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113 Cards in this Set
- Front
- Back
-We are born with it
-Nonspecific -Form the first and second line of defense |
Innate System
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Specific-Protects us against particular pathogens
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Adaptive system
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Form the third (elite) line of defense
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Adaptive System
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-May be able to destroy pathogens alone w/o help of adaptive system
-Reduces workload of adaptive system |
Innate Defenses
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Skin and mucous membrane barriers
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First Line of Defense
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The major barrier of the body
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Skin and mucous membrane barriers (First line of defense)
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The barriers of the Skin and Mucouse membrane
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-Physical barrier
-Epithelial cells produce protective chemicals |
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Acidity of the skin secretions inhibits (____).
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bacteria
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(____) secretes HCl and enzymes that kill bacteria.
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Stomach mucosa
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(____) contain lysozyme that kills bacteria.
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Saliva and lacrimal fluid
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(____) traps bacteria
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Mucus
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Structures - (____) of respiratory tract sweep mucus up to mouth away from lungs - (____) trap particles.
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cilia
nose hairs |
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Internal Defenses
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Second line of defense
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-Nonspecific cells and chemicals and responses
-Activated when specific carbohydrates on bacteria, virus, fungus are recognized. |
Internal Defenses (Second line of Defense)
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Pathogens that get thru skin barrier and into connective tissue encouter?
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phagocytes
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the chief phagocytes are?
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macrophages
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Macrophages come from?
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Monocytes (WBC's) that leave the blood and enter tissue.
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Wander from tissue to tissue
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Free macrophages
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kupffer cells in liver, microglia in brain, Langerhan cells in dermis
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fixed macrophages
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most numerous WBC-become phagocytic when encounter pathogen
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Neutrophils
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weakly phagocytic but good defense against parasitic worms
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Eosinophils
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ingest a wide range of bacteria
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Mast cells
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famous for containing histamine
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mast cells
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mechanism of phagocytosis
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1. Phagocyte recognizes CHO
2. Phagocyte adheres to pathogen 3. Phagocyte engulfs pathogen via pseudopods 4. Phagosome fuses with lysosome 5. Pathogen killed by enzymes |
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-Complex CHO that phagocyte cannot bind to
-Bacteria must be opsonized |
Pneumococcus
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coated with complement proteins and antibodies, then phagocyte can bind
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opsonized (i.e. pneumococcus)
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-resistant to lysozomal proteins
-need help of adaptive system -Neutrophils contain antibiotic like chemicals-but also kills neutrophil |
Tuberculosis Bacillus
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Prolonged Neutrophil activity=
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Cancer
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"police" blood and lymph
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Natural killer cells
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target cancer cells and virus infected cells, before adaptive system is activated
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Natural Killer Cells
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not phagocytic-release perforins-cytolytic chemicals
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Natural Killer Cells
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Release chemicals that enhance inflammatory response
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Natural killer cells
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-triggered when body tissue is injured
-prevent spread of damage -disposes debris and pathogens -allows repair |
Inflammatory response
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Signs-redness, heat, swelling, pain
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Inflammatory response
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The inflammatory response begins with a?
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chemical "alarm"
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What is the chemical "alarm" that begins the inflammatory response?
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A flood of inflammatory chemicals that are release into the extracellular fluid from:
1. Injured tissue cells 2. Phagocytes 3. Lymphocytes 4. Mast cells |
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Some of the inflammatory chemicals
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Histamines, kinins, prostaglandins, complement, cytokines
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Prostaglandins and kinins produce?
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pain part of the inflammatory response
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-All cause blood vessels to dilate
-Increase permeability-local edema-swelling -Prostaglandins and kinins-pain -Epithelial mucosa-beta defensins-have antibiotic activity |
The chemicals of the inflammatory response (histamine, kinins, prostaglandins, complement, and cytokines)
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First mast cells, neutrophils, macrophages
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Phagocyte influx
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The process of phagocyte influx
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1. Leukocytosis
2. Margination 3. Diapedisis 4. Chemotaxis |
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chemical released by injured cells promote release of neutrophils from red bone marrow during what step of phagocyte influx?
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Leukocytosis
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chemicals released by injured cells promote
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release of neutrophils from red bone marrow
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During the margination step of phagocyte influx endothelial cells sprout adhesion molecules called? Neutrophils have?
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selectins
integrins |
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During the margination step of phagocyte influx the selectins and integrins?
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bind together so neutrophils cling to capillary wall-called margination
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neutrophils squeeze out of capillary
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Diapedisis
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chemical attract neutrophils and WBC's to site of injury
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Chemotaxis
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-Enhance innate defenses
-Attacks pathaogens and prevent their proliferation |
Antimicrobial Proteins
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Virus infected cells secrete? Which?
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IFN's (Interferons)
diffuse to uninfected cells and stiumulate production of PKR production |
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(____) interferes with viral replication
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PKR
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Interferons activate (____)
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macrophages and mobilize NK cells
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(____) approved by FDA as an antiviral agent
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IFN
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-a system of 20 plasma proteins normally inactive in blood
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Complement
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Major mechanism for destroying pathogens in the body
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Complement
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complement system activated by either (1) or (2).
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1. classical pathway
2. alternative pathway |
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antibodies must bind to pathogen. The C1 binds to Ab/Ag complex - cascade of protein activation C1-C11
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Classical pathway
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triggered when 3 proteins - factors B, D, and P bind to surface of certain pathogens - activates cascade
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alternative pathway
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Process of cell lysis
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1. C3b binds to pathogen-insertion of a group of complement proteins MAC-membrane attack complex-open hole in membrane-lysis
2. C3b are proteins of opsonization-allow macrophages and neutrophils to adhere. 3. C3a stimulate mast cells and basophils to release histamine. |
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Increase cellular metabolism-speeds up repair
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Fever
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A specific defense system
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Adaptive system
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Must be "primed" by intial exposure to pathogen (antigen).
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Adaptive System
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-Antigen specific
-Is systemic (everywhere in the body) -Has memory |
Adaptive System
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The two overlapping sections of the Adaptive System
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1. Humoral immunity
2. Cell-mediated immunity |
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-Anitibody mediated immunity
-Abs circulate freely in blood and lymph (extracellular) -Bind to bacteria, toxins, virus -They do not destroy pathogens but mark them for destruction by-phagocytes and complement |
Humoral Immunity
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-Abs provide partial immunity
-Abs useless against tuberculosis bacillus infected cells -Need T cells |
Cell-mediated immunity
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Substances that evoke and immune response
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Antigens
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An antigen can be?
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Proteins, nucleic acids, lipids, pollen, bacteria, fungi, virus
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Cells of the Adaptive Immune system
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Antigen presenting cells - APC's
B lymphocytes - B cells T lymphocytes - T cells |
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Sticks part of antigen on its own surface
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Antigen Presenting Cells - APC's
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Made in red bone marrow of spongy bone
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B lymphocytes - B cells
T lymphocytes- T cells |
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If lymphocyte goes to thymus it becomes a?
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T cell
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Thymosin and thymopoietin induce?
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maturation of T cells
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T cells (____) divide
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rapidly
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(____) selection in thymic medulla - destroys T cells that bind too strongly to "self" proteins - autoimmune reactions
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Negative
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T cells interacting weakly with "self" proteins continue to develop in thymic cortex - T cells now become?
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immunocompetent
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(____) become immunocompetent in bone marrow - little is known of this process
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B cells
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When T and B cells become immunocompetent they?
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have unique receptors on their surface that recognize and bind to one specific antigen - now exported to lymph nodes, spleen, tonsils, etc.
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-These cells engulf pathogens and present fragments of these antigens on their surface.
-Now easily recognized by T cells |
Antigen Presenting Cells
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APC's include?
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Langerhan cells (in situ macrophages), (epidermis of skin) macrophages, and B cells.
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-Occurs when an immunocompetent B cell encounters an antigen
-Results in the production of abs -Primary immune response |
Humoral Immune Response
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Cells that make Abs
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Plasma Cells
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Mechanism of Humoral Response
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Ag binds to B cell receptors - Activates Ag/R complex is endocytosed stimulated B cell to divide rapidly produces a clone. Most cells of clone are plasma cells.
Plasma cells: are Ab secreting cells - secrete 2000 Abs/second for 4-5 days. Abs circulate in blood or lymph - bind to Ags and tag them for destruction by other cells. |
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In the Humoral Response the (____) acts as the key.
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Antigen
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In the Humoral Response the Rest of the Clone are (____)
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memory B cells
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The memory B cells are?
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-Primed
-If same Ag is encountered a second time immune response is much faster and Ab levels remain higher for longer - called secondary immune response. |
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-Immunoglobulins (Igs)
-Gamma globulins of blood proteins -Soluble -Secreted by activated B cells (few) or plasma cells (majority). -Each class has a different role and location in the body. |
Antibodies
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-First to be released by plasma cells
-Can fix complement -Exists as a monomer and as a pentamer (biggest Ab) |
IgM
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-Is a dimer
-The secretory Ig -Found mainly in mucus and other body secretions -help to prevent pathogens from entering body -Prevents attachment of pathogens to epithelial membranes. |
IgA
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-Always found on surface of B cells.
-Acts a B cell receptor |
IgD
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-Most abundant Ab (80%)
-Main Ab of primary and secondary response -Crosses placenta-transfers maternal immunity to baby |
IgG
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-Never found in blood
-"Trouble maker" antibodies involved in allergies -Causes cells to release histamines -Levels rise during severe allergic attacks and or chronic parasitic infections of GI tract. |
IgE
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What is the function of Abs?
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-They do not destroy antigens (pathogens).
-They can inactivate Ag's -They tag Ag's for destruction |
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Antibodies have four mechanisms. What are they?
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1. Neutralization
2. Agglutination 3. Precipitation 4. Complement Fixation |
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-Simplest mechanism
-Abs block specific sites on viruses and bacterial toxins -These cannot now bind to receptors on tissue cells and cause injury |
Neutralization
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-Clumping
-Mostly by IgM -E.g. mismatched blood transfusion |
Agglutination
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-Solube molecules (not cells) are cross linked - insoluble precipitate.
-Molecule now more easily captured and engulfed by phagocytes |
Precipitation
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Also known as opsinization gone wild
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Neutralization
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clumping of molecules
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Precipitation
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-Abs bind to cells
-Abs change shape and expose complement-binding sites - fixation - cell lysis -Amplifies inflammatory response -Promotes phagocytosis via opsonization (C3b) |
Complement fixation
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-Abs provide partial immunity
-Also need cellular immunity - mediated by T cells |
Cell-mediated immune response
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Based on the molecules displayed on the cell surface, the cell-mediated immune response can use?
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CD4 or CD8 cells
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CD4 cells replicate to make?
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T Helper Cells and Memory Cells
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CD8 cells replicate to make?
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-Suppressor T cells
-Cytotoxic T Cells -Memory Cells |
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T cells cannot recognize?
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"free" Ags
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T cells can recognize
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Ab/Ag complexes and "processed" Abs
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-Primed by APC
-Major role is to stimulate other T cells and B cells to divide |
T helper cells
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-Also called killer T cells
-Are the only T cells that attack and kill other cells -Circulate thru blood and lymph -Main targets are virus-infected cells -Also attack infected tissue cell (e.g. tuberculosis bacillus, parasites, cancer cells, and foreign cells) |
Cytotoxic T cells
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Mechanism action of T cells
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-T cell granules release perforin after T cell has bound to target cell
-T cell detaches -Target cell lysis |
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Some T cells secrete:
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-lymphotoxin-fragment DNA
-Tumor Necrosis factor-slowly kills target cells -Gamma Interferon-stimulates macrophages |
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-Secrete cytokines that suppress T and B cells - decrease and stop immune response
-Prevent excessive or uncontrolled immune system activity |
T Suppressor Cells
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Delayed hypersensitivity T cell
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TDH
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-Promote allergic reactions
-They secrete gamma interferon-stimulates macraphages |
TDH
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-Live in intestine
-Similar to NK cells |
Delta and Gamma T cells
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