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specific and non-specific immune response 

  • non specific (innate) immunity

    • barriers

    • repressive actions

    • blood clotting and wound repair

    • fevers

    • phagocytosis

  • neutrophils - lobed nucleus. Phagocytosis

  • lymphocytes - formed in the bone marrow and stored in the lymph

  • monocytes - macrophages - large kidney shaped nucleus. Phagocytosis

  • eosinophils - allergic response

  • basophils - mast cells - histamines

  • why is fever a useful adaptation:

    • cause it stops the pathogens from replicating

    • increases the body temperature

    • normal core body temperature is 37 degrees

    • this is controlled by the hypothalamus in the brain

    • during infection the large presents of white blood cells causes the hypothalamus to reset,increasing temperature

    • this is because pathogens cannot reproduce as quickly at temperature above 37 degrees,and the specific immune system can work faster

  • inflammatory response:

    • inflammation is swelling of skin immediately around the rupture

    • this is characterised by pain,heat and redness

    • mast cells are activated when skin is ruptured they release histamine and cytokines

    • histamine these make blood vessels dilate,causing localised heat and redness.high temperature prevent pathogen reproduction

    • histamines also increase the permeability of the cell wall,causing more tissue fluid to escape causing swelling and the pain

    • cytokines attract WBC to deal with any pathogens

specific immune response

  • phagocytes and lysosomes are involved in destroying macrophages

    • phagocytes engulf pathogens/macrophages

    • enclosed in a vacuole

    • lysosomes have enzymes that digests molecules

  • antibody actions

    • opsonisation

    • disable pathogen (antibody-antigen complex)

    • agglutination

    • deactivate antitoxins

  • how antibodies work

    • antibody - antigen complex acts similar to the opsonin chemical,by stimulating the digested by phagocytosis

    • most pathogens cannot affect the bodies cells once they formed an antibody-antigen complex

    • agglutination - one antibody binds to two pathogens,causing them to clump together

    • this makes pathogens more easily engulfed by phagocytosis

    • neutralisation - antibodies can act as antitoxins binding with toxins produced by pathogens

    • this makes them harmless

  • what are lymphocytes

    • lymphocytes are a type of WBC found in the blood and lymph nodes and a transition microscope should be used to see them

    • lymphocytes recognise antigen molecules on the surface of pathogens,and co-ordinate the immune response against that pathogen

    • collectively, lymphocytes can recognise millions

    • two main types of lymphocytes are B and T

    • b-lymphocytes mature in the bone marrow

    • t-lymphocytes mature in the thymus

    • t-helper cells - these cells produce interleukins, a type of cytokine.this stimulate B cell and antibody production,and attracts other t-cells and antibodies.

    • t-killer cells - these cells kill pathogens by producing a chemical called perforin, which makes holes in pathogens cell plasma membranes

    • t-memory cells - these act as the immunological memory,as they remain in the blood for long periods of time.when a second infection occurs,they divide rapidly to form many killer T cells.

    • t-regulator cells - these prevent an autoimmune response by repressing the immune system after the pathogens have been destroyed.

  • b-lymphocytes

    • plasma cells - these produce specific antibodies to an invading antigen.these only live for a few days but produce up to 2000 antibodies per second when active

    • b-effector cells - these divide to form plasma cell clones

    • b-memory cells - these remain in the blood for long periods of time,providing immunological memory.if infection occurs these reproduce rapidly and produce the same specific antigen.

humoral immunity

cell mediated response

main cells involved

B-cells

t-cells

where do cells develop?

they mature in the bone marrow and gain b-cell receptors which are displayed in the cell surface

they are produced in the thymus

antibodies

yes

no

how are pathogens identified

it fights the pathogens that are free in body fluids,or humours, it relies on antigens to identify the pathogens

t-cells rely on antigen-presenting cells that contain membrane bound MHC class I proteins I proteins to recognise antigens

how are pathogens dealt with

antibodies produced by the b-cells will bind to antigens, neutralising them,or causing lysis (destruction of cells by a lysin) or phagocytosis

they recognise infected cells and destroy them before the pathogens inside can replicated and spread to infect other cells

how do cells divide once they are stimulated

b-cells divide to produce plasma cells which rapidly secrete antibodies

MT

specific and non-specific immune response 

  • non specific (innate) immunity

    • barriers

    • repressive actions

    • blood clotting and wound repair

    • fevers

    • phagocytosis

  • neutrophils - lobed nucleus. Phagocytosis

  • lymphocytes - formed in the bone marrow and stored in the lymph

  • monocytes - macrophages - large kidney shaped nucleus. Phagocytosis

  • eosinophils - allergic response

  • basophils - mast cells - histamines

  • why is fever a useful adaptation:

    • cause it stops the pathogens from replicating

    • increases the body temperature

    • normal core body temperature is 37 degrees

    • this is controlled by the hypothalamus in the brain

    • during infection the large presents of white blood cells causes the hypothalamus to reset,increasing temperature

    • this is because pathogens cannot reproduce as quickly at temperature above 37 degrees,and the specific immune system can work faster

  • inflammatory response:

    • inflammation is swelling of skin immediately around the rupture

    • this is characterised by pain,heat and redness

    • mast cells are activated when skin is ruptured they release histamine and cytokines

    • histamine these make blood vessels dilate,causing localised heat and redness.high temperature prevent pathogen reproduction

    • histamines also increase the permeability of the cell wall,causing more tissue fluid to escape causing swelling and the pain

    • cytokines attract WBC to deal with any pathogens

specific immune response

  • phagocytes and lysosomes are involved in destroying macrophages

    • phagocytes engulf pathogens/macrophages

    • enclosed in a vacuole

    • lysosomes have enzymes that digests molecules

  • antibody actions

    • opsonisation

    • disable pathogen (antibody-antigen complex)

    • agglutination

    • deactivate antitoxins

  • how antibodies work

    • antibody - antigen complex acts similar to the opsonin chemical,by stimulating the digested by phagocytosis

    • most pathogens cannot affect the bodies cells once they formed an antibody-antigen complex

    • agglutination - one antibody binds to two pathogens,causing them to clump together

    • this makes pathogens more easily engulfed by phagocytosis

    • neutralisation - antibodies can act as antitoxins binding with toxins produced by pathogens

    • this makes them harmless

  • what are lymphocytes

    • lymphocytes are a type of WBC found in the blood and lymph nodes and a transition microscope should be used to see them

    • lymphocytes recognise antigen molecules on the surface of pathogens,and co-ordinate the immune response against that pathogen

    • collectively, lymphocytes can recognise millions

    • two main types of lymphocytes are B and T

    • b-lymphocytes mature in the bone marrow

    • t-lymphocytes mature in the thymus

    • t-helper cells - these cells produce interleukins, a type of cytokine.this stimulate B cell and antibody production,and attracts other t-cells and antibodies.

    • t-killer cells - these cells kill pathogens by producing a chemical called perforin, which makes holes in pathogens cell plasma membranes

    • t-memory cells - these act as the immunological memory,as they remain in the blood for long periods of time.when a second infection occurs,they divide rapidly to form many killer T cells.

    • t-regulator cells - these prevent an autoimmune response by repressing the immune system after the pathogens have been destroyed.

  • b-lymphocytes

    • plasma cells - these produce specific antibodies to an invading antigen.these only live for a few days but produce up to 2000 antibodies per second when active

    • b-effector cells - these divide to form plasma cell clones

    • b-memory cells - these remain in the blood for long periods of time,providing immunological memory.if infection occurs these reproduce rapidly and produce the same specific antigen.

humoral immunity

cell mediated response

main cells involved

B-cells

t-cells

where do cells develop?

they mature in the bone marrow and gain b-cell receptors which are displayed in the cell surface

they are produced in the thymus

antibodies

yes

no

how are pathogens identified

it fights the pathogens that are free in body fluids,or humours, it relies on antigens to identify the pathogens

t-cells rely on antigen-presenting cells that contain membrane bound MHC class I proteins I proteins to recognise antigens

how are pathogens dealt with

antibodies produced by the b-cells will bind to antigens, neutralising them,or causing lysis (destruction of cells by a lysin) or phagocytosis

they recognise infected cells and destroy them before the pathogens inside can replicated and spread to infect other cells

how do cells divide once they are stimulated

b-cells divide to produce plasma cells which rapidly secrete antibodies

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