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Ch 31 immune system AP lecture

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Page 1: Ch 31 immune system AP lecture  hill.com/sites/0072507470/student_view0/ch apter22/animation__the_immune_response.h tml

Ch 31 immune system

AP lecture

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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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sss

s

ss

ss

ss

ss

ss

ss

ss

ss

s

ss

ss

s

ss

ss

ss

ss

ss

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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