3.2.4 immunity

non-specific and specific

non-specific: - response is immediate and same for all pathogens. - done via phagocytosis (engulfing) or through physical barriers. specific: - response is slower and specific to each pathogen. - done via cell-mediated response (T lymphocytes) or humoral response (B lymphocytes).

a macrophage, with a lobed nucleus, (a type of white blood cell) that carries out phagocytosis.

• phagocytes are attracted to the pathogens by chemicals released by the pathogen, causing the phagocyte to move towards the pathogen along a concentration gradient. • phagocyte uses its complementary receptors to bind to chemicals or antigens on surface of pathogen. • phagocyte changes shape and engulfs the pathogen, forming a phagosome. • lysosomes move towards and fuse with phagosome. • lysosomes then release their lysozymes (lytic enzyme) into the phagosome, where they then hydrolyse the pathogen. • hydrolysis products are either absorbed by the phagocyte or expelled from the cell.

antigen-receptors

molecules, usually a protein, which are recognised as non-self by the immune system, that cause an immune response.

bone marrow and then migrate to the lymph nodes.

thymus gland and then migrate to the lymph nodes.

a quaternary protein produced by B cells/plasma cells that is specific and complementary to an antigen.

• two lighter chains. • two heavier chains. • two antigen binding sites. • two variable regions. and constant regions. • disulphide bridges.

• phagocytes engulf pathogens by phagocytosis and become antigen presenting cells. • t helper cells bind to antigens on antigen presenting cells using complementary receptors, which activate t helper cells. • activated t helper cells undergo mitosis, producing a clone of cells. • some helper t cells become memory cells. • cytotoxic T cell binds to antigens on infected cell using complementary receptors. • activated t helper cell also binds to cytotoxic t cell, activating it. • activated cytotoxic T cells undergo mitosis, producing a clone of cells. • cytotoxic T cells destroy infected cells. • cytotoxic t memory cells produced.

• phagocytes engulf pathogens by phagocytosis and become antigen presenting cells. • t helper cell binds to antigen on antigen presenting cell using complementary receptors. • t helper cell activated • activated t helper cells undergoes mitosis, producing a clone of cells. • memory t helper cells produced. • b cells engulfs antigens and become antigen presenting b cells. • active t helper cell binds to antigen presenting b cell using complementary receptors, activating b cell. • active b cell undergoes mitosis/ clonal expansion. • memory b cells produced. • active b cells differentiate into plasma cells. • plasma cells released antibodies.

• cytotoxic T cell binds to infected cell. • perforin makes holes in infected cell’s membrane and enzyme enters. • holes result in the cell surface membrane becoming freely permeable to all substances.

• agglutination. • opsonisation. • neutralise.

binding of antibodies causing pathogens to clump together, preventing them spreading and easier to engulf and locate.

antibodies act as an opsonisation, a chemical making pathogens more easily recognisable.

neutralise affects of bacterial toxins by binding to them.

antibodies injected from one person to another

most immunisation programs

mother to baby with breast milk containing antibodies

contact with foreign antigen

occurs when a significant proportion of the population is vaccinated.

human immunodeficiency virus

acquired immunodeficiency syndrome