Module 6: The Lymphatic and Immune Systems

Lesson 6: Diseases Associated with Depressed or Overactive Immune Responses

Bệnh Lý Liên Quan Đến Suy Giảm Hoặc Tăng Quá Mức Đáp Ứng Miễn Dịch

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Dưới đây là danh sách những thuật ngữ Y khoa của module The Lymphatic and Immune Systems.
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Medical Terminology: The Lymphatic and Immune Systems

active immunity
immunity developed from an individual’s own immune system
acute inflammation
inflammation occurring for a limited time period; rapidly developing
adaptive immune response
relatively slow but very specific and effective immune response controlled by lymphocytes
afferent lymphatic vessels
lead into a lymph node
antigen-specific protein secreted by plasma cells; immunoglobulin
molecule recognized by the receptors of B and T lymphocytes
antigen presentation
binding of processed antigen to the protein-binding cleft of a major histocompatibility complex molecule
antigen processing
internalization and digestion of antigen in an antigen-presenting cell
antigen receptor
two-chain receptor by which lymphocytes recognize antigen
antigenic determinant
(also, epitope) one of the chemical groups recognized by a single type of lymphocyte antigen receptor
B cells
lymphocytes that act by differentiating into an antibody-secreting plasma cell
barrier defenses
antipathogen defenses deriving from a barrier that physically prevents pathogens from entering the body to establish an infection
bone marrow
tissue found inside bones; the site of all blood cell differentiation and maturation of B lymphocytes
bronchus-associated lymphoid tissue (BALT)
lymphoid nodule associated with the respiratory tract
central tolerance
B cell tolerance induced in immature B cells of the bone marrow
soluble, long-range, cell-to-cell communication molecule
chronic inflammation
inflammation occurring for long periods of time
lipid-rich lymph inside the lymphatic capillaries of the small intestine
cisterna chyli
bag-like vessel that forms the beginning of the thoracic duct
class switching
ability of B cells to change the class of antibody they produce without altering the specificity for antigen
clonal anergy
process whereby B cells that react to soluble antigens in bone marrow are made nonfunctional
clonal deletion
removal of self-reactive B cells by inducing apoptosis
clonal expansion
growth of a clone of selected lymphocytes
clonal selection
stimulating growth of lymphocytes that have specific receptors
group of lymphocytes sharing the same antigen receptor
enzymatic cascade of constitutive blood proteins that have antipathogen effects, including the direct killing of bacteria
constant region domain
part of a lymphocyte antigen receptor that does not vary much between different receptor types
soluble, short-range, cell-to-cell communication molecule
cytotoxic T cells (Tc)
T lymphocytes with the ability to induce apoptosis in target cells
delayed hypersensitivity
(type IV) T cell-mediated immune response against pathogens infiltrating interstitial tissues, causing cellular infiltrate
early induced immune response
includes antimicrobial proteins stimulated during the first several days of an infection
effector T cells
immune cells with a direct, adverse effect on a pathogen
efferent lymphatic vessels
lead out of a lymph node
erythroblastosis fetalis
disease of Rh factor-positive newborns in Rh-negative mothers with multiple Rh-positive children; resulting from the action of maternal antibodies against fetal blood
fas ligand
molecule expressed on cytotoxic T cells and NK cells that binds to the fas molecule on a target cell and induces it do undergo apoptosis
Fc region
in an antibody molecule, the site where the two termini of the heavy chains come together; many cells have receptors for this portion of the antibody, adding functionality to these molecules
germinal centers
clusters of rapidly proliferating B cells found in secondary lymphoid tissues
graft-versus-host disease
in bone marrow transplants; occurs when the transplanted cells mount an immune response against the recipient
apoptosis-inducing substance contained in granules of NK cells and cytotoxic T cells
heavy chain
larger protein chain of an antibody
helper T cells (Th)
T cells that secrete cytokines to enhance other immune responses, involved in activation of both B and T cell lymphocytes
high endothelial venules
vessels containing unique endothelial cells specialized to allow migration of lymphocytes from the blood to the lymph node
vasoactive mediator in granules of mast cells and is the primary cause of allergies and anaphylactic shock
antibody whose dimer is secreted by exocrine glands, is especially effective against digestive and respiratory pathogens, and can pass immunity to an infant through breastfeeding
class of antibody whose only known function is as a receptor on naive B cells; important in B cell activation
antibody that binds to mast cells and causes antigen-specific degranulation during an allergic response
main blood antibody of late primary and early secondary responses; passed from carrier to unborn child via placenta
antibody whose monomer is a surface receptor of naive B cells; the pentamer is the first antibody made blood plasma during primary responses
immediate hypersensitivity
(type I) IgE-mediated mast cell degranulation caused by crosslinking of surface IgE by antigen
immune system
series of barriers, cells, and soluble mediators that combine to response to infections of the body with pathogenic organisms
protein antibody; occurs as one of five main classes
immunological memory
ability of the adaptive immune response to mount a stronger and faster immune response upon re-exposure to a pathogen
basic innate immune response characterized by heat, redness, pain, and swelling
innate immune response
rapid but relatively nonspecific immune response
early induced proteins made in virally infected cells that cause nearby cells to make antiviral proteins
light chain
small protein chain of an antibody
fluid contained within the lymphatic system
lymph node
one of the bean-shaped organs found associated with the lymphatic vessels
lymphatic capillaries
smallest of the lymphatic vessels and the origin of lymph flow
lymphatic system
network of lymphatic vessels, lymph nodes, and ducts that carries lymph from the tissues and back to the bloodstream.
lymphatic trunks
large lymphatics that collect lymph from smaller lymphatic vessels and empties into the blood via lymphatic ducts
white blood cells characterized by a large nucleus and small rim of cytoplasm
lymphoid nodules
unencapsulated patches of lymphoid tissue found throughout the body
ameboid phagocyte found in several tissues throughout the body
macrophage oxidative metabolism
metabolism turned on in macrophages by T cell signals that help destroy intracellular bacteria
major histocompatibility complex (MHC)
gene cluster whose proteins present antigens to T cells
mast cell
cell found in the skin and the lining of body cells that contains cytoplasmic granules with vasoactive mediators such as histamine
memory T cells
long-lived immune cell reserved for future exposure to a pathogen
MHC class I
found on most cells of the body, it binds to the CD8 molecule on T cells
MHC class II
found on macrophages, dendritic cells, and B cells, it binds to CD4 molecules on T cells
MHC polygeny
multiple MHC genes and their proteins found in body cells
MHC polymorphism
multiple alleles for each individual MHC locus
precursor to macrophages and dendritic cells seen in the blood
mucosa-associated lymphoid tissue (MALT)
lymphoid nodule associated with the mucosa
naïve lymphocyte
mature B or T cell that has not yet encountered antigen for the first time
natural killer cell (NK)
cytotoxic lymphocyte of innate immune response
negative selection
selection against thymocytes in the thymus that react with self-antigen
inactivation of a virus by the binding of specific antibody
phagocytic white blood cell recruited from the bloodstream to the site of infection via the bloodstream
enhancement of phagocytosis by the binding of antibody or antimicrobial protein
passive immunity
transfer of immunity to a pathogen to an individual that lacks immunity to this pathogen usually by the injection of antibodies
pattern recognition receptor (PRR)
leukocyte receptor that binds to specific cell wall components of different bacterial species
molecule in NK cell and cytotoxic T cell granules that form pores in the membrane of a target cell
peripheral tolerance
mature B cell made tolerant by lack of T cell help
movement of material from the outside to the inside of the cells via vesicles made from invaginations of the plasma membrane
plasma cell
differentiated B cell that is actively secreting antibody
polyclonal response
response by multiple clones to a complex antigen with many determinants
positive selection
selection of thymocytes within the thymus that interact with self, but not non-self, MHC molecules
primary adaptive response
immune system’s response to the first exposure to a pathogen
primary lymphoid organ
site where lymphocytes mature and proliferate; red bone marrow and thymus gland
study of the connections between the immune, nervous, and endocrine systems
regulatory T cells (Treg)
(also, suppressor T cells) class of CD4 T cells that regulates other T cell responses
right lymphatic duct
drains lymph fluid from the upper right side of body into the right subclavian vein
secondary adaptive response
immune response observed upon re-exposure to a pathogen, which is stronger and faster than a primary response
secondary lymphoid organs
sites where lymphocytes mount adaptive immune responses; examples include lymph nodes and spleen
first exposure to an antigen
clearance of pathogen in the serum and the simultaneous rise of serum antibody
severe combined immunodeficiency disease (SCID)
genetic mutation that affects both T cell and B cell arms of the immune response
secondary lymphoid organ that filters pathogens from the blood (white pulp) and removes degenerating or damaged blood cells (red pulp)
T cell
lymphocyte that acts by secreting molecules that regulate the immune system or by causing the destruction of foreign cells, viruses, and cancer cells
T cell tolerance
process during T cell differentiation where most T cells that recognize antigens from one’s own body are destroyed
T cell-dependent antigen
antigen that binds to B cells, which requires signals from T cells to make antibody
T cell-independent antigen
binds to B cells, which do not require signals from T cells to make antibody
Th1 cells
cells that secrete cytokines that enhance the activity of macrophages and other cells
Th2 cells
cells that secrete cytokines that induce B cells to differentiate into antibody-secreting plasma cells
thoracic duct
large duct that drains lymph from the lower limbs, left thorax, left upper limb, and the left side of the head
immature T cell found in the thymus
primary lymphoid organ; where T lymphocytes proliferate and mature
tissue typing
typing of MHC molecules between a recipient and donor for use in a potential transplantation procedure
lymphoid nodules associated with the nasopharynx
type I hypersensitivity
immediate response mediated by mast cell degranulation caused by the crosslinking of the antigen-specific IgE molecules on the mast cell surface
type II hypersensitivity
cell damage caused by the binding of antibody and the activation of complement, usually against red blood cells
type III hypersensitivity
damage to tissues caused by the deposition of antibody-antigen (immune) complexes followed by the activation of complement
variable region domain
part of a lymphocyte antigen receptor that varies considerably between different receptor types
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This article is about how the immune system goes wrong. When it goes haywire, and becomes too weak or too strong, it leads to a state of disease. The factors that maintain immunological homeostasis are complex and incompletely understood.
As you have seen, the immune system is quite complex. It has many pathways using many cell types and signals. Because it is so complex, there are many ways for it to go wrong. Inherited immunodeficiencies arise from gene mutations that affect specific components of the immune response. There are also acquired immunodeficiencies with potentially devastating effects on the immune system, such as HIV.

A. Inherited Immunodeficiencies

A list of all inherited immunodeficiencies is well beyond the scope of this book. The list is almost as long as the list of cells, proteins, and signaling molecules of the immune system itself. Some deficiencies, such as those for complement, cause only a higher susceptibility to some Gram-negative bacteria. Others are more severe in their consequences. Certainly, the most serious of the inherited immunodeficiencies is severe combined immunodeficiency disease (SCID). This disease is complex because it is caused by many different genetic defects. What groups them together is the fact that both the B cell and T cell arms of the adaptive immune response are affected.

Children with this disease usually die of opportunistic infections within their first year of life unless they receive a bone marrow transplant. Such a procedure had not yet been perfected for David Vetter, the “boy in the bubble,” who was treated for SCID by having to live almost his entire life in a sterile plastic cocoon for the 12 years before his death from infection in 1984. One of the features that make bone marrow transplants work as well as they do is the proliferative capability of hematopoietic stem cells of the bone marrow. Only a small amount of bone marrow from a healthy donor is given intravenously to the recipient. It finds its own way to the bone where it populates it, eventually reconstituting the patient’s immune system, which is usually destroyed beforehand by treatment with radiation or chemotherapeutic drugs.

New treatments for SCID using gene therapy, inserting nondefective genes into cells taken from the patient and giving them back, have the advantage of not needing the tissue match required for standard transplants. Although not a standard treatment, this approach holds promise, especially for those in whom standard bone marrow transplantation has failed.

B. Human Immunodeficiency Virus/AIDS

Although many viruses cause suppression of the immune system, only one wipes it out completely, and that is the previously mentioned HIV. It is worth discussing the biology of this virus, which can lead to the well-known AIDS, so that its full effects on the immune system can be understood. The virus is transmitted through semen, vaginal fluids, and blood, and can be caught by risky sexual behaviors and the sharing of needles by intravenous drug users. There are sometimes, but not always, flu-like symptoms in the first 1 to 2 weeks after infection. This is later followed by seroconversion. The anti-HIV antibodies formed during seroconversion are the basis for most initial HIV screening done in the United States. Because seroconversion takes different lengths of time in different individuals, multiple AIDS tests are given months apart to confirm or eliminate the possibility of infection.

After seroconversion, the amount of virus circulating in the blood drops and stays at a low level for several years. During this time, the levels of CD4+ cells, especially helper T cells, decline steadily, until at some point, the immune response is so weak that opportunistic disease and eventually death result. HIV uses CD4 as the receptor to get inside cells, but it also needs a co-receptor, such as CCR5 or CXCR4. These co-receptors, which usually bind to chemokines, present another target for anti-HIV drug development. Although other antigen-presenting cells are infected with HIV, given that CD4+ helper T cells play an important role in T cell immune responses and antibody responses, it should be no surprise that both types of immune responses are eventually seriously compromised.

Treatment for the disease consists of drugs that target virally encoded proteins that are necessary for viral replication but are absent from normal human cells. By targeting the virus itself and sparing the cells, this approach has been successful in significantly prolonging the lives of HIV-positive individuals. On the other hand, an HIV vaccine has been 30 years in development and is still years away. Because the virus mutates rapidly to evade the immune system, scientists have been looking for parts of the virus that do not change and thus would be good targets for a vaccine candidate.
The word “hypersensitivity” simply means sensitive beyond normal levels of activation. Allergies and inflammatory responses to nonpathogenic environmental substances have been observed since the dawn of history. Hypersensitivity is a medical term describing symptoms that are now known to be caused by unrelated mechanisms of immunity. Still, it is useful for this discussion to use the four types of hypersensitivities as a guide to understand these mechanisms (Figure 1).

A. Immediate (Type I) Hypersensitivity

Antigens that cause allergic responses are often referred to as allergens. The specificity of the immediate hypersensitivity response is predicated on the binding of allergen-specific IgE to the mast cell surface. The process of producing allergen-specific IgE is called sensitization, and is a necessary prerequisite for the symptoms of immediate hypersensitivity to occur. Allergies and allergic asthma are mediated by mast cell degranulation that is caused by the crosslinking of the antigen-specific IgE molecules on the mast cell surface. The mediators released have various vasoactive effects already discussed, but the major symptoms of inhaled allergens are the nasal edema and runny nose caused by the increased vascular permeability and increased blood flow of nasal blood vessels. As these mediators are released with mast cell degranulation, type I hypersensitivity reactions are usually rapid and occur within just a few minutes, hence the term immediate hypersensitivity.

Most allergens are in themselves nonpathogenic and therefore innocuous. Some individuals develop mild allergies, which are usually treated with antihistamines. Others develop severe allergies that may cause anaphylactic shock, which can potentially be fatal within 20 to 30 minutes if untreated. This drop in blood pressure (shock) with accompanying contractions of bronchial smooth muscle is caused by systemic mast cell degranulation when an allergen is eaten (for example, shellfish and peanuts), injected (by a bee sting or being administered penicillin), or inhaled (asthma). Because epinephrine raises blood pressure and relaxes bronchial smooth muscle, it is routinely used to counteract the effects of anaphylaxis and can be lifesaving. Patients with known severe allergies are encouraged to keep automatic epinephrine injectors with them at all times, especially when away from easy access to hospitals.

Allergists use skin testing to identify allergens in type I hypersensitivity. In skin testing, allergen extracts are injected into the epidermis, and a positive result of a soft, pale swelling at the site surrounded by a red zone (called the wheal and flare response), caused by the release of histamine and the granule mediators, usually occurs within 30 minutes. The soft center is due to fluid leaking from the blood vessels and the redness is caused by the increased blood flow to the area that results from the dilation of local blood vessels at the site.

B. Type II and Type III Hypersensitivities

Type II hypersensitivity, which involves IgG-mediated lysis of cells by complement proteins, occurs during mismatched blood transfusions and blood compatibility diseases such as erythroblastosis fetalis (see section on transplantation). Type III hypersensitivity occurs with diseases such as systemic lupus erythematosus, where soluble antigens, mostly DNA and other material from the nucleus, and antibodies accumulate in the blood to the point that the antigen and antibody precipitate along blood vessel linings. These immune complexes often lodge in the kidneys, joints, and other organs where they can activate complement proteins and cause inflammation.

C. Delayed (Type IV) Hypersensitivity

Delayed hypersensitivity, or type IV hypersensitivity, is basically a standard cellular immune response. In delayed hypersensitivity, the first exposure to an antigen is called sensitization, such that on re-exposure, a secondary cellular response results, secreting cytokines that recruit macrophages and other phagocytes to the site. These sensitized T cells, of the Th1 class, will also activate cytotoxic T cells. The time it takes for this reaction to occur accounts for the 24- to 72-hour delay in development.

The classical test for delayed hypersensitivity is the tuberculin test for tuberculosis, where bacterial proteins from M. tuberculosis are injected into the skin. A couple of days later, a positive test is indicated by a raised red area that is hard to the touch, called an induration, which is a consequence of the cellular infiltrate, an accumulation of activated macrophages. A positive tuberculin test means that the patient has been exposed to the bacteria and exhibits a cellular immune response to it.

Another type of delayed hypersensitivity is contact sensitivity, where substances such as the metal nickel cause a red and swollen area upon contact with the skin. The individual must have been previously sensitized to the metal. A much more severe case of contact sensitivity is poison ivy, but many of the harshest symptoms of the reaction are associated with the toxicity of its oils and are not T cell mediated.
The worst cases of the immune system over-reacting are autoimmune diseases. Somehow, tolerance breaks down and the immune systems in individuals with these diseases begin to attack their own bodies, causing significant damage. The trigger for these diseases is, more often than not, unknown, and the treatments are usually based on resolving the symptoms using immunosuppressive and anti-inflammatory drugs such as steroids. These diseases can be localized and crippling, as in rheumatoid arthritis, or diffuse in the body with multiple symptoms that differ in different individuals, as is the case with systemic lupus erythematosus (Figure 2).

Environmental triggers seem to play large roles in autoimmune responses. One explanation for the breakdown of tolerance is that, after certain bacterial infections, an immune response to a component of the bacterium cross-reacts with a self-antigen. This mechanism is seen in rheumatic fever, a result of infection with Streptococcus bacteria, which causes strep throat. The antibodies to this pathogen’s M protein cross-react with an antigenic component of heart myosin, a major contractile protein of the heart that is critical to its normal function. The antibody binds to these molecules and activates complement proteins, causing damage to the heart, especially to the heart valves. On the other hand, some theories propose that having multiple common infectious diseases actually prevents autoimmune responses. The fact that autoimmune diseases are rare in countries that have a high incidence of infectious diseases supports this idea, another example of the hygiene hypothesis discussed earlier in this chapter.

There are genetic factors in autoimmune diseases as well. Some diseases are associated with the MHC genes that an individual expresses. The reason for this association is likely because if one’s MHC molecules are not able to present a certain self-antigen, then that particular autoimmune disease cannot occur. Overall, there are more than 80 different autoimmune diseases, which are a significant health problem in the elderly. Table 1 lists several of the most common autoimmune diseases, the antigens that are targeted, and the segment of the adaptive immune response that causes the damage.

OpenStax. (2022). Anatomy and Physiology 2e. Rice University. Retrieved June 15, 2023. ISBN-13: 978-1-711494-06-7 (Hardcover) ISBN-13: 978-1-711494-05-0 (Paperback) ISBN-13: 978-1-951693-42-8 (Digital). License: Attribution 4.0 International (CC BY 4.0). Access for free at

Components of the immune system cause four types of hypersensitivity. Notice that types I–III are B cell mediated, whereas type IV hypersensitivity is exclusively a T cell phenomenon.

(a) Extensive damage to the right hand of a rheumatoid arthritis sufferer is shown in the x-ray. (b) The diagram shows a variety of possible symptoms of systemic lupus erythematosus.

Celiac diseaseTissue transglutaminaseDamage to small intestine
Diabetes mellitus type IBeta cells of pancreasLow insulin production; inability to regulate serum glucose
Graves’ diseaseThyroid-stimulating hormone receptor (antibody mimics hormone and stimulates receptor)Hyperthyroidism
Hashimoto’s thyroiditisThyroid-stimulating hormone receptor (antibody blocks receptor)Hypothyroidism
Lupus erythematosusNuclear DNA and proteinsDamage of many body systems
Myasthenia gravisAcetylcholine receptor in neuromuscular junctionsDebilitating muscle weakness
Rheumatoid arthritisJoint capsule antigensChronic inflammation of joints
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Dưới đây là video và các luyện tập (practice) của bài này. Nghe là một kĩ năng khó, đặc biệt là khi chúng ta chưa quen nội dung và chưa có nhạy cảm ngôn ngữ. Nhưng cứ đi thật chậm và đừng bỏ cuộc.
Xem video và cảm nhận nội dung bài. Bạn có thể thả trôi, cảm nhận dòng chảy ngôn ngữ và không nhất thiết phải hiểu toàn bộ bài. Bên dưới là script để bạn khái quát nội dụng và tra từ mới.
  1. The immune response can be under-reactive or over-reactive.
  2. Suppressed immunity can result from inherited genetic defects or by acquiring viruses.
  3. Over-reactive immune responses involve excessive B cell- and T cell-mediated immune reactions that result in symptoms or medical complications.
  4. Inherited and acquired immunodeficiencies disrupt the immune system’s balance, leading to susceptibility to infections and diseases like severe combined immunodeficiency disease (or SCID).
  5. SCID, exemplified by the case of David Vetter, underscores the importance of bone marrow transplants and the potential of gene therapy as a treatment option.
  6. Human Immunodeficiency Virus severely compromises the immune system, primarily targeting CD4 cells, leading to opportunistic infections and eventual death.
  7. Treatment involves antiviral drugs targeting viral replication, while vaccine development faces challenges due to the virus’s rapid mutation.
  8. Hypersensitivities can manifest as allergic reactions (or Type I), cytotoxic reactions (or Type II), immune complex-mediated reactions (or Type III), and delayed cellular reactions (which is Type IV).
  9. Allergies, anaphylaxis, and contact sensitivity are examples of hypersensitivity reactions with varying degrees of severity.
  10. Autoimmune diseases result from the immune system attacking the body’s own tissues due to breakdowns in self-tolerance.
  11. Environmental triggers and genetic factors play significant roles in autoimmune diseases, leading to conditions like rheumatoid arthritis and systemic lupus erythematosus.
  12. These diseases are more common in the aged, so treating them will be a challenge in the future as the aged population in the world increases.
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