ch 31 immune system ap lecture hill.com/sites/0072507470/student_view0/ch...
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Ch 31 immune system
AP lecture
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• http://highered.mcgraw-hill.com/sites/0072507470/student_view0/chapter22/animation__the_immune_response.html
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Immunity
• The ability to avoid disease when invaded by a pathogen
• Animals have two ways – Innate immunity – nonspecific • First line of defense • Second line of defense
– Adaptive immunity – specific • Involves antibody proteins • Only vertebrates
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White blood cells
• Phagocytes- engulf pathogens – Innate and adaptive
• Lymphocytes– Adaptive
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Innate, nonspecific defense
• 1st line: – Skin – Salt concentration on skin – Normal flora –Musuc – Lysozyme– Defensins– Internal condition
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• 2nd line of defense – Phagocyte activation – Natural killer cells – Complement proteins • One protein binds to invading cell and helps
phagocyte recognize and destroy cell • Other protein activates the inflammation
response and attract phagocytes to site • Other proteins lyse the invading cell
– interferons
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Inflammation
• Bodies response to damaged tissue, causes redness, swelling and heat near the damaged tissue – Isolates damage, stops the spread– Promotes other cells to help with healing – First response mast cells • Adhere to skin and lining of organ and
release chemicals
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–Tumor necrosis factor- cytokine that kills target cells and activated immune system –Prostaglandins- initiate inflammation in nearby tissue –Histamine- increase permeability of blood vessels to white blood cells so they can act in nearby tissue
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Redness and heat caused by dilation. Phagocytes and neutrophils responsible for healing associated with inflammation. Also produce cytokines that signal the brain to produce fever. Rise in body temp causes increased production of phagocytes and lymphocytes – speeding up the immune system.
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• Medical problems- sometimes too strong– Allergic reaction – Autoimmune disease – no recognition
between self and non self cells – Sepsis – inflammation do to bacterial
infection that does not stay local.
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Adaptive players
1. Antibodies – proteins that bind to substances identified as nonself - Inactive or destroy pathogen - Tag for immune system to attack - Produced by B cells
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• 2. major histocompatibility complex–MHC I- found on the surface of most
cells • Present antigen to TC cells
–MHC II- found on most immune cells • Present antigen to TH cells
– Coordinate interactions between lymphocytes and macrophages
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• 3. T cell receptors – integral proteins – Expressed on T cells – Recognize and bind to nonself cells
presented by MHC proteins
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• 4. Cytokines- soluble signaling proteins – Bind and later behavior of the target cell – Activate or inactive B cells,
macrophages and T cells
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Adaptive immune response
• key features – Specific – pathogen present – Diverse- respond to several pathogens – Identifies self from non self – Immunological memory – more efficient
when pathogen present again
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• Specificity – B and T lymphocytes– B cells make proteins and T cells that
bind to antigens (non self substances) – Initiates immune response – Antibodies react with antigenic
determinates (sites on antigen)
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• Diversity – Need for a wide range of lymphocytes
for all the pathogens that can be encountered
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• Self from non self – Should recognize self – Failure leads to autoimmune disorders
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• Immunological memory– Immune system can remember
pathogens and respond more rapidly – primary response take several days to
produce antibodies and T cells –Memory happens because lymphocytes
divide and differentiate into • Effector cells • Memory cells
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• Effector cells – Only live a few days – Carry out attack on the antigen – Effector B cells and plasma cells secrete
antibodies – Effector T cells release cytokines to
destroy non self
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• Memory cells – Have ability to start dividing on short
notice– Produce effector and more memory cells –Memory B and T cells can survive
decades in the body
Principle behind vaccinations
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• Three phases of adaptive immune response – Recognition- self or non self– Activation- fight the invaders– Effector- destroy the invaders
• Two types of adaptive immune response– Humoral immune response – B cells – Cellular immune response – Tc cells and
cytotoxic T cells
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Humoral Immune response
• Recognition is when an antigen binds to a B cell holding the antibody specific to that antigen
• Antibodies
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Antibodies
• Two regions – Constant region • General structure and function • When acting as a B cell receptor, this part
inserts into the membrane
– Variable region • Different for each specific antibody • Antigen binding site Bivalent: two antigen binding sites; forms
clusters and makes for easier ingestion by phagocyte.
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Structure of antibodies
light chains
antigen-bindingsite
heavy chains
antigen-bindingsite
lightchain
B cellmembrane
heavychains
lightchain
variable region
antigen-binding siteY
Y
YY Y
Y
Y
YY
Y Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
YY
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macrophage
plasma cellsrelease antibodies
Y
Y
Y
YY
Y
Y
YY
YY
Y
Y
B cell immune responsetested by B cells(in blood & lymph)
10 to 17 days for full response
invader(foreign antigen) B cells + antibodies
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
recognition
Y
Y
YY Y
Y
Y
Y
clones1000s of clone cellsY
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Ymemory cells“reserves”
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
YY
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
YY
Y
Y
YY Y
YY
Y
Y
Y
Y
YYY
Y
Ycapturedinvaders
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Cellular immune system
• Recognition when an antigen is inserted in the plasma membrane of an antigen presenting cell.
• Antigen is then recognized because it matches the T cell receptor on a T helper (TH) cell
• B cells binds to antigenic fragment that has been ingested, so TH cell binds to B cell
• TH cell stimulates B cell to divide and make clones and activates the adaptive immune response
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• TH cell binding to antigen presenting cells also releases cytokines that stimulate the cytotoxic T cell (TC) with the same T cell receptor to divide
So we have Clone of B cells with specific antibody against antigen clone of TC cells that can bind to the antigen
Trying to eliminate the antigen presenting cell (target cell)
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T cell response
stimulateB cells &antibodies
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
Y
Y
YY Y
Y
Y
Y
YYY
YY
Y
Y
Y
killerT cell
activatekiller T cells
or
interleukin 1
interleukin 2
interleukin 2
helperT cell
helperT cell
helperT cell
helperT cell
helperT cell
recognition
clones
recognition
APC:activatedmacrophage
APC:infected cell
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• Tregs- regulatory T cells –Make sure immune response does not
get out of control –Made in thymus – Express T cell receptors – Activate when bound to antigen MHC
complex– BUT the antigens they recognize are self
antigens– Release cytokine interleukin 10 which
blocks T cell activation and leads to apoptosis of TC and TH cells
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Immune response
free antigens in blood antigens on infected cells
humoral response cellular response
B cells T cells
macrophages(APC)
helperT cells
plasmaB cells
memoryB cells
memoryT cells
cytotoxicT cells
YYY
Y
YY
Y
YantibodiesY
Y Y
skinskin pathogen invasionantigen exposure
YY
Y
Y
YY
Y
YantibodiesY
Y Y
alert alert
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AIDS
• Inherited or acquired immune deficiency disorder
• T and B cells, so also plasma cells, never form
• HIV infects macrophages, TH cells and antigen presenting cells
• Immune response starts but then fails
• HIV may decrease but then the immune system fails
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• http://bcs.whfreeman.com/thelifewire/content/chp18/1802004.html
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