly destroying the infected cells, the virus is deprived of its host and can no longer
replicate itself. The T-cell receptor of a CTL recognizes peptides derived from cytosolic pathogens (like
viruses) presented by MHC-I molecules on the surface of the infected cell. Some viruses can induce
downregulation of these MHC-I molecules by the cells that they infected. As a consequence, these
infected cells can no longer be recognized by the specific CTLs. Fortunately, another lymphocyte, the
large granular lymphocyte (LGL), also called natural killer (NK) cell, recognizes and kills cells with
, down-regulated MHC-I molecules. These NK cells do not have variable receptors and are part of the
innate immune system.
Cells that are important in the initiation of inflammation are basophils, masT-cells and platelets.
These cells have receptors that can sense pathogens or tissue damage and respond by releasing
factors from their granules that induce inflammation in the surrounding tissue.
Complement system: the major humoral innate defence mechanism. Three different pathways are
distinguished: the classical pathway that is activated by antibody binding to a microbe, the
alternative pathway that is activated by microbial surfaces, and the lectin pathway that is activated
by mannose binding lectin (MBL). Mannose binding
lectin is an acute phase protein that can bind to
mannose groups on microbial surfaces. Once the
complement system is activated, it can have a number
of functions. It is able to lyse many bacterial species
due to the forming of pores in the microbial cell wall. It
can also coat bacteria with complement molecules
that promote phagocytosis. Complement components
C3a and especially C5a strongly promote
inflammation: they increase the vascular permeability and produce molecules that attract
phagocytes, a process called chemotaxis. They also prevent immune complexes from becoming too
big and promote removal of these complexes by phagocytic cells.
Cytokines: messenger molecules that act over a short distance, responsible for communication
between the immune cells. Types:
Interferons: particularly important in controlling viral infections. The type-I interferons (IFN
and IFN) are produced by cells that have become infected by a virus. As a response to
these interferons, the protein synthesis of the infected cell and cells in the direct vicinity, is
strongly reduced. As a consequence, the replication rate of the virus is strongly reduced too.
Another type of interferon, IFN, is produced by activated Th1 cells and can also induce viral
resistance in cells. IFN has many other functions as well, among which the activation of
macrophages.
Interleukins: mainly produced by T-cells, cause other cells to divide and differentiate. They
are also involved in the initiation and downregulation of inflammation.
Colony stimulating factors (CSFs): involved in division and differentiation of bone marrow
cells and the precursors of blood leukocytes.
Chemokines: chemotactic proteins that direct (immune) cells to the right place.
Other: tumour necrosis factor alpha (TNF) is particularly important in promoting
inflammation and cytotoxic reactions. Transforming growth factor beta (TGF) is involved in
the downregulation of inflammatory responses.
Principle components of inflammation:
1. Increase in blood supply to the infected tissue
2. Increased vascular permeability due to retraction of the endothelial cells lining the vessels,
enabling transfer of larger molecules (like antibodies) form the blood to the infected tissue
3. Migration of leukocytes from the blood vessels to the infected tissue
Failure of the immune system:
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