Phil's Study Guide - Chapters 4, 10

Disease and Etiology

Homeostasis	State of relative stability of the body’s internal environment with respect to the external environment. Maintained by adaptive mechanisms Negative feedback Positive feedback
Disease	Disruption in the Homeostatic balance Loss of homeostasis= loss of functional capacity
Etiology	Cause of disease Three types of Etiology: Genetic Congenital Acquired
Idiopathic	Medical term used to describe diseases of unknown Etiology
Pathogenesis	Medical term used to describe the progression of a Disease or time course. Time course: Acute Chronic
Stress and Homeostasis	Stress = Note: some forms of stress are normal and beneficial. Cell Injury can have different distribution. Distribution may be: local systemic With regard to organ damage, injury may be: focal- meaning localized to a single region diffuse- meaning distributed throughout
Causes of cell injury	Three major processes: Deficiency Primary Secondary Intoxication endogenous exogenous Trauma Effects and Responses Reversible: functional structural Irreversible: functional structural

Note: Injury is dependent upon:

1. intensity
2. duration
3. exposures
4. nature

Reversible injury can be described as either functional or structural.

• Functional:
  1. hydropic change
  2. fatty change
  3. altered metabolism
  4. altered size
     1. hypertrophy
     2. atrophy
  5. organelle change
     
     
• Structural:
  1. Stretched or distorted membrane
     1. membrane blebs
  2. Intracellular
     1. loss of ribosomes
     2. loss of mitochondrial matrix

Irreversible injury

• Functional:
  1. plasma membrane extremely distorted
  2. increased membrane permeability
     1. increased influx of sodium
     2. increased efflux of potassium
     3. increased influx of calcium
  3. increased loss of cellular constituents
     
     
• Structural:
  1. altered nucleus
     1. karyolysis
     2. pyknosis
     3. karyohexis

Cells, Tissues and Organs are surrounded by fluid. These fluids represents specific fluid compartments. Changes in the composition of these fluid compartments can have direct effects on the function and structure of the cell, tissues or organ. These compartments are:

• Fluid compartments
  • Intracellular
  • Intravascular
  • Interstitial

Edema is defined as the accumulation of fluid within the interstitium.
Edema can be either:

• Local
• Systemic

What is the effect of changes in the composition of the extracellular compartment fluid on a typical cell?

Hypertonic solutions

Hypotonic solutions

Isotonic solutions

Inflammation - Injury or breach of defense barriers triggers localized response.

1. Acute inflammation
   1. Acute increase in blood flow
   2. Localized swelling as a result of increased fluid and cells in the interstitium.

Classical terminology used to describe inflammation

• Rubor - redness
• Calor - heat
• Tumor - swelling
• Dolor - pain
• Functio laesa - loss of function

Vessels involved in the inflammatory response are,

• Capillaries
• Post capillary venules

Blood flow through the capillaries is regulated by the

• Pre-capillary sphincter tone

Blood vessels are impermeable to certain substances. This vascular barrier to permeability due to the presence of:

• Endothelium - a special type of epithelial cell that lines the surfaces of all blood vessels and chambers of the heart.
  
  Tight junctions - are protein structures that seal one cells membrane to another. Usually found on the apical surface of the cell that prevents fluids and solutes from passing between the cells of the blood vessels. As a result, fluid and solutes must pass through the cells (across the cell membrane) and not between them. This results in the cell regulating what passes to the underlying tissues.

The space between cells is termed the Interstitium. It is composed of different cell types:

• Fibroblast
• Macrophages
• Mast cells
• Extracellular matrix, ( gelatinous structure composed of proteoglycans).

Formation of EDEMA?

• Exudate vs transudate
• Benefits of Edema

Acute inflammatory response has two components:

• Vascular - Increased blood flow and Vascular permeability
• Cellular - Increased migration of neutrophils and macrophages

Acute inflammation can be classified based on the differences
in exudate formed

• Serous
• Fibrinous
• Purulent
  • abscess
  • cyst

Hemorrhagic

Cellular factors

Emigration or migration of leukocytes to site of injury

1. axial flow
2. margination
3. pavementing
4. adhesion

Phagocytosis

Involves several steps

1. activation
2. recognization and attachment
3. engulfment and destruction

Chemotaxis - The movement of cells towards an area of damaged tissue due to the release of a chemotactic factor.

Opsonins - are proteins that coat the surface of a foreign substance in order for the bodies defense mechanisms to see them as foreign.

Specialized task of the phagocytic cells such as macrophages

• Killing of microorganisms
• Destruction or inactivation of toxic agents
• Degradation of macromolecules

Two broad mechanisms for the killing process

• Oxygen- dependent process
• Oxygen-independent process

Overview of Body Defenses

We are born with some general defenses and acquire other, specific ones. We have many defenses to protect us from pathogens—those viruses, bacteria, fungi, protozoa, and parasitic worms that cause disease. Antigens on these pathogens identify them as nonself. Antigens are usually proteins, lipids, or oligosaccharides. Immunity is the body’s overall ability to resist and combat anything that is nonself. Innateimmunity encompasses preset responses that activate rapidly and in a generalized way to detected damage or invasion. Adaptive immunity responds to specific antigens on specific pathogens; this response takes longer to develop, but the body “remembers” what it sees and responds quicker the next time the same pathogen is seen.

Adaptive and Innate Immunity
	Innate Immunity	Adaptive Immunity
Response time	Immediate	Slower
How antigen is detected	About 1,000 preset receptors	Billions of different receptors
Triggers	Damage to tissues; proteins on microbes	Pathogens, toxins, altered body cells
Memory	None	Long-term

Three lines of defense protect the body. Intact skin and mucous membranes are important first-line physical barriers. Innate immunity forms the second line of defense. Adaptive immunity forms the third line of defense.

White blood cells and their chemicals are the defenders in immune responses. White blood cells are the core of the immune system. Phagocytes release chemicals called cytokines to further defense responses. Cytokines regulate different aspects of the immune response; interleukins affect inflammation and fever, interferons defend against viruses, and tumor necrosis factor also affects inflammation and stimulates tumor cell death.

Complement is a group of about 30 blood proteins that can kill microbes or identify them for phagocytes to destroy. White blood cells serve a variety of different functions in the immune response:

• Neutrophils make up two-thirds of all white blood cells and work at the site of inflammation or damage.
• Basophils and mast cells produce histamines in response to antigens.
• Macrophages are the predominant phagocytes that patrol the bloodstream.
• Eosinophils target pathogens that are too large for the macrophages.
• Dendritic cells signal when antigens are present in skin and body linings.
• B and T lymphocytes (B and T cells) function in adaptive immunity.
• Natural killer cells (NK cells) are lymphocytes that function in innate responses.

Click here for the Animation: White Blood Cells. Please make sure that your sound is on and your volume is up.

Chemical Weapons of Immunity
Complement		Directly kills cells; stimulates lymphocytes
Cytokines		Cell-cell and cell-tissue communication:
	Interleukins	Cause inflammation and fever, cause T cells and B cells to divide and specialize; stimulate bone marrow stem cells, attract phagocytes, activate NK cells
	Interferons	Confer resistance to viruses; activate NK cells
	Tumor Necrosis Factor	Causes inflammation; kills tumor cells, causes T cells to accumulate in lymph nodes during infection
Other Chemicals		Various antimicrobial and defensive effects Enzymes and peptides; clotting factors; protease inhibitors; toxins; hormones

Neutrophil	Eosinophil
Basophil	Mast Cell
Tlymphocyte (T-cell)	Blymphocyte (B-cell)

Macrophage	Dendritic cell	Natural Killer (NK) cell

The Lymphatic System

Click to enlarge image

The lymphatic system has two key roles: to work with the cardiovascular system to cycle fluids back into the circulation; and to circulate lymph from the spleen, lymph nodes, and other lymphoid tissues throughout the body.

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The lymph vascular system functions in drainage, delivery, and disposal. The lymph vascular system consists of lymph capillaries and other vessels linking it to the cardiovascular system. Water and solutes that drain from the blood vessels collect in the lymphatic vessels and are returned to the blood via these vessels. The lymphatic vessels pick up absorbed fats and deliver them to the blood. Lymphatic vessels also transport foreign material to the lymph nodes for disposal. Lymph capillaries and vessels are structured much like blood capillaries and veins.

Lymphoid organs and tissues are specialized for body defense. Lymph nodes are located at intervals along the lymph vessels; lymphocytes congregate in these nodes, making them key battlefields in fighting off pathogens.

The spleen filters blood and serves as a holding station for large numbers of lymphocytes. T cells are produced and become specialized in the thymus.

Click here for the Animation: Human Lymphatic System. Please make sure that your sound is on and your volume is up.

Some of the lymph capillaries at the start of the drainage network called the lymph vascular system. (b) Cutaway diagram of a lymph node. Its inner chambers are packed with highly organized arrays of infection.fighting white blood cells.	Lymph Node Cross sectionSome of the lymph capillaries at the start of the drainage network called the lymph vascular system. (b) Cutaway diagram of a lymph node. Its inner chambers are packed with highly organized arrays of infection.fighting white blood cells.

Surface Barriers

Propionibacterium acnes	Streptococcus mutans

The normal microorganisms living on your skin help prevent the growth of unwanted pathogens through competition. Some microorganisms, such as the Lactobacillus species of the vaginal tract in women, lower the pH of their surroundings to prevent growth of other microbes.

The mucus coating your lungs contains enzymes such as lysozyme that can attack and destroy many bacteria; cilia can also sweep out pathogens. Chemicals in tears, saliva, and gastric fluid offer similar protection. The natural low pH of urine, as well as its flushing action, helps protect the urinary tract.

Innate Immunity

Once a pathogen enters the body, macrophages engulf it and release cytokines to attract dendritic cells, neutrophils, and more macrophages.

Circulating complement proteins can detect pathogens and become activated. Activated complement attracts phagocytes, which can destroy the pathogens. Activated complement can also form membrane attack complexes in the pathogen; these are holes that cause the pathogen to disintegrate.

Macrophange about to engulf a yeast cell	Pores form

A white blood cell squeezing through the wall of a cpillary.

Click here for the Animation: Membrane Attack Complexes. Please make sure that your sound is on and your volume is up.

Activated complement and cytokines stimulate inflammation, characterized by redness, swelling, warmth, and pain. Tissue irritation causes mast cells to release histamine and cytokines that cause the blood vessels to dilate (tissue redness and warmth) and capillary walls to become leaky (edema). Plasma proteins and phagocytes leave the blood vessels. Plasma proteins contain clotting agents that help wall off the pathogen and promote repair of tissues. Macrophages release cytokines that tell the brain to release prostaglandins, which in turn stimulates fever production; moderate fevers inhibit pathogen growth.

Click here for the Animation: Inflammatory Response. Please make sure that your sound is on and your volume is up.

a. Bacteria invadea tissue and directly kill cells or release metabolic products that damage tissue.	b. Mast cells in tissue release histamine, which then triggers arteriolar vasodilation (hence redness and warmth) as well as increased capillary permeability.	c. Fluid and plasma proteins leak out of capillaries; localized edema (tissue swelling) and pain result.	d. Plasma proteins attack bacteria. Clotting factors wall off inflamed area.	e. Neutrophils, macrophages, and other phagocytes engulf invaders and debris. Activated complement attracts phagocytes and directly kills invaders.

Overview of Adaptive Defenses

A life history of B cells and T cells

Adaptive immunity is the body’s third line of defense and has three defining features:

• Adaptive immunity is specific; each B and T cell only recognizes one antigen.
• Adaptive immunity is diverse; B and T cells collectively can recognize at least a billion different threats.
• Adaptive immunity has memory.

Recognition of an antigen results in rapid cell division to produce huge numbers of identical B and T cells that recognize the stimulating antigen. Some of these new cells are effector cells that can immediately destroy pathogens. Others are memory cells, held in reserve for future battles against the same threat; memory cells are what make you “immune” to various pathogens.

B cells and T cells become specialized to attack antigens in different ways. Both B and T lymphocytes arise in stem cells in the bone marrow. B cells continue to develop within bone marrow. T cells travel to the thymus to finish developing; T cells divide into two populations - helper T cells and cytotoxic (“killer”) T cells. When mature, B and T cells can be found in the lymph nodes, spleen, and other lymphoid tissues where they remain “naive” until they recognize antigen. B cells and T cells respond to pathogens in different ways. B cells produce antibodies (proteins) and are responsible for antibody-mediated immunity. T cells directly attack invaders; their response is called cell-mediated immunity.

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Overview of the links between antibody-mediated and cell-mediated immune responses - the two arms of adaptive immunity.

Proteins called MHC markers label body cells as self. All body cells have MHC markers (from Major Histocompatibility Complex genes) to identify them as “self.” T cells have TCRs (T Cell Receptors) that see MHC in context with antigen and respond.

Antigen-presenting cells introduce antigens to T cells and B cells. T cells and B cells can only “see” antigens that have been processed by an antigen-presenting cell (APC). Macrophages, dendritic cells, and B cells can all present antigen. The antigen is ingested and digested; then its fragments are linked with MHC markers and displayed on the cell’s surface as antigen-MHCcomplexes.

Helper T cells see the antigen-MHC complex, release cytokines, and trigger repeated rounds of division to produce the large numbers of activated B and T cells. Specialization of activated cells into effector or memory cells also occurs. An effector B cell is called a plasma cell; it can flood the bloodstream with antibodies.

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The Human Body's Three Lines of Defense against Pathogens
Barriers at Body Surfaces (nonspecific targets)	Intact skin; mucous membranes at other body surfaces Infection-fighting chemicals in tears, saliva, gastric fluid Normally harmless bacteria on body surfaces, which outcompete pathogens Flushing effect of tears, saliva, urination, diarrhea, sneezing and coughing
Innate Immune Responses (nonspecific targets)	Inflammation Fast-acting white blood cells (neutrophils, eosinophils, and basophils) Macrophages (also take part in immune responses) Complement proteins, blood-clotting proteins, and other infections-fighting cytokines Organs with pathogen-killing functions (such as lymph nodes) Some cytotoxic cells (e.g., NK cells) with a range of targets
Adaptive Immune Responses (specific targets only)	White blood cells (T cells, B cells, and macrophages that interact with them) Communication signals (e.g., interleukins) and chemical weapons (e.g., antibodies, perforins)

Antibody-Mediated Immunity: Defending Against Threats Outside Cells

Antibodies develop while B cells are in bone marrow. An antibody has a Y-shaped protein structure; antigens are bound by the two “arms” of the antibody. No two B cells make antibodies that are alike; this allows both diversity and specificity. B cells make many copies of their antibodies, which are inserted in the plasma membrane, arms sticking out and ready to bind antigen.

The Y-shaped structure of many antibodies.	How an antibody binds to an antigen. Each antibody can bind only one kind of antigen, which fits into grooves and onto bumps on the antibody molecule. In this example

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Antibody-mediated immune response. This example is a response to a bacterial invasion.

Antibodies target pathogens that are outside cells. Prior to activation, B cells serve as antigen-presenting cells. Antibodies on the B cell surface bind antigens, internalize them, process them, and then display antigen-MHC complexes. TCRs of a helper T cell see the antigen-MHC complex and bind; binding causes the cells to exchange signals. The T cell disengages, but the B cell is now activated; when it recognizes unbound antigen, the B cell will divide into plasma cells and memory cells.

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Click here for the Animation: Antibody-Mediated Immune Response. Please make sure that your sound is on and your volume is up.

Plasma cells can release up to 2,000 antibodies per minute into the bloodstream; these antibodies “flag” invaders for destruction by phagocytes and complement. There are five classes of antibodies, each with a particular function. Collectively, antibodies are referred to as immunoglobulins, or Igs. The five different classes of Igs are the protein products of gene shuffling that takes place as the B cells mature:

1. IgM antibodies cluster into a structure with 10 binding sites, making them more efficient at binding clumped targets; IgM is the first antibody produced in a response.
2. IgA antibodies are present in secretions of exocrine glands (tears, saliva, breast milk) and in the mucus of the respiratory, digestive, and reproductive tracts.
3. IgG antibodies neutralize toxins, turn on complement, are long lasting, can cross the placenta, and are found in mother’s milk.
4. IgD is the most common antibody bound to naive B cells; it may help activate T cells.
5. IgE antibodies are involved in allergic reactions; they bind to basophils and mast cells where they act as traps for antigen, causing the release of histamine.

Click here for the Animation: Generating Antibody Diversity. Please make sure that your sound is on and your volume is up.

Click here for the Video: Germs in Pakistan. Please make sure that your sound is on and your volume is up.

The Y-shaped structure of many antibodies

Cell-Mediated Responses—Defending Against Threats Inside Cells

A cytotoxic T cell caught in the act of tough-killing a tumor cell.

Cell-mediated responses fight those pathogens (viruses, bacteria, and some fungi and protozoans) that can enter cells to avoid antibody defenses; cell-mediated responses also fight abnormal body cells such as cancer cells. APCs present antigen to T cells, similar to their role in antibody-mediated immunity.

Helper T cells can be stimulated this way to divide into effector and memory cells. Effector helper T cells or APCs directly can stimulate cytotoxic T cells to divide. Cytotoxic T cells rapidly multiply and release molecules that can “touch-kill” infected and abnormal body cells. Cytotoxic T cells also secrete chemicals that stimulate apoptosis—the programmed cell death of the infected cell.

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Click here for the Video: Cell-Mediated Response Overview. Please make sure that your sound is on and your volume is up.

Diagram of a T cell-mediated immune response Click to enlarge

Helper T cells can also stimulate NK cells; they will attack any cell that has too few or altered MHC, any cells that have been tagged by antibodies, and cells showing “stress markers” as indicators of infection or cancer. Cytotoxic T cells cause the body to reject transplanted tissue. During organ transplants, donor tissues must be matched to a recipient to ensure that the MHC markers do not differ enough to stimulate rejection by cytotoxic T cells.

Donor and recipient usually must share at least 75% of their MHC markers for the transplant to succeed; close relatives make the best donors because of this. Recipients usually also take drugs to suppress the immune system to prevent rejection; often they will also take antibiotics to ward off potential infections. Tissues of the eye and testicles do not stimulate rejection; instead, cells of these tissues secrete signals that cause lymphocytes to undergo apoptosis, thus preventing the lymphocytes from attacking.

Immunological Memory

A positive reaction to a tuberculosis skin test

Memory cells form during the primary (first) response to an antigen and remain in the blood for years or decades. Secondary responses to the same antigen are much faster; plasma cells and effector T cells form sooner and in greater numbers, preventing infection.

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Comparison of a primary and secondary immune response Applications of Immunology Immunization gives “borrowed” immunity. Immunization increases immunity against specific diseases. In active immunization, a vaccine is given by injection or is taken orally. The first dose of vaccine elicits a primary immune response; a second dose (“booster”) elicits a secondary, and more long-lasting, response. Vaccines are made from killed or very weak pathogens, inactivated forms of toxins, or transgenic (genetically engineered) viruses. Passive immunization involves injecting antibodies into already infected individuals. Vaccines are not risk free. Recommended Vaccines Recommended Ages Hepatitis B Birth - 2 months Hepatitis B booster 1 1-4 months Hepatitis B booster 2 6-18 months DTP Diphtheria, tetanus, and pertussis (whooping cough) 2, 4, and 6 months DTP booster 1 15-18 months DTP booster 2 4-6 years DT 11-12 years HiB (Haemophilus influenzae) 2, 4, and 6 months HiB booster 12-15 months Polio 2 and 4 months Polio booster 1 6 - 18 months Polio booster 2 4-6 years MMR (Measles, Mumps, Rubella) 12-15 months MMR booster 4-6 years Pneumococcal 2, 4, and 6 months Pneumococcal booster 1 12-15 months Pneumococcal booster 2 2 - 18 years Varicella 12-18 months Hepatitis A series (in some areas) 2-12 years Influenza Yearly, 1-18 years Monoclonal antibodies are used in research and medicine. Monoclonal antibodies are antibodies made by cells cloned from a single antibody-producing B cell; they are generally produced using genetically altered bacteria or sometimes plants. Monoclonal antibodies are being used commercially in home pregnancy tests, screening for prostate cancer, and other uses. Immunotherapies reinforce defenses. Immunotherapy alters the body’s own immune mechanisms to enhance defense against infections and cancer. Cytokines can be used to activate B and T cells to fight cancer. Monoclonal antibodies can be used to bind to proteins on cancer cells to draw NK cells to the tumor. Other monoclonal antibodies are bound to toxins to make immunotoxins; these substances bind to cancer cells, enter them, and prevent growth. Gamma interferon, produced by T cells, stimulates NK cells and boosts activity of macrophages; it is currently being used to treat hepatitis C. Beta interferon is being used to treat multiple sclerosis. Immunotherapies, as with vaccines, do not come without risks. Click here for the Video: Polio Scare. Please make sure that your sound is on and your volume is up. Disorders of the Immune System Diseases of the immune system can be divided into four groups: Hypersensitivity reactions T-Cell deficiencies B- cell deficiencies Complement deficiencies Hypersensitivity reactions can be subdivided into four types: Type I Type II Type III Type IV T- cell deficienceies are sudivided into tow type (see supplement to this section entitled, “Immune Deficiency Diseases”): Primary Secondary Like T- cell deficiencies, B-cell deficiencies are subdivided into two groups (see supplement to this section entitled, “Immune Deficiency Diseases”): Allergen Primary Secondary Compliment deficiencies can come about when ever there is a inability to produce any of the twenty compliment proteins or the factors that regulate compliment activity. Type I hypersensitivities, or Allergies, harmless substances provoke an immune attack. An allergy is an immune response to a normally harmless substance called an allergen. Allergens include: pollen, some foods and drugs, dust mites, fungal spores, insect venom, and certain ingredients in cosmetics. Allergens trigger mild to severe inflammation of various tissues. A variety of causes, from genetic to emotional, lead to allergies. Exposure to an allergen triggers production of IgE antibodies, which cause the release of histamines and prostaglandins from mast cells. Histamines and prostaglandins fuel inflammation. Hay fever manifests as stuffed sinuses, a drippy nose, and sneezing. In a few individuals, explosive inflammatory responses trigger life-threatening anaphylactic shock in which air passages constrict and fluid rushes out of the capillaries. Food allergies, such as peanut allergies, and wasp and bee venom allergies, can trigger anaphylactic shock. Rapid injections of the hormone epinephrine can prevent shock and save lives. Antihistamines are often used to relieve the short-term symptoms of allergies; desensitization can be used to “train” the body not to see allergens. Allergen enters the body Micrograph of ragweed pollen Type II Autoimmune disorders attack “self.” In an autoimmune response, lymphocytes turn against the body’s own cells. Examples of autoimmune diseases include the following: Hand of a person affected by rheumatoid arthritis Rheumatoid arthritis, an inflammation of the joints caused by immune attack against collagen and antibodies in the joints; inflammation, complement and faulty repair mechanisms contribute to the damage. Type 1 diabetes, a type of diabetes mellitus, caused when the immune system attacks and destroys the insulin-secreting cells of the pancreas, impairing glucose absorption from the blood. Systemic lupus erythematosus, where patients develop antibodies to their own DNA and other “self” components. Autoimmune diseases tend to be more frequent in women than in men. In T –cell or B-cell Deficiencies immune responses can be deficient due to a lack of immune cells. Immunodeficiency is used to describe the state where a person’s immune system is weakened or lacking; under these conditions the body is vulnerable and infections that would normally not be serious become life threatening. An example of a T-cell deficiency would be in acquired immune deficiency syndrome (AIDS), the HIV virus attacks the body’s macrophages and helper T cells, crippling the immune response. Sometimes Immune cell diseases are due to a deficiency of both T and B-cells. One such type is termed: In severe combined immune deficiency (SCID) both B and T cells are in low numbers; infants born with SCID usually die early in life. In acquired immune deficiency syndrome (AIDS), the HIV virus attacks the body’s macrophages and helper T cells, crippling the immune response. The Immune system Chronic Inflammation Distinguishing factors Length of time Persistence of injurious agent Involvement of lymphocytes Diseases of the Immune System Lymph tissues Spleen Thymus Tonsils Appendix Lymph nodes Lymph formation Lymphatic circulation Lymphocytes T-cells B-cells NK cells K cells Immunity Non-specific (Innate Immunity) Specific (Adaptive Immunity) Antibodies Structural features Types and function Immune response Cell mediated Humoral Immunization Vaccines Antibody production Active immunity Passive immunity Hypersensitivity reactions Type I Type II Type III Type IV Diseases due to hypersensitivity reactions Type I Allergies Type II Myasthenia Gravis Erythroblastosis Fetalis Graves Disease Goodpasture Disease Type III Serum sickness Rheumatoid Arthritis Immune-complex Glomerulonephritis Type IV Contact dermatitis Tuberculosis Fungal, viral and parasiteinfections Acute and chronic transplant rejection Major histocompatibility complex (MHC) MHC-1 MHC-2 Tissue transplant Immune Deficiency Syndromes Primary - genetic B-cells deficiency T-cells deficiency B and T cells deficiency Secondary - acquired AIDS

In immune responses, some plasma cells adn T cells are set aside as memory cells