t/b cells

where are t cells made + where do they mature?

bone marrow and thymus

T cell mediated response?

• T_H cell receptors attach to APC antigens

• attachment activates T_H cells to divide by mitosis + make clones

• clones stay the same or differentiate into B cells, cytotoxic T cells or phagocytes

how do cytotoxic T cells destroy abnormal/infected cells?

• release perforin that embeds in cell membrane + makes pore so substance can exit/enter

• causing cell death

why do we get sore throat from viruses?

infected cells in throat have to be destroyed by cytotoxic T cells to prevent viral replication

where are B cells made + where do they mature?

bone marrow

how are B cells activated?

• antigens collide w/ complimentary antibody on B cell

• B cell takes it in by endocytosis + presents it on cell surface

• T_H receptor collides w/ antigen, activating the B cell to release cytokines and divide by mitosis

• clones differentiate into plasma cells that make antibodies or memory B cells

role of memory B cells?

divide into plasma cells when reinfected w/ same pathogen for rapid antibody production, before symptoms are present

allows for active immunity and acts a secondary response

antigen?

molecule/protein that is recognised as foreign by immune system and stimulates an immune response

how do lymphocytes identify non-cell selfs?

• made as a foetus, only exposed to self-cells

• lymphocytes complimentary to antigens on self-cells killed

• prevents attack of own cells

• remaining are complimentary to pathogens/non-self cells

• same process occurs after birth in bone marrow

antigen variability?

• pathogen DNA mutates often, may take place in gene coding for antigen, changing its shape

• previous immunity no longer effective as memory cells only remember previous shape

• antibodies no longer complimentary changed antigen

why does influenza virus require a new vaccine every year?

it is constantly mutating

antibody structure?

quaternary protein

antigen binding sites at top, tip is the variable region, remaining is constant region

outer, shorter section is lighter chain

inner, longer section is heavy chain

joined via disulphide bridge

agglutination?

antibodies bind to multiple antigens (pathogens) as they have 2 binding sites, causing pathogens to clump together, making them easier to locate + engulf

phagocytosis?

• phagocyte recognises pathogen’s foreign antigens

• surrounds pathogen with cell membrane + engulfs

• pathogen contained in vesicle/phagosome

• lysosome fuses with phagosome

• lysozymes hydrolyse pathogen

• leads to APC production, stimulating immune response

how do antibodies lead to the destruction of pathogens?

• antibodies bind to pathogen antigens → antigen - antibody complex → antibody specific tertiary structure allows for specific active site shape complimentary to antigens

• each antibody binds to 2 pathogens at a time → agglutination

• antibodies attract phagocytes

• that bind to antibodies + engulf the pathogens

primary response/1st exposure?

• antibodies produced slower + at lower conc.

• takes time for B plasma cells to be stimulated

• memory cells produced

secondary response/2nd exposure?

• antibodies produced faster + at higher conc.

• B memory cells rapidly undergo mitosis + produce plasma cells to produce antibodies

vaccine?

dead/weakened pathogen resulting in formation of memory cells

vaccine process?

• specific B cells w/ complimentary receptor binds to antigen

• specific T helper cells bind to APC + stimulates B cells

• B cells divide by mitosis

• clones differentiate into plasma + memory cells

• on secondary exposure, memory cells differentiate into plasma cells that produce high conc. of antibodies quickly

how do vaccines. protect the population?

herd immunity → large proportion vaccinated, reducing spread of pathogen

• large proportion immune so dont become ill

• fewer infected people to spread pathogen

• less likely for the unvaccinated to encounter someone infected