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Pain Terms

Allodynia
Pain due to a stimulus which does not normally provoke pain. Note: The term allodynia was
originally introduced to separate from hyperalgesia and hyperesthesia, the conditions seen in
patients with lesions of the nervous system where touch, light pressure, or moderate cold or
warmth evoke pain when applied to apparently normal skin. Allo means "other" in Greek and is
a common prefix for medical conditions that diverge from the expected. Odynia is derived from
the Greek word "odune" or "odyne," which is used in "pleurodynia" and "coccydynia" and is
similar in meaning to the root from which we derive words with -algia or -algesia in them.
Allodynia was suggested following discussions with Professor Paul Potter of the Department of
the History of Medicine and Science at The University of Western Ontario.

The words "to normal skin" were used in the original definition but later were omitted in order to
remove any suggestion that allodynia applied only to referred pain. Originally, also, the pain-
provoking stimulus was described as "non-noxious." However, a stimulus may be noxious at
some times and not at others, for example, with intact skin and sunburned skin, and also, the
boundaries of noxious stimulation may be hard to delimit. Since the Committee aimed at
providing terms for clinical use, it did not wish to define them by reference to the specific
physical characteristics of the stimulation, e.g., pressure in kilopascals per square centimeter.
Moreover, even in intact skin there is little evidence one way or the other that a strong painful
pinch to a normal person does or does not damage tissue. Accordingly, it was considered to be
preferable to define allodynia in terms of the response to clinical stimuli and to point out that the
normal response to the stimulus could almost always be tested elsewhere in the body, usually in
a corresponding part. Further, allodynia is taken to apply to conditions which may give rise to
sensitization of the skin, e.g., sunburn, inflammation, trauma.

It is important to recognize that allodynia involves a change in the quality of a sensation, whether
tactile, thermal, or of any other sort. The original modality is normally non-painful, but the
response is painful. There is thus a loss of specificity of a sensory modality. By contrast,
hyperalgesia (q.v.) represents an augmented response in a specific mode, viz., pain. With other
cutaneous modalities, hyperesthesia is the term which corresponds to hyperalgesia, and as with
hyperalgesia, the quality is not altered. In allodynia the stimulus mode and the response mode
differ, unlike the situation with hyperalgesia. This distinction should not be confused by the fact
that allodynia and hyperalgesia can be plotted with overlap along the same continuum of
physical intensity in certain circumstances, for example, with pressure or temperature.

See also the notes on hyperalgesia and hyperpathia.

Analgesia
Absence of pain in response to stimulation which would normally be painful. Note: As with
allodynia (q.v.), the stimulus is defined by its usual subjective effects.

Anesthesia Dolorosa
Pain in an area or region which is anesthetic.

Causalgia
A syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion,
often combined with vasomotor and sudomotor dysfunction and later trophic changes.

Central Pain
Pain initiated or caused by a primary lesion or dysfunction in the central nervous system.

Dysesthesia
An unpleasant abnormal sensation, whether spontaneous or evoked. Note: Compare with pain
and with paresthesia. Special cases of dysesthesia include hyperalgesia and allodynia. A
dysesthesia should always be unpleasant and a paresthesia should not be unpleasant, although it
is recognized that the borderline may present some difficulties when it comes to deciding as to
whether a sensation is pleasant or unpleasant. It should always be specified whether the
sensations are spontaneous or evoked.

Hyperalgesia
An increased response to a stimulus which is normally painful. Note: Hyperalgesia reflects
increased pain on suprathreshold stimulation. For pain evoked by stimuli that usually are not
painful, the term allodynia is preferred, while hyperalgesia is more appropriately used for cases
with an increased response at a normal threshold, or at an increased threshold, e.g., in patients
with neuropathy. It should also be recognized that with allodynia the stimulus and the response
are in different modes, whereas with hyperalgesia they are in the same mode. Current evidence
suggests that hyperalgesia is a consequence of perturbation of the nociceptive system with
peripheral or central sensitization, or both, but it is important to distinguish between the clinical
phenomena, which this definition emphasizes, and the interpretation, which may well change as
knowledge advances.

Hyperesthesia
Increased sensitivity to stimulation, excluding the special senses. Note: The stimulus and locus
should be specified. Hyperesthesia may refer to various modes of cutaneous sensibility including
touch and thermal sensation without pain, as well as to pain. The word is used to indicate both
diminished threshold to any stimulus and an increased response to stimuli that are normally
recognized.

Allodynia is suggested for pain after stimulation which is not normally painful. Hyperesthesia
includes both allodynia and hyperalgesia, but the more specific terms should be used wherever
they are applicable.

Hyperpathia
A painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a
repetitive stimulus, as well as an increased threshold. Note: It may occur with allodynia,
hyperesthesia, hyperalgesia, or dysesthesia. Faulty identification and localization of the stimulus,
delay, radiating sensation, and after-sensation may be present, and the pain is often explosive in
character. The changes in this note are the specification of allodynia and the inclusion of
hyperalgesia explicitly. Previously hyperalgesia was implied, since hyperesthesia was mentioned
in the previous note and hyperalgesia is a special case of hyperesthesia.

Hypoalgesia
Diminished pain in response to a normally painful stimulus. Note: Hypoalgesia was formerly
defined as diminished sensitivity to noxious stimulation, making it a particular case of
hypoesthesia (q.v.). However, it now refers only to the occurrence of relatively less pain in
response to stimulation that produces pain. Hypoesthesia covers the case of diminished
sensitivity to stimulation that is normally painful.

The implications of some of the above definitions may be summarized for convenience as
follows:
Allodynia: lowered threshold: stimulus and response mode differ
Hyperalgesia: increased response: stimulus and response mode are the same
Hyperpathia: raised threshold: stimulus and response mode may be the increased response: same
or different
Hypoalgesia: raised threshold: stimulus and response mode are the same lowered response:
The above essentials of the definitions do not have to be symmetrical and are not symmetrical at
present. Lowered threshold may occur with allodynia but is not required. Also, there is no
category for lowered threshold and lowered response - if it ever occurs.

Hypoesthesia
Decreased sensitivity to stimulation, excluding the special senses. Note: Stimulation and locus to
be specified.
Neuralgia
Pain in the distribution of a nerve or nerves. Note: Common usage, especially in Europe, often
implies a paroxysmal quality, but neuralgia should not be reserved for paroxysmal pains.

Neuritis
Inflammation of a nerve or nerves. Note: Not to be used unless inflammation is thought to be
present.

Neurogenic Pain
Pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the
peripheral or central nervous system.

Neuropathic Pain
Pain initiated or caused by a primary lesion or dysfunction in the nervous system. Note: See also
Neurogenic Pain and Central Pain. Peripheral neuropathic pain occurs when the lesion or
dysfunction affects the peripheral nervous system. Central pain may be retained as the term when
the lesion or dysfunction affects the central nervous system.

Neuropathy
A disturbance of function or pathological change in a nerve: in one nerve, mononeuropathy; in
several nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy. Note:
Neuritis (q.v.) is a special case of neuropathy and is now reserved for inflammatory processes
affecting nerves. Neuropathy is not intended to cover cases like neurapraxia, neurotmesis,
section of a nerve, or transitory impact like a blow, stretching, or an epileptic discharge. The
term neurogenic applies to pain due to such temporary perturbations.

Nociceptor
A receptor preferentially sensitive to a noxious stimulus or to a stimulus which would become
noxious if prolonged. Note: Avoid use of terms like pain receptor, pain pathway, etc.
Noxious Stimulus
A noxious stimulus is one which is damaging to normal tissues. Note: Although the definition of
a noxious stimulus has been retained, the term is not used in this list to define other terms.
Pain
An unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in terms of such damage. Note: The inability to communicate verbally
does not negate the possibility that an individual is experiencing pain and is in need of
appropriate pain-relieving treatment. Pain is always subjective. Each individual learns the
application of the word through experiences related to injury in early life. Biologists recognize
that those stimuli which cause pain are liable to damage tissue. Accordingly, pain is that
experience we associate with actual or potential tissue damage. It is unquestionably a sensation
in a part or parts of the body, but it is also always unpleasant and therefore also an emotional
experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, should not be
called pain. Unpleasant abnormal experiences (dysesthesias) may also be pain but are not
necessarily so because, subjectively, they may not have the usual sensory qualities of pain.

Many people report pain in the absence of tissue damage or any likely pathophysiological cause;
usually this happens for psychological reasons. There is usually no way to distinguish their
experience from that due to tissue damage if we take the subjective report. If they regard their
experience as pain and if they report it in the same ways as pain caused by tissue damage, it
should be accepted as pain. This definition avoids tying pain to the stimulus. Activity induced in
the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a
psychological state, even though we may well appreciate that pain most often has a proximate
physical cause.

Pain Threshold
The least experience of pain which a subject can recognize. Note: Traditionally the threshold has
often been defined, as we defined it formerly, as the least stimulus intensity at which a subject
perceives pain. Properly defined, the threshold is really the experience of the patient, whereas the
intensity measured is an external event. It has been common usage for most pain research
workers to define the threshold in terms of the stimulus, and that should be avoided. However,
the threshold stimulus can be recognized as such and measured. In psychophysics, thresholds are
defined as the level at which 50% of stimuli are recognized. In that case, the pain threshold
would be the level at which 50% of stimuli would be recognized as painful. The stimulus is not
pain (q.v.) and cannot be a measure of pain.

Pain Tolerance Level


The greatest level of pain which a subject is prepared to tolerate. Note: As with pain threshold,
the pain tolerance level is the subjective experience of the individual. The stimuli which are
normally measured in relation to its production are the pain tolerance level stimuli and not the
level itself. Thus, the same argument applies to pain tolerance level as to pain threshold, and it is
not defined in terms of the external stimulation as such.

Paresthesia
An abnormal sensation, whether spontaneous or evoked. Note: Compare with dysesthesia. After
much discussion, it has been agreed to recommend that paresthesia be used to describe an
abnormal sensation that is not unpleasant while dysesthesia be used preferentially for an
abnormal sensation that is considered to be unpleasant. The use of one term (paresthesia) to
indicate spontaneous sensations and the other to refer to evoked sensations is not favored. There
is a sense in which, since paresthesia refers to abnormal sensations in general, it might include
dysesthesia, but the reverse is not true. Dysesthesia does not include all abnormal sensations, but
only those which are unpleasant.

Peripheral Neurogenic Pain


Pain initiated or caused by a primary lesion or dysfunction or transitory perturbation in the
peripheral nervous system.

Peripheral Neuropathic Pain


Pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous system.
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LYMPHATIC SYSTEM AND IMMUNITY.


Table of Contents

The Lymphatic System | Immunity | General Defenses | Specific Defenses


Antibody-mediated Immunity | Blood Types, Rh, and Antibodies
Organ Transplants and Antibodies | Allergies and Disorders of the Immune System
Links
The Lymphatic System | Back to Top
The lymphatic system is composed of lymph vessels, lymph nodes, and organs. The
functions of this system include the absorbtion of excess fluid and its return to the
blood stream, absorption of fat (in the villi of the small intestine) and the immune
system function.
Lymph vessels are closely associated with the circulatory system vessels. Larger
lymph vessels are similar to veins. Lymph capillaries are scatted throughout the body.
Contraction of skeletal muscle causes movement of the lymph fluid through valves.
Lymph organs include the bone marrow, lymph nodes, spleen, and thymus. Bone
marrow contains tissue that produces lymphocytes. B-lymphocytes (B-cells) mature in
the bone marrow. T-lymphocytes (T-cells) mature in the thymus gland. Other blood
cells such as monocytes and leukocytes are produced in the bone marrow. Lymph
nodes are areas of concentrated lymphocytes and macrophages along the lymphatic
veins. The spleen is similar to the lymph node except that it is larger and filled with
blood. The spleen serves as a reservoir for blood, and filters or purifies the blood and
lymph fluid that flows through it. If the spleen is damaged or removed, the individual
is more susceptible to infections. The thymus secretes a hormone, thymosin, that
causes pre-T-cells to mature (in the thymus) into T-cells.
Immunity | Back to Top
Immunity is the body's capability to repel foreign substances and cells. The
nonspecific responses are the first line of defense. Highly specific responses are the
second line of defense and are tailored to an individual threat. The immune response
includes both specific and nonspecific components. Nonspecific responses block the
entry and spread of disease-causing agents. Antibody-mediated and cell-mediated
responses are two types of specific response. The immune system is associated with
defense against disease-causing agents, problems in transplants and blood
transfusions, and diseases resulting from over-reaction (autoimmune, allergies) and
under-reaction (AIDS).
General Defenses | Back to Top
Barriers to entry are the skin and mucous membranes. The skin is a passive barrier to
infectious agents such as bacteria and viruses. The organisms living on the skin
surface are unable to penetrate the layers of dead skin at the surface. Tears and saliva
secrete enzymes that breakdown bacterial cell walls. Skin glands secrete chemicals
that retard the growth of bacteria. Mucus membranes lining the respiratory, digestive,
urinary, and reproductive tracts secrete mucus that forms another barrier. Physical
barriers are the first line of defense.
When microorganisms penetrate skin or epithelium lining respiratory, digestive, or
urinary tracts, inflammation results. Damaged cells release chemical signals such as
histamine that increase capillary blood flow into the affected area (causing the areas to
become heated and reddened). The heat makes the environment unfavorable for
microbes, promotes healing, raises mobility of white blood cells, and increases the
metabolic rate of nearby cells. Capillaries pass fluid into interstitial areas, causing the
infected/injured area to swell. Clotting factors trigger formation of many small blood
clots. Finally, monocytes (a type of white blood cell) clean up dead microbes, cells,
and debris.
The inflammatory response is often strong enough to stop the spread of disease-
causing agents such as viruses, bacteria, and fungi. The response begins with the
release of chemical signals and ends with cleanup by monocytes. If this is not enough
to stop the invaders, the complement system and immune response act.
Protective proteins that are produced in the liver include the complement system of
proteins. The complement system proteins bind to a bacterium and open pores in its
membrane through which fluids and salt move, swelling and bursting the cell.
The complement system directly kills microbes, supplements inflammatory response,
and works with the immune response. It complements the actions of the immune
system. Complement proteins are made in the liver and become active in a sequence
(C1 activates C2, etc.). The final five proteins form a membrane-attack complex
(MAC) that embeds itself into the plasma membrane of the attacker. Salts enter the
invader, facilitating water to cross the membrane, swelling and bursting the microbe.
Complement also functions in the immune response by tagging the outer surface of
invaders for attack by phagocytes.

The complement system of proteins and their functioning. Image from Purves et al., Life: The
Science of Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and WH Freeman
(www.whfreeman.com), used with permission.
Interferon is a species-specific chemical produced by cells that are viral attack. It
alerts nearby cells to prepare for a virus. The cells that have been contacted by
interferon resist all viral attacks.
Specific Defenses | Back to Top
The immune system also generates specific responses to specific invaders.
The immune system is more effective than the nonspecific methods, and has a
memory component that improves response time when an invader of the same type (or
species) is again encountered.
Immunity results from the production of antibodies specific to a given antigen
(antibody-generators, located on the surface of an invader). Antibodies bind to the
antigens on invaders and kill or inactivate them in several ways. Most antibodies are
themselves proteins or are a mix of protein and polysaccharides. Antigens can be any
molecule that causes antibody production.
Lymphocytes
White blood cells known as lymphocytes arise from by mitosis of stem cells in the
bone marrow. Some lymphocytes migrate to the thymus and become T cells that
circulate in the blood and are associated with the lymph nodes and spleen. B cells
remain in the bone marrow and develop before moving into the circulatory and lymph
systems. B cells produce antibodies.

Macrophage Attacking E.coli (SEM x8,800). This image is copyright Dennis Kunkel at
www.DennisKunkel.com, used with permission.
Antibody-mediated (humoral immunity)
Antibody-mediated (humoral) immunity is regulated by B cells and the antibodies
they produce. Cell-mediated immunity is controlled by T cells. Antibody-mediated
reactions defend against invading viruses and bacteria. Cell-mediated immunity
concerns cells in the body that have been infected by viruses and bacteria, protect
against parasites, fungi, and protozoans, and also kill cancerous body cells.

Human T-lymphocyte (SEM x12,080). This image is copyright Dennis Kunkel at


www.DennisKunkel.com, used with permission.
The cell-mediated immune responses. Images from Purves et al., Life: The Science of
Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and WH Freeman
(www.whfreeman.com), used with permission.
Antibody-mediated Immunity | Back to Top
Stages in this process are:
1. antigen detection
2. activation of helper T cells
3. antibody production by B cells
Each stage is directed by a specific cell type.
Macrophages
Macrophages are white blood cells that continually search for foreign (nonself)
antigenic molecules, viruses, or microbes. When found, the macrophages engulfs and
destroys them. Small fragments of the antigen are displayed on the outer surface of
the macrophage plasma membrane.

The role of macrophages in the formation of antibodies. Image from Purves et al., Life:
The Science of Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and WH
Freeman (www.whfreeman.com), used with permission.

Helper T Cells
Helper T cells are macrophages that become activated when they encounter the
antigens now displayed on the macrophage surface. Activated T cells identify and
activate B cells.
The display path of an antigen as accomplished by a macrophage. Image from Purves et
al., Life: The Science of Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and
WH Freeman (www.whfreeman.com), used with permission.

B Cells
B cells divide, forming plasma cells and B memory cells. Plasma cells make and
release between 2000 and 20,000 antibody molecules per second into the blood for the
next four or five days. B memory cells live for months or years, and are part of the
immune memory system.
The activation of T cells by the action of macrophages and interleukin-2. Images from
Purves et al., Life: The Science of Biology, 4th Edition, by Sinauer Associates
(www.sinauer.com) and WH Freeman (www.whfreeman.com), used with permission.

Antibodies
Antibodies bind to specific antigens in a lock-and-key fashion, forming an antigen-
antibody complex. Antibodies are a type of protein molecule known as
immunoglobulins. There are five classes of immunoglobulins: IgG, IgA, IgD, IgE, and
IgM.
The five classes of Ig antibodies. Image from Purves et al., Life: The Science of Biology, 4th
Edition, by Sinauer Associates (www.sinauer.com) and WH Freeman (www.whfreeman.com),
used with permission.
Antibodies are Y-shaped molecules composed of two identical long polypeptide
(Heavy or H chains) and two identical short polypeptides (Light or L chains).
Function of antibodies includes:
1. Recognition and binding to antigens
2. Inactivation of the antigen

Structural regions of an antibody molecule. Image from Purves et al., Life: The Science of
Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and WH Freeman
(www.whfreeman.com), used with permission.
A unique antigenic determinant recognizes and binds to a site on the antigen, leading
to the destruction of the antigen in several ways. The ends of the Y are the antigen-
combining site that is different for each antigen. Click here to learn more about the
different classes of antibodies.
Formation of an antigen-antibody complex. Image from Purves et al., Life: The Science of
Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and WH Freeman
(www.whfreeman.com), used with permission.
Helper T cells activate B cells that produce antibodies. Supressor T cells slow down
and stop the immune response of B and T cells, serving as an off switch for the
immune system. Cytotoxic (or killer) T cells destroy body cells infected with a virus
or bacteria. Memory T cells remain in the body awaiting the reintroduction of the
antigen.
A cell infected with a virus will display viral antigens on its plasma membrane. Killer
T cells recognize the viral antigens and attach to that cell's plasma membrane. The T
cells secrete proteins that punch holes in the infected cell's plasma membrane. The
infected cell's cytoplasm leaks out, the cell dies, and is removed by phagocytes. Killer
T cells may also bind to cells of transplanted organs.
The immune system is the major component of this defense. Lymphocytes,
monocytes, lymph organs, and lymph vessels make up the system. The immune
system is able to distinguish self from non-self. Antigens are chemicals on the surface
of a cell. All cells have these. The immune system checks cells and identifies them as
"self" or "non-self". Antibodies are proteins produced by certain lymphocytes in
response to a specific antigen. B-lymphocytes and T-lymphocytes produce the
antibodies. B-lymphocytes become plasma cells which then generate antibodies. T-
lymphocytes attack cells which bear antigens they recognize. They also mediate the
immune response.
The immune system and memory of infections
Secondary immunity, the resistance to certain diseases after having had them once,
results from production of Memory B and T cells during the first exposure to the
antigen. A second exposure to the same antigen produces a more massive and faster
response. The secondary response is the basis for vaccination.
Vaccination
Vaccination is a term derived from the Latin vacca (cow, after the cowpox material
used by Edward Jenner in the first vaccination). A vaccine stimulates the antibody
production and formation of memory cells without causing of the disease. Vaccines
are made from killed pathogens or weakened strains that cause antibody production
but not the disease. Recombinant DNA techniques can now be used to develop even
safer vaccines.
The immune system can develop long-term immunity to some diseases. Man can use
this to develop vaccines, which produce induced immunity. Active immunity develops
after an illness or vaccine. Vaccines are weakened (or killed) viruses or bacteria that
prompt the development of antibodies. Application of biotechnology allows
development of vaccines that are the protein (antigen) which in no way can cause the
disease. Passive immunity is the type of immunity when the individual is given
antibodies to combat a specific disease. Passive immunity is short-lived.
Blood Types, Rh, and Antibodies | Back to Top
There are 30 or more known antigens on the surface of blood cells. These form the
blood groups or blood types. In a transfusion, the blood groups of the recipient and
donor must be matched. If improperly matched, the recipient's immune system will
produce antibodies causing clotting of the transfused cells, blocking circulation
through capillaries and producing serious or even fatal results.
ABO blood types are determined by a gene, I (for isoagglutinin). There are three
alleles, IA, IB and IO. Proteins produced by the A and B alleles are antigenic.
Individuals with blood type A have the A antigen on the surface of their red blood
cells, and antibodies to type B blood in their plasma. People with blood type B have
the B antigen on their blood cells and antibodies against type A in their plasma.
Individuals with type AB blood produce have antigens for A and B on their cell
surfaces and no antibodies for either blood type A or B in their plasma. Type O
individuals have no antigens on their red blood cells but antigens to both A and B are
in their plasma.
People with type AB blood can receive blood of any type. Those with type O blood
can donate to anyone. If a transfusion is made between an incompatible donor and
recipient, the recipient's blood will undergo a cascade of events. Reaction of antigens
on cells and antibodies in plasma will produce clumping that clogs capillaries, other
cells burst, releasing hemoglobin that can crystallize in the kidney and lead to kidney
failure.
The Rh (for the rhesus monkey in which it was discovered) blood group is made up of
those Rh positive (Rh+) individuals who can make the Rh antigen and those Rh
negative (Rh-) who cannot.
Hemolytic disease of the newborn (HDN) results from Rh incompatibility between an
Rh- mother and Rh+ fetus. Rh+ blood from the fetus enters the mother's system during
birth, causing her to produce Rh antibodies. The first child is usually not affected,
however subsequent Rh+ fetuses will cause a massive secondary reaction of the
maternal immune system. To prevent HDN, Rh- mothers are given an Rh antibody
during the first pregnancy with an Rh+ fetus and all subsequent Rh+ fetuses.
Organ Transplants and Antibodies | Back to Top
Success of organ transplants and skin grafts requires a matching of histocompatibility
antigens that occur on all cells in the body. Chromosome 6 contains a cluster of genes
known as the human leukocyte antigen complex (HLA) that are critical to the
outcome of such procedures. The array of HLA alleles on either copy of our
chromosome 6 is known as a haplotype.
The large number of alleles involved mean no two individuals, even in a family, will
have the same identical haplotype. Identical twins have a 100% HLA match. The best
matches are going to occur within a family. The preference order for transplants is
identical twin > sibling > parent > unrelated donor. Chances of an unrelated donor
matching the recipient range between 1 in 100,000-200,000. Matches across racial or
ethnic lines are often more difficult. When HLA types are matched survival of
transplanted organs dramatically increases.
Allergies and Disorders of the Immune System | Back to Top
The immune system can overreact, causing allergies or autoimmune diseases.
Likewise, a suppressed, absent, or destroyed immune system can also result in disease
and death.
Allergies result from immune system hypersensitivity to weak antigens that do not
cause an immune response in most people. Allergens, substances that cause allergies,
include dust, molds, pollen, cat dander, certain foods, and some medicines (such as
penicillin). Up to 10% of the US population suffer from at least one allergy.
After exposure to an allergen, some people make IgE antibodies as well as B and T
memory cells. Subsequent exposure to the same allergen causes a massive secondary
immune response that releases plenty of IgE antibodies. These bind to mast cells
found usually in connective tissues surrounding blood vessels. Mast cells then release
histamine, which starts the inflammatory response. In some individuals the histamine
release causes life-threatening anaphylaxis or anaphylactic shock.
The immune system usually distinguishes "self" from "nonself". The immune system
learns the difference between cells of the body and foreign invaders. Autoimmune
diseases result when the immune system attacks and destroys cells and tissues of the
body. Juvenile diabetes, Grave's disease, Multiple sclerosis, Systemic lupus
erythematosus, and Rheumatoid arthritis are some of the autoimmune diseases.
Myasthenia gravis (MG) is a muscle weakness caused by destruction of muscle-nerve
connections. Multiple sclerosis (MS) is caused by antibodies attacking the myelin of
nerve cells. Systemic lupus erythematosis (SLE) has the person forming a series of
antibodies to their own tissues, such as kidneys (the leading cause of death in SLE
patients) and the DNA in their own cellular nuclei. In systemic lupus erythematosus
(SLE), the immune system attacks connective tissues and major organs of the body.
Rheumatoid Arthritis; sufferers have damage to their joints. Some evidence supports
Type I diabetes as an auto immune disease. Juvenile diabetes results from the
destruction of insulin-producing cells in the pancreas.
Immunodeficiency diseases result from the lack or failure of one or more parts of the
immune system. Affected individuals are susceptible to diseases that normally would
not bother most people. Genetic disorders, Hodgkin's disease, cancer chemotherapy,
and radiation therapy can cause immunodeficiency diseases.
Severe Combined Immunodeficiency (SCID) results from a complete absence of the
cell-mediated and antibody-mediated immune responses. Affected individuals suffer
from a series of seemingly minor infections and usually die at an early age. A small
group suffering from adenosine deaminase (ADA) deficiency, a type of SCID, are
undergoing gene therapy to provide them with normal copies of the defective gene.
Acquired Immunodeficiency Syndrome (AIDS) is currently receiving the most
attention among the immunodeficiency diseases. AIDS is a collection of disorders
resulting from the destruction of T cells by the Human Immunodeficiency Virus
(HIV), a retrovirus. When HIV replicates in the human T cells, it buds from the T cell
plasma membrane encased in a coat derived from the T cell plasma membrane. HIV
selectively infects and kills T4 helper cells. The viral RNA is converted into DNA by
the enzyme reverse transcriptase; this DNA can become incorporated into a human
chromosome for months or years.
Structure and replication cycle of HIV. Images from Purves et al., Life: The Science of
Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and WH Freeman
(www.whfreeman.com), used with permission.
When the infected T cell is needed in the immune response, the viral genes are
activated and the virus replicates, killing the infected cell and producing a new round
on T4 cell infection. Gradually the number of T4 cells, the master on switch for the
immune system, decline. The immune response grows less powerful, eventually
failing. Premature death results from a series of rare diseases (such as fungal
pneumonia and Kaposi's sarcoma, a rare cancer) that overwhelm the body and its
compromised immune system.
Links | Back to Top
• AIDS: The War Within Museum of Science and Industry, Chicago. A very nicley
illustrated series of pages that walk you through the replication/infection
cycle of HIV.
• Our Immune System Written by Sara Le Bien, this site uses clever cartoon T
and B cells to explain the function of the immune syste. Very worth a visit.
• Jerry's Immunology Page
• Immunology and AIDS Another fine problem set with tutorials from the
University of Arizona's Biology Project.
• What The Heck Does Protease Inhibitor Have To Do With HIV? An article from
"Bugs in the News"
• Immunology Problem Set Another fine problem set with tutorials from the
University of Arizona's Biology Project. As of 4/21 the tutorials were not yet
online but were expected soon.
• The Lupus Foundation of America Learn about a serious illness and some of
the treatment options.
• SLE Lupus A page on "the great imposter" by the National Jewish Medical
Research Center
• The Lupus Home Page Hamline University
• Cells Alive! Excellent coverage of a range of immune-related topics, including

inflammation and AIDS.


• Microbiology Video Library Beware....some of these files are large and not for
the faint-of-modem!
• Welcome to Histo A site dedicated to the Major Histocompatibility Complex. I
can't wait!
• Dr. Kadar's Immune System Page
• Bloodline: The Online Hematology Resource
• Cells of the Blood A cool interface by clicking of a type of blood cell.
• Atlas of Hematology Nagoya University School of Medicine
• Inflammation and Fever An online book that I was ferverish to finish.
• Immunity Full text and graphics (after 1 May) from a journal devoted to
immunity.
• Cancer and the Immune System The Cancer Research Institute presents a
tasty series of graphics detailing the immune response to cancerous cells.
• Development of Vaccines to Infectious Diseases Brown University page for
BIO 160.

Text ©1992, 1994, 1997, 1998, 2000, 2001, by M.J. Farabee, all rights reserved.
Use for educational purposes is encouraged.
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Email: mj.farabee@emcmail.maricopa.edu
Last modified: Wednesday June 06 2007
The URL of this page is:
www.emc.maricopa.edu/faculty/farabee/BIOBK/BioBookIMMUN.html

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