Chapter 21- Immunity Flashcards
1
Q
Immunity
A
The ability of the body to defend itself against “unfamiliar” microorganisms. Has a basis in the lymphatic system- a lot of WBCs stay there but can leave to provide immune functions
2
Q
What do WBCs use to identify self vs non-self cells?
A
Antigens
3
Q
2 intrinsic systems of immunity
A
- Innate defenses
2. Adaptive defenses- adapt to new pathogens as we are introduced to them
4
Q
Non specific immunity
A
cells or chemicals involved are looking for a pathogen in general, not a specific type
5
Q
Innate defenses
A
Nonspecific defense mechanism that is able to be initiated very quickly in the body. Exposure to pathogen not necessary for body defense to occur. Consists of physical barriers and certain cells that initially encounter pathogens- primarily responsible for preventing bacteria, viruses, etc. from entering the body
6
Q
2 lines of defense for innate defenses
A
- Surface barriers
2. Cells and chemicals- antimicrobial proteins, macrophages, etc.
7
Q
Surface barriers definition
A
Physically prevent pathogens from entering the body, first line of defense.
8
Q
Types of surface barriers (2)
A
- Skin
2. Mucous membranes
9
Q
What 2 characteristics of skin allow it to act as a surface barrier?
A
- Keratin
2. Acid mantle
10
Q
Keratin
A
Tough protein resistant to weak acids, weak bases, bacterial enzymes- allows skin to be both tough and dry. If nowhere for bacteria to go, it will die on the skin unless it’s transferred to something else
11
Q
Acid mantle of the skin
A
Sweat and sebum on skin surface are slightly acidic. Bactericidal in nature- inhibits bacterial growth
12
Q
Mucous membranes definition
A
Line all body cavities that open to the exterior (digestive, respiratory, and reproductive tracts).
13
Q
Characteristics that can be found on some mucous membranes (6)
A
- Mucus
- Nasal hairs
- Cilia
- Acid mantle
- Tears and saliva
- Urine
14
Q
Mucus immune function
A
Traps microorganisms in respiratory and digestive tracts
15
Q
Nasal hairs immune function
A
Trap microorganisms in nasal cavity
16
Q
Cilia immune function
A
Takes mucus (with trapped microorganisms) and propels it away from nasal cavity and respiratory tract
17
Q
Acid mantle immune function (mucous membranes)
A
Stomach- secretes very acidic gastric juices, pH 2-3
Vagina- acidic nature prevents bacterial and fungal growth in reproductive tract
18
Q
Tears and saliva immune function
A
Cleanses eyes and mouth- contains lysozyme digestive protein that destroys bacteria
19
Q
Urine immune function
A
Acidic in nature, physically removes bacteria during urination
20
Q
What is the purpose of cellular and chemical innate defenses?
A
Used when surface barriers are breached as a second line of defense. Skin and mucous membranes can suffer physical damage- allows microorganisms an entry point. Several different types of cells and chemicals are the back up to the surface barriers
21
Q
Pattern recognition receptors
A
Non-specific proteins found on cells of the innate immune system. They can recognize potentially harmful substances by presence of a molecule with a certain shape found on a pathogen, but not normal human cells. When it encounters a protein that doesn’t belong, you have an immune response.
22
Q
Cells of innate defense (2)
A
- Natural killer cells
2. Phagocytes
23
Q
Natural killer cells
A
Target cancerous cells and virus infected cells. Non specific- will recognize/destroy a wide range of cancerous and virus infected cells. Therefore, NK cells do not need to recognize a specific antigen before destroying the cell- act against the cell itself. Do not phagocytize- directly contact target cell, induces apoptosis (programmed cell death). They releases protein perforin, which creates pores in the membrane of the cell, then release proteases and other chemicals
24
Q
What is the difference between apoptosis and cellular lysis?
A
Lysis- when a cell is so full it bursts. Apoptosis is shutting down a cell
25
Why is it more beneficial for NK cells to induce apoptosis rather than lysis?
Viruses hijack cell machinery to reproduce, and eventually rips open the cell so the virus can go to other places. With lysis, NK cells would make infection worse by releasing viruses. Apoptosis shuts down the cell so that no more virus can be produced or released
26
Examples of phagocytes (2)
neutrophils and macrophages
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Phagocytosis definition
Process by which cells engulf and destroy pathogenic cells or substances
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Neutrophils function
Become phagocytic upon encountering a pathogen. Can also use defensins to pierce the pathogen membrane- induce lysis
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Types of macrophages (2)
1. Free macrophage
| 2. Fixed macrophage
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Free macrophage
Capable of traveling through tissue to search for pathogens
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Fixed macrophages
Permanent location in tissue of a particular organ- wait for something to pass by them
32
When is phagocytosis initiated?
Initiated when pathogen comes in contact with the membrane of the phagocytic cell
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Phagocytosis process (5 steps)
1. Phagocyte adheres to pathogens or debris
2. Phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome
3. Lysosome fuses with the phagocytic vesicle, forming a phagolysosome
4. Lysosomal enzymes digest the particles, leaving a residual body
5. Exocytosis of the vesicle removes indigestible and residual material
34
Respiratory burst
Cells produce a large amount of harsh chemicals to destroy the more resistant form of the pathogen. Causes release of large amounts of free radicals, and produces oxidizing chemicals (hydrogen peroxide, etc.)
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Why is phagocytosis not always successful? (3)
1. Pathogens can be resistant to phagocytic lysosomes
2. Some bacteria are surrounded by a capsule
3. Pathogens can be too large for the phagocyte to ingest
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What happens if pathogens are resistant to phagocytic enzymes?
Additional enzymes must be released to create respiratory burst
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What happens if bacteria are surrounded by a capsule and phagocytosis isn't successful?
In these cases, the phagocyte is unable to "recognize" the infectious organism. The cell can use opsonins- substance that binds to pathogen surface- allows phagocytes to recognize and bind to pathogen easily. Ex- antibodies, complement
38
What happens if pathogens are too large for the phagocytic cell to digest?
Very large pathogens can’t even fit in the phagocytic cell in these cases, so phagocytes release toxic chemicals to surrounding extracellular fluid. However, neutrophils are killed off in this process. It can be necessary to sacrifice cells so the pathogen can't do a lot of damage. Macrophages are more resistant than neutrophils and can usually survive to kill more
39
Inflammation definition
Nonspecific localized response to tissue injury
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Symptoms of inflammation
Redness, heat, swelling, pain, impaired function. Impaired function stems from pain and swelling, and might not happen depending on the extent of damage. Swelling can impair movement
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Benefits of inflammation (4)
1. Prevents spread of pathogens to surrounding non damaged tissue
2. Disposes of cell debris and pathogens
3. Alerts immune system
4. Allows repair to occur
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Histamine
Inflammatory chemicals released by mast cells, basophils. Mast cells are important for generating immune responses, help speed things up. Effect- vasodilation (brings more blood to the area), increases permeability of local capillaries
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Kinins
Inflammatory chemicals derived from plasma protein kininogen. Effect- vasodilation, attracts other leukocytes, induces pain. By inducing pain, your body is telling you to stop doing what you’re doing
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Prostaglandins
Inflammatory chemicals generated by neutrophils, basophils, mast cells, etc.. Effect- vasodilation, neutrophil chemotaxis, induces pain
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Important events for inflammation (6)
1. Vasodilation
2. Increase in capillary permeability
3. Phagocytes flood area after inflammation begins
4. Neutrophils are usually the first to be mobilized and arrive to injury site
5. Monocytes take longer to be mobilized and form macrophages
6. Once pathogens are destroyed and cellular debris is cleared, healing can begin
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Purpose of vasodilation/hyperemia in inflammation
Hyperemia is an important component of inflammation. Increased blood flow brings more cells and chemicals to injury site- results in redness (same color as blood) and heat that is typical of inflammation
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Purpose of increased capillary permeability in inflammation
Squeezes out excess fluid from bloodstream, results in formation of exudate
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Exudate
Excess fluid containing clotting factors and antibodies (mark any pathogens that have already entered the body). Exudate is produced continuously but also consistently moved back into the lymphatic system to prevent extreme swelling. Formation of clot physically prevents microorganisms from entering and blood from leaving. Exudate in tissue space carried away by lymph vessels to the nodes. Exudate causes swelling and pain associated with inflammation
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Neutrophils and macrophages mobilization process during inflammation (4 steps)
1. Leukocytosis
2. Margination
3. Diapedesis
4. Chemotaxis
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Leukocytosis
An increase in the number of white blood cells in the blood-leukocytosis inducing factors released by injured/damaged cells. Neutrophils released by red bone marrow to blood
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Margination
Phagocytes cling to endothelial walls of capillaries near injury site. Sets the stage for the next step
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Diapedesis definition
Inflammatory chemicals increase capillary permeability, allowing for diapedesis- cells clinging to the wall will flatten and squeeze between cells of the endothelial wall to travel to the site of injury.
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Diapedesis importance
Allows WBCs to leave bloodstream, move to injury site. If WBCs are only in the blood, pathogens can get to the blood before encountering a WBC. That is a huge risk- the pathogen might not be killed by a WBC, and would have the opportunity to circulate throughout the body.
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Chemotaxis
Inflammatory chemicals are chemotactic agents. Phagocytes and WBCs use positive chemotaxis to locate injury site
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What cells are macrophages formed from?
Monocytes differentiate to form macrophages
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Benefits of macrophages (2)
1. Macrophages can replace destroyed/worn out neutrophils to continue defense
2. Macrophages can dispose of cellular debris (pathogens, dead body cells, etc.). Clean up duty of the macrophages helps speed up repair (create new tissue, etc.)
57
Pus
Yellow substance that accumulates in the wound area. Composed of dead/dying neutrophils, dead pathogens, dead/dying tissue cells. Collagen fibers are often laid down to “wall off” pus, forming an abscess. If minor, body can take care of abscess on its own, if severe, abscess needs to be surgically drained
58
Antimicrobial proteins
Proteins that can attack microorganisms directly or interfere with their reproduction
59
Interferons
Antimicrobial proteins released by cells infected with a virus to protect surrounding non infected cells. Nonspecific- protects cells from multiple types of pathogens. Diffuse into cell- non infected cell synthesizes proteins to degrade viral RNA. Virus can no longer use cell machinery to replicate itself
60
Complement definition
Group of about 20 plasma proteins synthesized by the liver. Normally inactive in blood, must be activated. Activation causes massive release of inflammatory chemicals- “complements” innate defenses and inflammation
61
Complement functions during inflammation (2)
1. Stimulates phagocytes to clear debris/damaged and dead cells
2. Can lyse/kill several types of bacteria and other cell types
62
Fever definition
Body wide systemic response to pathogens- characteristic abnormally high body temperature. Leukocytes and macrophages release pyrogens, which reset the hypothalamus to raise body temperature. To get rid of a fever, you need to get rid of the pathogen.
63
Benefits of fever (2)
1. Fever causes spleen and liver to store more iron so bacteria can’t use it for growth and spread will slow down
2. Fever increases metabolic rate of tissue cells- can speed up repair
64
Which body temperature is abnormal?
Normal body temperature is 98.6 degrees. A low grade fever is 99-100.4 for 24+ hours. Fever of 103 degrees or higher is concerning, especially in children
65
When is taking a fever reducer necessary?
For low fevers, taking a fever reducer usually isn’t necessary. The medications drop the fever, not the infection- could mean that you stay sick for a longer period of time
66
Adaptive defenses
Defense system that is more specific than innate defenses. Benefit- more “specialized” for defense than the innate system. Drawback- slower response than innate system- cells involved here must be exposed to an antigen before they react
67
2 features of adaptive defenses
1. Humoral immunity
| 2. Cellular immunity
68
Humoral immunity
Antibodies present in body’s fluids (“humors”)- circulate freely after release, mark and temporarily inactivate target cells for destruction. Concerned with B lymphocytes
69
Cellular immunity
When lymphocytes directly defend the body- cells can either directly kill target cells or release chemicals that increase inflammatory response and active macrophages. Concerned with T lymphocytes
70
Differences of adaptive defense from innate defense (4)
1. Adaptive defense uses lymphocytes
2. Adaptive is more specific- pathogens are identified
3. Adaptive is systemic- not restricted to the site of infection, more widespread
4. Adaptive has “memory”- previously identified pathogens can be recognized, quickly destroyed before infection can occur again
71
Antigens
Any substance that can mobilize the adaptive defense system, how the immune system recognizes “self” vs “non-self”. Can be complete or incomplete
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Complete antigens
Are capable of stimulating lymphocyte proliferation (immunogenicity)- launching an immune response on its own. Can react with activated lymphocytes and antibodies. Nearly any foreign molecule can act as a complete antigen- proteins, polysaccharides, lipids, and nucleic acids. Proteins stimulate the strongest immune response- the most immunogenic
73
Incomplete antigen (Hapten)
Can only generate immune response when they are attached to a protein carrier. Ex- peptides, nucleotides, and hormones will not trigger reactions by themselves. If bound to a body protein, the immune system may recognize it as “nonself”- poison ivy, pet dander, detergents, etc.
74
What binds to antigens to distinguish self from non self?
Lymphocytes and antibodies bind to antigenic determinants when it encounters an antigen to tell whether it’s self or nonself. Determinants are usually found on the antigen surface- one antigen can have several determinants on its surface. Different antibodies can recognize different determinants
75
Self antigens (MHC proteins)
Our own cells also have a wide variety of structures on the surface. Self antigens- antigens that “belong” to your own body
76
Major histocompatibility complex (MHC) proteins
Class of glycoproteins- genes code for this class of proteins- highly unlikely that 2 individuals have the exact same “set” of genes (except for possibly identical twins). This is why people tend to react to illness differently
77
When does an MHC protein generate an immune response?
MHC protein holds an antigen. MHC protein plus self antigen= no immune response. If the protein doesn’t have a self antigen, immune response is generated against the cell
78
Why are the MHC proteins necessary for immune function?
Without these proteins, you run the risk of autoimmune disorders, responsible for T lymphocytes
79
Lymphocytes
B and T cells. All lymphocytes must mature/be educated before they can launch an immune response and be reactive
80
Maturation and action of lymphocytes (5 steps)
1. Originate from hematopoietic stem cells in red bone marrow
2. Education of cells
3. Seeding and circulation
4. Antigen exposure
5. Proliferation
81
Where do lymphocytes mature?
B cells mature in the bone marrow, T cells mature in the thymus
82
Immunocompetence
Part of cellular education. Lymphocytes must be able to recognize a single antigen to act against. Individual lymphocytes form a specific receptor that binds to a specific antigen
83
Self tolerance
Part of cellular education. Lymphocytes must be able to recognize self vs non-self. Helps prohibit autoimmune responses
84
Seeding and circulation of lymphocytes
B cells and T cells colonize secondary lymphoid organs. Lymphocytes (especially T cells) circulate through the body
85
Antigen exposure of lymphocytes
First encounter with antigen leads to clonal selection- lymphocyte development continues. There are usually millions of viral molecules during an infection- more lymphocytes with the specific receptor produced to destroy the virus
86
Proliferation of lymphocytes
Activated lymphocyte proliferates to form lymphocytes with the same receptor. Same antigen specificity, can form effector cells or memory cells
87
Effector cells
The cells that do the work in killing off the pathogen
88
Memory cells
Remember that specific antigen in case we are infected with it again
89
Antigen-presenting cells (APCs)
Cells that engulf an antigen and display some of its fragments to the lymphocytes. Alerts the lymphocytes to a pathogen in the body. Benefit- APCs make it easy for T cells (especially immature T cells) to recognize non-self antigens
90
Types of APCs (3)
1. Dendritic cells
2. Macrophages
3. B lymphocytes
91
Dendritic cells
Transport an antigen back to the lymphoid organ (lymph nodes specifically) and display it to local lymphocytes. Extremely important for antigen encounters- allows for an earlier encounter and faster response. Most likely cell to stimulate an immune response
92
Macrophages
Take in the pathogen and destroy it, then display the antigens of that pathogen, then present antigens to T cells to maintain T cell activation- immune response can continue. In contrast to dendritic cells- the immune response has already started, just keeping it going. T cells activate macrophages that transport antigens
93
B lymphocytes
Present antigens to helper T cells to be activated, helper T cells help launch immune responses
94
The process of producing plasma cells and antibodies (4 steps)
1. Primary response
2. Clonal selection
3. Clones differentiate into one of two cell types
4. Secondary response and immunological memory
95
Primary response- when are B cells activated?
B cells are activated by binding of an antigen to multiple receptors on B cell surface
96
Clonal selection
Clones all have a similar receptor to recognize the same antigen. B cells proliferate, resulting B cells have the same antigen specificity
97
Cell types clones can differentiate into (2)
1. Plasma cells
| 2. Memory B cells
98
Plasma cells
Cells that produce and secrete antibodies- B lymphocytes do not produce antibodies themselves. Antibodies bind the same type of antigen, mark it for destruction
99
Memory B cells
Remember previous antigen encounters can launch a very fast response to subsequent encounters. Memory B cells can retain the ability to produce massive numbers of plasma cells for a lifetime. If an individual is infected with a new pathogen, it’s just a primary response- no memory for that pathogen
100
Secondary response
Immune system has already been exposed to an antigen. Secondary responses are often faster, more prolonged, and more effective. Antibody concentration in secondary response is much higher than in primary response. Release is also prolonged- often by weeks or months
101
Active humoral immunity
B cells encounter antigens, produce plasma cells and antibodies to act against them. Can be naturally or artificially acquired.
102
How is active humoral immunity acquired naturally?
Bacterial or viral infection occurs in the body- illness/infection occurs. Just getting sick normally and waiting for the body to fight it off
103
How is active humoral immunity acquired artificially?
Use of vaccines. Vaccines are composed of dead antigens (or parts of them)- enough to launch an immune response, but without the actual infection. You still launch a primary immune response and produce memory B cells and effector cells. Actual infection after exposure to vaccine will recruit memory B cells- secondary immune response occurs
104
Passive humoral immunity
Antibodies are supplied to the body, rather than produced by it. B cells are not introduced to antigen- memory cells are not produced. There is no primary response. Generally short lived- protection ends when the antibody “supply” ends. Can be acquired naturally or artificially.
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How is passive humoral immunity acquired naturally?
Antibodies passed from mother to fetus/infant, occurs through placenta or through breast milk. Fetus/infant is protected from antigens that mother has already been exposed to. Protection ends when birth occurs and/or breastfeeding ends- infant’s immune system has to take over
106
How is passive humoral immunity acquired artificially?
Antibodies supplied by an “immune donor”. Protects from antigens that can kill a person before the body can produce antibodies. Ex- snakebites, rabies, tetanus
107
How does each antibody fit an antigen?
Each type of antibody has an antigen-binding site. This site fits a specific antigen determinant
108
5 classes of antibodies/immunoglobulins
IgM, IgA, IgD, IgG, IgE
109
IgM
First class of antibodies that is secreted by plasma cells during a primary response. Largest antibody in size
110
IgA
Found in body secretions (sweat, saliva, etc.). Prevents pathogens from attaching to epithelial surfaces- skin and mucous membranes
111
IgD
Functions as a B cell antigen receptor. Found on the surface of a B lymphocyte. When something binds to IgD, the B cell becomes active
112
IgG
Most abundant antibody- main antibody of primary and secondary responses. Main antibody supplied to a fetus
113
IgE
Release histamine from mast cells and basophils- mediates inflammation and allergic reaction. Important for innate responses
114
Which antibodies can B cells produce?
B lymphocytes with different antigen specificity can produce antibodies of the same class, but they have different binding specificity. B lymphocytes can produce antibodies of a different class, but they all have the same binding specificity (recognize the same antigen?)
115
4 mechanisms of antibody action
1. Neutralization
2. Agglutination
3. Precipitation
4. Complement activation
116
Neutralization
Antibody binds to antigen and blocks specific sites on virus or bacteria- virus/bacteria can no longer bind to receptors on healthy tissue cells. Neutralize the pathogen by preventing it from binding to the body cells, also makes the pathogen very visible to macrophages. Phagocytes destroy antibody-antigen complex
117
Agglutination
Antibody can have multiple antigen binding sites- can bind multiple antigens. Antigens are clumped together- easy access for phagocytes
118
Precipitation
Antibody is binding to a soluble antigen, making them insoluble. Soluble molecules are clumped together and settle out of solution- they are visible to phagocytes. Phagocytes can engulf precipitate
119
Complement activation
Multiple antibodies binding closely to same cell activates complement. Effects- antigen lysis, increases inflammatory response, and promotes phagocytosis
120
Functions of cellular immunity (2)
1. Directly attack cancerous cells, virus infected cells, “foreign” transplant cells
2. Mediate/manage immune responses- ensures that the T lymphocytes become active and their activity doesn’t fly out of control
121
How do T cells find free antigens?
T cells do not have the ability to “see” free antigens. Activation of T cell occurs via antigen presentation. Remember- cell surface proteins on which antigens are presented to T cell is the MHC- if MHC proteins of body cell display a self antigen, T cell will ignore cell. If MHC protein displays a foreign antigen (antigen-MHC complex)- immune response begins
122
Helper T cell definition
Help in generating immune response, especially with humoral immunity
123
Helper T cell functions (3)
1. Activate B cells- B cells divide more rapidly, signals production of antibody formation
2. Helper T cells stimulate production of destructive (cytotoxic/killer) T cells
3. Activation of the innate system- activate macrophages to become more voracious and release chemicals to attract more white blood cells to area- positive chemotaxis
124
Cytotoxic T cells
Directly kill cells. Highly mobile- circulate through the body consistently . Cytotoxic T cells bind their targets tightly, and once bound, cytotoxic T cells release perforin. Perforin inserts a pore in the target cell membrane, and granzyme is pumped into this pore- triggers apoptosis
125
Regulatory T cells
Dampen immune responses that have already started- prevent them from spiraling out of control. Extremely important for preventing autoimmune responses- suppresses reactive lymphocytes outside of the lymphoid organs
126
Regulatory T cells could potentially be used for (2)
1. Organ transplants to prevent rejection by the body
| 2. Autoimmune conditions to lessen severity of disease
127
Immunodeficiencies
Any condition that impairs the production or function of immune cells or molecules. One of the most dangerous issues in medicine, can be congenital (present at birth) or acquired
128
Severe combined immunodeficiency (SCID) syndrome
Caused by congenital genetic defects that result in markedly reduced lymphocyte production (meaning you don’t have much of an immune system at all). Infants with this condition have virtually no protection- minor infections are often life threatening or fatal. Hematopoietic stem cells from a donor can be used to improve survival rates
129
Acquired immune deficiency syndrome (AIDS)
A disease that interferes with helper T cell activity- if you kill off helper T cells, your immune system is destroyed. Caused by HIV.
130
Human immunodeficiency virus (HIV)
Retrovirus passed from person to person through exchange of bodily fluids. Ex- contaminated needles, sexual intercourse, mother to infant during birth. A drug cocktail (several different medications) of antivirals is used to treat the different variants of the disease- no cure currently exists
131
How does HIV replicate itself?
HIV uses the enzyme reverse transcriptase to replicate itself . Virus spreads to and infects other cells- hijacks cell machinery to reproduce. Reverse transcriptase is not accurate- creates several mutations as it produces viral RNA. This changes how the virus responds to medical treatment- AIDS is characterized by relatively high level of drug resistance. This is why HIV is called a retrovirus
132
Autoimmune disorders
Any disease in which the immune system cannot recognize “self” from “non-self”. Autoimmunity is when auto-antibodies and cytotoxic T cells destroy body tissues. Auto-antibodies bind to self-antigens. The macrophages just see that an antibody is attached, so it destroys the body cell
133
Examples of autoimmune disorders (4)
1. Rheumatoid arthritis (joints)- bones will eventually fuse together as the disease progresses
2. Multiple sclerosis (CNS)- the myelin sheath is destroyed
3. Graves’ disease (thyroid)- disrupts release of hormone thyroxine and therefore metabolism
4. Type 1 diabetes (pancreas)- immune system destroys the beta cells of the pancreas, no insulin is produced to regulate blood sugar
134
Treatment for autoimmune disorders
Any drug that suppresses the entire immune system. No cure. People undergoing these treatments have less of an ability to fight off infection
135
Hypersensitivity definition
The immune system damages normal tissue cells while fighting off a perceived threat (not an actual threat). There are immediate and delayed hypersensitivities
136
Immediate hypersensitivities
Allergies- immune response begins within seconds of contact with allergen. Results in mast cells and basophils releasing very large amounts of histamine and other inflammatory chemicals- histamine is a powerful vasodilator, makes blood vessels leaky. Effect- runny nose, hives, watery eyes. People with more severe hypersensitivities can experience tongue swelling, difficulty breathing, and anaphylactic shock
137
Delayed hypersensitivity
Appears 1-3 days after exposure. Macrophages and cytotoxic T cells cause inflammation and tissue damage. An example is contact dermatitis
138
Contact dermatitis
Red, itchy rash caused by direct skin contact with a substance, or an allergic reaction to the substance. Severity depends on exposure- will go away on its own, but some drugs can be used to alleviate it. Common causes- certain plants (poison ivy and poison oak), certain metals (nickel in jewelry), cosmetic and deodorant chemicals. These substances act as haptens
