Chapter 21: The Immune System Flashcards

1
Q

The 3 Lines of Defense Against Pathogens:

A
o	External Barriers (innate)
o	a)  skin
o	b)  mucous membranes
o	Non-specific (innate) Internal Body Defenses
o	a)  antimicrobial proteins
o	b)  antimicrobial CELLS
o	c)  fever
o	d)  inflammatory process
o	Specific Immune System = “immunity”
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2
Q

Characteristics of Innate Defenses:

A

o Present at birth.
o Act instantly or very quickly.
o No prior exposure necessary.
o Response is the same EACH TIME the body is exposed to any foreign thing.
o Responses are effective against a wide range of pathogens, even pathogens our body has never seen before!
o Reduces the workload for our SPECIFIC defense mechanisms.

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3
Q

First Line of Defense:

External Barriers

A

o Skin:
o Hostile surface (dry, low pH, keratin).
o Closely packed cells; shed periodically.
o Coated with antimicrobial chemicals.
• Defensins (peptide that pokes holes).
• Lactic acid & dermcidin (from sweat).
• Lysozyme (from sweat, tears, mucus, saliva).
o Mucous Membranes:
o Mucus (sticky trap).
o Lysozyme (enzyme that is disruptive to pathogen cell walls).
o Cilia in respiratory tract.
o Coughing and sneezing.
o Tears.
o Cerumen.
o Low pH of gastric juice.
o Emesis.
o Diarrhea.
o Acid secretions of vagina.
o Acid pH of urine + periodic flow of urine.

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4
Q

Second Line of Defense:

Non-Specific Internal Body Defenses (4 Categories)

A

o 1. Antimicrobial Proteins.
o 2. Antimicrobial cells.
o 3. Pyrexia (fever).
o 4. Inflammatory process.

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5
Q

Second Line of Defense:

Antimicrobial Proteins

A
o	Interferons.
o	Complement proteins.
o	Epithelial cell-derived chemicals.
o	Bacterial-derived chemicals (normal flora).
o	Proteins secreted by epithelial cells:
o	Cathelicidins.
o	Defensins.
o	Collectins.
o	Proteins secreted by bacteria that normally populate our mucous membranes.
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6
Q

Antimicrobial Proteins:

Interferons

A

o Small proteins that provide protection against viruses.
o Secreted by your own body cells that have become infected by a virus.
o These infected body cells (especially lymphocytes) secrete interferons into the IF (interstitial fluid), they bind to surface receptors on neighboring cells.
o Neighboring cells receive the signal and make anti-viral substances.
o Interferons also activate macrophages and NK cells.
o Alpha-Interferons: Produced by cells infected with viruses. Attract and stimulate NK cells and enhance resistance to viral infection.
o Beta-Interferons: Secreted by fibroblasts, slow inflammation in a damaged area.
o Gamma-Interferons: Secreted by T cells and NK cells, stimulate macrophate activity.

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7
Q

Antimicrobial Proteins:

Complement Proteins

A

o The complement system = 30 or more antimicrobial proteins that circulate in the blood in an inactive state.
o Many ways to activate the complement system!!!!
o When activated, 3 important effects:
o Inflammation.
o Enhanced Phagocytosis via opsonization.
o Cytolysis via membrane attack complexes (MACs).

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8
Q

Second Line of Defense:

Antimicrobial Cells

A
o	Natural Killer Cells (NK Cells):
o	Immune surveillance.
o	Secrete perforins and granzymes.
o	Phagocytes:
o	Microphages:
•	Neutrophils.
•	Eosinophils.
•	Basophils.
o	Macrophages, from monocytes.
o	(Most lymphocytes are involved in specific defense mechanisms).
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9
Q

Antimicrobial Cells:

Natural Killer Cells

A

o Destroy bacteria, viruses, cancer cells, and cells of transplanted organs and tissues.
o The cells within a primary tumor may grow rapidly, and if the tumor has a surrounding capsule, the cells within may not provoke a massive response by NK cells.
o As a malignant tumor cells begin migrating into surrounding tissues, they can be detected and destroyed by NK cells.
o Sometimes a daughter cell will be produced that either doesn’t display tumor-specific antigens, or that secretes chemicals that destroy NK cells. Such as a cell will survive and be free to grow and divide.
o Once immunological escape has occurred, cancer cells can multiply and spread without interference by NK cells. They can even move throughout the body, establishing potentially lethal secondary tumors.

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10
Q

Antimicrobial Cells:

Phagocytes

A

o Neutrophils: Abundant, mobile, and quick to phagocytize cellular debris or invading bacteria. They circulate in the bloodstream and roam through peripheral tissues, especially at sites of injury or infection.
o Eosinophils: Less abundant than neutrophils. Phagocytize foreign compounds or pathogens that have been coated with antibodies.
o The two major classes of macrophages derived from the monocytes of the circulating blood.
o Fixed macrophages: Permanent residents of specific tissues and organs and are scattered among connective tissues. Normally don’t move within these tissues.
o Free macrophages: Travel throughout the body, arriving at the site of an injury by migrating through adjacent tissues or by recruitment from the circulating blood.

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11
Q

Neutrophils:

A
o	Most abundant of the microphages.
o	First to arrive; usually first to die.
o	Really good at killing bacteria.
o	Phagocytosis (eating one/few at a time).
o	Respiratory burst (via degranulation).
•	Superoxide anions.
•	Hydrogen peroxide.
•	Hypochlorite ion.
o	Unfortunately, they kill just about everything in the vicinity (including themselves, and our body cells).
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12
Q

Eosinophils:

A

o Weak but useful phagocytes (antigen- antibody complexes).
o Surround much bigger parasites.
o Round worms, tapeworms, etc.
o Produce superoxide, hydrogen peroxide, and even a neurotoxin.
o Do induce inflammation, but then seem to modulate the inflammatory response by secreting the enzyme histaminase to limit allergic and inflammatory responses.

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13
Q

Basophils:

A

o Help out other WBCs.
o Release histamine (vasodilator).
o Release heparin (inhibits formation of clots, making it easier for WBCs to move around the infection site).
o Involved in hypersensitivity reactions, such as anaphylactic shock.

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14
Q

Monocytes:

A

o Monocytes emigrate from the blood in the tissue spaces to become MACROPHAGES (5X normal size).
o Fixed macrophages:
o Kupffer cells of liver.
o Alveolar dust cells of lung alveoli.
o Many fixed in spleen, lymph nodes and red bone marrow.
o Wandering macrophages (lookin’ for trouble).
o Not the first to arrive (8-12 hr), but they are deadly to pathogens and also “clean up”.

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15
Q

Macrophages are APCs (tattle-tales):

A
o	Macrophages:
o	1. Eat the pathogen.
o	2. Digest the pathogen.
o	3. Recycle/spit out parts of pathogen.
o	4. Insert fragments of the pathogen into their own membrane.
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16
Q

Second Line of Defense:

Pyrexia

A

o Fever = abnormal elevation of body temp from many different causes.
o Exogenous pyrogens (e.g., endotoxins).
o Endogenous pyrogens (e.g., our own neutrophils and macrophages secrete “pyrogens” when they eat bacteria).
o IL-1 and IL-6 (interleukins).
o TNF-alpha (tumor necrosis factor).
o Pyrogens stimulate the hypothalamus (via release of prostaglandins) to raise the set point for body temp.
o 1. Pyrogens stimulate the hypothalamus to release PGE (prostaglandin E).
o 2. PGE increases the Hypothalamic set point.

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17
Q

Benefits of Moderate Fever:

A

o Intensifies effects of interferons.
o Enhances phagocytosis.
o Increases lymphocytic activity.
o Elevates metabolic rate, which accelerates tissue repair.
o Causes liver and spleen to sequester iron, zinc & copper (needed for bacterial replication).
o Kills and/or inhibits the growth of some microbes (but many like heat).

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18
Q

Dangers of High Fever:

A

o Proteins denature at high temps, including ENZYMES.
o Proteins in cell membranes can coagulate.
o Nerve damage begins at 41Degrees C (105.8 degrees F).
o Greater than 103 Degrees F: danger of heat stroke.
o Greater than 105 Degrees F: delirious/convulsions/coma.
o Greater than 110 Degrees F: irreversible brain damage or death.

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19
Q

Second Line of Defense:

Inflammation

A

o Inflammation is a non-specific LOCAL defensive response to tissue damage.
o Common response to most dz states!!!
o Purpose of inflammation:
o Dispose of pathogens and dead cells/debris.
o Prevent spread of infection.
o Prepare the site for tissue repair.
o Inflammation is regulated by cytokines.
o Inflammatory Chemicals: Histamine, Kinins, Prostaglandins, Complement proteins, cytokines (Interferons, Interleukins).

20
Q

Inflammatory Process:

A
o	Mast cells, basophils and damaged cells secrete or activate vasoactive chemicals.
o	Histamine.
o	Kinins and prostaglandins.
o	Interleukins.
o	Local vasodilation of blood vessels.
o	Heat.
o	Erythema (redness).
o	Local increased capillary permeability.
o	Edema.
o	Pain.
21
Q

Benefits of Inflammation:

A

o Heat:
o Increased metabolic rate leads to increased mitosis and tissue repair.
o Increased capillary permeability:
o Easier for WBCs, fluid and plasma proteins (complement, antibodies, clotting proteins) to get into injured area.
o Edema:
o Compresses local veins and sends more interstitial fluid into lymphatic vessels.
o Attracts WBCs into the area.

22
Q

Specific (Adaptive/Acquired) Immunity:

A

o Different from innate (non-specific) immunity because it is:
o 1. Systemic —not restricted to the initial site of infection.
o 2. Specific —fights a very specific pathogen or part of a pathogen.
o 3. Has memory —when the body is exposed a second time to the same pathogen, the specific immune system responds more quickly and more forcefully.
o 4. Depends heavily on lymphocytes.

23
Q

The 2 Main Forms of Specific Immunity:

A

o CELLULAR IMMUNITY = Cell-mediated immunity
o T-lymphocytes (T-cells) directly attack foreign cells or diseased host cells.
o Many different types of T-cells!
o HUMORAL IMMUNITY
o Antibody-mediated immunity.
o B-lymphocytes (B-cells) differentiate into Plasma cells then secrete antibodies (good at targeting pathogens in ECF).

24
Q

Antigens:

A

o Specific immunity requires recognition of a foreign antigen.
o Antigen (Ag) is any molecule that can trigger an immune response.
o Foreign proteins and glycoproteins.
o Foreign complex polysaccharides.
o Foreign lipids, lipoproteins, glycolipid.
o Some antigens are free molecules.
o Bacterial toxins, snake venoms, etc.
o Some antigens are components of cell membranes of pathogens.

25
Q

Epitopes:

A
o	Antigens are large, and usu. only certain PARTS of this large molecule triggers the immune response = EPITOPE = antigenic determinant.
o	Each antigen may have MANY different epitopes, let’s say that this Antigen #32 (found in a toxin) has 3 different epitopes on its surface, can specifically react with 3 different lymphocyte receptors.
o	Epitopes (antigenic determinants) can also interact with 
o	ANTIBODIES (Ab) that are specific to their specific and unique shapes, more on antibodies (Ab) later.
26
Q

Antigen Receptors:

A

o There are more than 7 billion unique individuals on our planet.
o There are at least 1 billion unique lymphocytes in our body.
o Each lymphocyte displays only one type of antigen receptor (but the lymphocyte has hundreds of receptors that are all the same).
o Each lymphocyte spends its entire life waiting to combine with a specific epitope.
o Antigen receptors are inserted in lymphocyte membranes:
o Before B-cells leave the red bone marrow.
o Before T-cells leave the thymus.
o Antigen receptors even recognize “artificial” molecules that don’t exist naturally.

27
Q

Major Histocompatibility Proteins:

A

o All human nucleated cells (i.e., except RBCs) have hundreds of MHC proteins displayed on the surface of their cell membranes
o MHCs are glycoproteins (thus, these MHC proteins would be an antigen to someone else, but because they are on our very OWN cells, we sometimes call them “self antigens.”).
o MHC proteins are unique to each person (except for identical twins), serve as “identification tags” that label every cell of your body as “SELF”
o MHC proteins are the basis of histocompatibility testing = tissue compatibility between a donor organ and the recipient.

28
Q

2 Types of MHC Proteins:

A

o MHC Type I proteins on cell membranes of all body cells except RBCs.
o MHC-I displays stuff produced/processed INSIDE our human cells:
o “This is what I MADE today”.
o MHC Type II proteins on cell membranes of Antigen Presenting Cells (APCs):
o MHC-II proteins display antigens eaten/engulfed by APCs: “This is what I ATE today”.
o This is a SIGNAL that stimulates other immune cells (e.g., T-Helper cells) to respond to the foreign Ag in ways that ENHANCE specific immunity.
o Types:
o Dendritic cells.
o Macrophages.
o B lymphocytes.

29
Q

Types of T-Cells:

A

o T-cells with CD-8 markers:
o Cytotoxic T cells.
o T-cells with CD-4 markers:
o T-Helper Cells– Critical to all types of immunity!!!!
o T-HELPER CELLS ENHANCE ALL ASPECTS OF THE IMMUNE SYSTEM!

30
Q

Process of Cytotoxic T-Cells in Cellular Immunity:

A

o 1. T cell identifies foreign antigens on MHC I proteins and binds tightly to target cell.
o 2. T cell releases perforin and granzyme molecules from its granules by exocytosis.
o 3. Perforin molecules insert into the target cell membrane, polymerize, and form transmembrane pores similar to those produced by compliment activation.
o 4. Granzymes enter the target cell via the pores. Once inside, granzymes activate enzymes that trigger apoptosis.
o 5. The T cell detaches and searches for another prey.

31
Q

Process Where Helper T Cells Help in Humoral Immunity:

A

o 1. T Helper Cell binds with the self-nonself complexes of a B cell that has encountered its antigen and is displaying it on MHC II on its surface.
o 2. T Helper Cell releases interleukins as co-stimulatory signals to complete B cell activation.

32
Q

Process Where Helper T Cells Help in Cellular Immunity:

A

o 1. T Helper Cell binds to dendritic cell.
o 2. T Helper Cell stimulates dendritic cell to express co-stimulatory molecules.
o 3. Dendritic cell can now activate CD8 cell with the help of interleukin 2 secreted by T Helper Cell.

33
Q

Antibodies:

A

o Antibodies are small PROTEINS that can help out in a lot of different ways.
o Tips of Ab have a variable region that has a very specific antigen-binding site!
o IgG, IgA, IgM, IgE, and IgD are the Classes of Antibodies.
o Gawk At Monkey Dancing Enthusiastically most to least IgG, IgA, IgM, IgD, IgE.

34
Q

Antibodies:

IgG

A

o Most abundant (80 percent of Abs in blood).
o Only antibody that crosses the placenta—passive immunity.
o Can fix complement.

35
Q

Antibodies:

IgA

A

o 10-15 percent of Abs in blood.
o Found in sweat, tears, saliva, mucus, breast milk, GI secretions.
o Prevents pathogens from adhering to mucous membranes.
o Provides passive natural immunity to newborn.

36
Q

Antibodies:

IgM

A

o 5-10 percent of Abs in blood.
o FIRST Ab to be secreted by plasma cells during primary response.
o Can fix complement.

37
Q

Antibodies:

IgE

A

o 0.1 percent of Abs in blood.
o Found mainly on surface of mast cells and basophils.
o Involved in allergies and anaphylactic shock reactions.

38
Q

Timing Affects Antibody Response:

A

o First exposure: Slow
o IgM is first antibody to be released
o Second exposure: Very rapid.
o IgG response is rapid and enormous!

39
Q

Classes of Specific Immunity:

A

o ACTIVE IMMUNITY: Your body makes its own antibodies or activates its own T-cells against the pathogen.
o Natural (natural exposure to an antigen).
o Artificial (exposure via vaccination).
o PASSIVE IMMUNITY: Your body acquires antibodies or T-cells from another person or an animal.
o Natural (fetus via placenta; newborn via breast milk).
o Artificial (injection of immune serum).

40
Q

Immune Disorders:

A
o	Hypersensitivity reactions:
o	Immune system overacts.
o	Autoimmune diseases:
o	Immune system attacks your OWN body cells for no good reason.
o	Immunodeficiency diseases:
o	SCID.
o	AIDs.
41
Q

Hypersensitivity Reactions:

A

o Type I (acute hypersensitivity):
o Includes most allergic reactions (involves IgE).
o Type II (antibody-dependent cytotoxic):
o Involves Abs bound to cell surfaces and complement rxns (e.g., blood transfusions).
o Type III (immune complex):
o Ag-Ab complex precipitates out beneath blood vessels/in tissues with intense inflammation (e.g.,Systemic Lupus Erythematosus).
o Type IV (delayed hypersensitivity):
o Cell-mediated (T-cell) mediated responses.

42
Q

Autoimmune Disorders:

A

o Your own immune system attacks your OWN body cells.
o RA.
o Myasthenia gravis.
o MS.
o Graves’ disease.
o Type I Diabetes mellitus.
o SLE (systemic lupus).
o 5 percent of adults have autoimmune d/o (2/3 of them are women).
o Make AUTOANTIBODIES to own tissues & cytotoxic T-cells destroy own cells.
o Etiology unknown, but some hypothesize:
o Foreign antigens resemble self-antigens.
o T-reg cells don’t inhibit cell-mediated immunity.
o New self antigens appear (from mutations).
o Treat by using meds that suppress the entire immune system (e.g., prednisone).

43
Q

Immunodeficiency Diseases:

A

o SCIDS: Severe Combined Immunodeficiency Disease.
o Bubble babies.
o Non-functioning T-cells or B-cells.
o AIDS: Acquired Immunodeficiency Syndrome.
o Caused by HIV (human immunodeficiency VIRUS = a retro virus).
o NOT an autoimmune disease, your immune system is attacking a VIRUS.

44
Q

How HIV Spreads:

A
o	Transmitted in body secretions.
o	Blood.
o	Dirty needles.
o	Hemophiliacs.
o	Tearing of mucous membranes with sexual intercourse.
o	Semen.
o	Vaginal secretions.
o	Saliva and tears—extremely rare transmission, although documented cases of oral sex transmission.
o	Breast milk from AIDS-infected mother.
45
Q

AIDS:

A

o Virus loves to get inside T-Helper cells.

o AIDS victims don’t die of AIDS…they die of opportunistic infections (Kaposi’s sarcoma, pneumocystis pneumonia, etc.).

46
Q

Invasion of HIV:

A

o Virus glycoprotein (gp120/gp4) docks on host cell membrane proteins.
o Requires a second docking receptor (CXCR4).
o Virus gains entry to cell.
o Virus uses it’s own reverse transcriptase enzyme to produce DNA that is inserted into host DNA.
o New DNA directs host cell to crank out new HIV.

47
Q

Treatment of AIDS:

A

o Meds that prevent the virus from DOCKING on your body cells.
o Fusion inhibitors (e.g. Enfuvirtide).
o Meds that prevent the virus from replicating inside your cells.
o Reverse transcriptase inhibitors (e.g. AZT and ddC).
o Protease inhibitors (e.g., Saquinavir, Ritonavir).
o Meds that block viral integrase enzyme that puts provirus into cell’s DNA (new).