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utilizes molecules & immune cells to keep body safe from invading organisms, cancer cells & transplanted tissue; not comprised of organs but is a functional system:
immune system
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non-specific defense system
innate
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specific defense system
adaptive
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non-specific - external body membranes (skin and mucosae)
first line of defense
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non-specific - antimicrobial proteins, phagocytes & other cells; inhibit spread of invaders and inflammation is most important mechanism:
2nd line of defense
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attacks particular foreign substances; takes longer to react than the innate system:
third line of defense - specific
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most abundent white blood cell; become phagocytic on encountering infectious material in tissue:
neutrophils
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mechanism of phagocytosis:
- 1. adherence of phagocyte to pathogen
- 2. engulf the particle & form a phagosome vessicle
- 3. fuse w/a lysosome & form a phagolysosome
- 4. lysosomal enzymes digest the particle
- 5. exocytosis of the vessicle removes residual material
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inflammatory response:
- 1. triggered whenever body tissues are injured or infected
- 2. prevents the spread of damagin agents
- 3. disposes of cell debris & pathogens
- 4. sets the stage for repair
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large non-specific granular lymphocytes; induce apoptosis in cancer cells & virus-infected cells; secrete potent chemicals that enhance the inflammatory response:
natural killer (nk) cells
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cardinal signs of accute inflammation:
- 1. redness
- 2. heat
- 3. swelling
- 4. pain
- 5. sometimes impairment of function
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inflammatory mediators:
- 1. histamine (from mast cells)
- 2. blood proteins
- 3. kinins, prostaglandins (PGs), leukotienes & complement
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inflammatory chemicals cause:
- 1. dilation of arterioles, resulting in hypermia (blood congestion), causes redness & heat
- 2. increased permeability of local capillaries & edema
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fluid that contains proteins, clotting factors & antibodies:
exudate
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functions of the surge of exudate:
- 1. moves foreign material into lymphatic vessels
- 2. delivers clotting proteins to form a scaffold for repair & to isolate the area
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steps for phagocyte mobilization:
- 1. leukocytosis: release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells
- 2. margination: neutrophils cling to the walls of capillaries in the inflamed area
- 3. diapedesis of neutrophils
- 4. chemotaxis: inflammatory chemotaxis promote positive chemotaxis of neutrophils
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dead or dying neutrophils, broken down tissue cells, living & dead pathogens that fill a severly infected wound:
pus
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sac of pus walled off by collagen fibers, must be drained in order for healing to occur:
abscess
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when a macrophage engulfs an organism that cannot be broken down:
infectious granuloma (a person can harbor an infection for years & if the immune system is ever compromised the infection can activate & cause disease)
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attack microorganisms directly; hinder microorganisms ability to reproduce:
interferons & complement proteins
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anti-viral, reduce inflammation, activate macrophages & mobilize Natural Killer cells:
interferons
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amplifies all aspects of the inflammatory response; kills bacteria & certian other cell types by cell lysis; enhances both nonspecific and specific defenses:
complement proteins
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systemic response to invading microorganisms; leukocytes & macrophages exposed to foreign substances secrete pyrogens (reset the body's thermostat upward):
fever
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benefits of moderate fever:
- 1. causes the liver & spleen to sequester iron & zinc (needed by microorganisms)
- 2. increases metabolic rate, which speeds up repair
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antibody-mediated immunity:
humoral
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cell-mediated immunity:
cellular
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substances that can mobilize the adaptive defenses & provoke an immune response; most are large, complex molecules not normally found in the body (nonself)
antigens
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antibody generating:
antigen
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ability to stimulate proliferation of specific lymphocytes & antibodies:
immunogenicity
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ability to react with products of activate lymphocytes & antibodies released:
reactivity
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incomplete antigens:
haptens
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small molecules; not immunogenic by themselves; are immunogenic when attached to body proteins; cause the immune system to mount a harmful attack:
haptens ex (poison ivy, animal dander, detergents & cosmetics)
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protein molecules (self antigens) on the surface of cells; antigenic to others in transfusions or grafts; are unique to an individual:
self-antigens (MHC proteins)
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able to recognize & bind to a specific antigen:
immunocompetence
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unresponsive to self antigens so that it doesn't attack it's own cells:
self-tolerance
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selects T cells capable of binding to self-MHC proteins (MHC restriction):
positive selection
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prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC; ensures self-tolerance (only 2% make it to maturity)
negative selection
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engulf antigens; present fragments of antigens to be recognized by T cells:
antigen-presenting cells (APCs)
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major types of APCs:
- 1. dendritic cells in connective tissues & epidermis
- 2. macrophages in connective tissues & lymphoid organs
- 3. B cells
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uses lymphocytes, APCs & specific molecules to identify & destroy nonself substances; depends upon the ability of its cells to recognize antigens by binding to them & communicate w/one another so that the whole system mounts a specific response:
adaptive immunity
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1st encounter between an antigen & a naive immunocompetent lymphocyte; usually occurs in spleen or lymph node; if lymphocyte is a B cell the antigen provokes a humoral (antibody) immune response & antibodies are produced:
humoral immunity response
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B cell is activated when antigens bind to its surface receptors & cross-link them; receptor-mediated endocytosis of cross-linked antigen-receptor complexes occurs; stimulated B cells grows to form a clone of identical cells bearing the same antigen-specific receptors:
clonal selection
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clone cells that don't become plasma cells become memory cells; what do they do:
- provide immunological memory
- mount an immediate response to future exposures of the same antigen
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occurs on the 1st exposure to a specific antigen; lag period is 3-6 days; peak levels of plasma antibody are reached in 10 days; antibody levels then decline:
primary immune response
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occurs on re-exposure to same antigen; sensitized memory cells respond w/i hours; antibody levels peak in 2-3 days at much higher levels; antibodies bind w/greater affinity; antibody level can remain high for weeks to months:
secondary immune response
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occurs when B cells encounter antigens & produce specific antibodies against them:
active humoral immunity
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response to a bacterial or viral infection:
naturally acquired active humoral immunity
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response to a vaccine of dead or attenuated pathogens:
artificially acquired active humoral immunity
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spare us the symptoms of the primary response; provide antigenic determinants that are immunogenic & reactive; target only 2 type of helper T cell, so fail to fully establish cellular immunological memory:
- vaccines
- ;
- B cells aren't challenged by antigens; immunological memory doesn't occur:
- passive humoral immunity
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antibodies delivered to a fetus via the placenta or to infant though milk:
naturally acquired passive humoral immunity
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injection of serum, such as gamma globulin (protection is immediate but ends when antibodies naturally degrade in the body:
artificially acquired passive humoral immunity
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first antibody released; potent agglutinating agent; readily fixes & activates complement
IgM
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monomer or dimer; in mucus and other secretions; helps prevent entry of pathogens:
IgA
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monomer attached to the surface of B cells; functions as a B cell receptor:
IgD
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monomer; 75-85% of antibodies in plasma; from secondary to late primary respones; crosses the placental barrier:
IgG
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monomer active in some allergies & parasitic infections; causes mast cells & basophils to release histamine:
IgE
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defensive mechanisms used by antibodies:
- 1. neutralization & agglutination (2 most important)
- 2. precipitation & complement fixation
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"plan" of antibody function:
- Precipitation
- Lysis (by complement)
- Agglutination
- Neutralization
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used in pregnancy, STD and rabies test, research and cancer treatment:
monoclonal antibodies ( commercially prepared pure antibody); produced indefinitely & have the ability to produce a single type of antibody
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becomes helper T cells when activated (call for help/helper cells):
CD4
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become cytotoxic T cells that destroy cells harboring foreign antigens (destroyer cells):
CD8
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two types of MHC proteins are important to T cell activation:
- Class I MHC
- Class II MHC (both are synthesized at the ER and bind to peptide fragments)
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displayed by all cells except RBCs; interact w/CD8 cells:
Class I MHC proteins
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displayed by antigen presenting cells (APC), dendritic cells, macrophages and B cells; interact w/CD4 cells:
Class II MHC proteins
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endogenous (from within) antigen is a self-antigen in a normal cell; a nonself antigen in an infected or abnormal cell; informs cytotoxic T cells of the presence of microorganisms hiding in cells:
Class I MHC proteins
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bind with fragments of exogenous antigens that have been engulfed & broken down in a phagolysosome; recognized by helper T cells:
Class II MHC proteins
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directly attack & kill other cells; activated T cells circulate in blood & lymph & lymphoid organs in search of body cells displaying antigen they recognize:
roles of cytotoxic cells
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targets of cytotoxic cells:
- 1. virus - infected cells
- 2. cells w/intracellular bacteria or parasites
- 3. cancer cells
- 4. foreign cells (transfusions or transplants)
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from one body site to another in the same person:
autograft
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between identical twins:
isografts
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between individuals who aren't identical twins:
Allografts
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from another animal species:
Xenografts
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removing the patients bone marrow & transplanting the donors red marrow into the patient; allows the organ to be treated as self instead of foreign; similiar method has been shown to cure HIV infection in 1 case in Europe:
Chimeric Immune System
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congential & acquired condition that cause immune cells, phagocytes or complement to behave abnormally:
immunodeficiencies
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genetic defect; marked deficit in B & T cells; abnormalities in interleukin receptors; defective adenosine deaminase enzyme (ADA); is fatal if untreated:
SCID (severe combined immunodeficiency syndrome
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an acquired immunodeficiency; cancer of the B cells; leads to immunodeficiency by depressing lymph node cells:
Hodgkins Disease
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cripples the immune system by interfering w/ the activity of helper T cells; characterized by severe weight loss, night sweats & swollen lymph nodes; opportunistic infections occur, including pneumocystis pneumonia & Kaposi's sacroma:
AIDS (acquired immune deficiency syndrome)
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immune system loses the ability to distinguish self from foreign; production of autoantibodies & sensitized TC cells that destroy body tissues:
Autoimmune diseases ex(mulitple sclerosis, graves disease, type I diabetes)
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destroys myelin sheath on neural tissue:
multiple sclerosis
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impaired communication between nerves & skeletal muscle:
myasthenia gravis
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prompts excessive thryoxine produced by thyroid:
graves disease
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destroys beta cells of the pancreas that produce insulin:
type I diabetes
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systemic disease that destroys the kidney, heart, lungs and skin:
lupus
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severe impairment of renal function:
glomerulonephritis
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destroys joints of the body:
rheumatoid arthritis
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mechanisms of autoimmune diseases:
- 1. foreign antigens may resemble self-antigens
- 2. new self-antigens may appear
- 3. release of novel self-antigens by trauma of a barrier
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immune responses to a perceived threat; causes tissue damage; antibodies cause immediate & subcute hypersensitivites; T cells cause delayed hypersensitivity:
hypersensitivites
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