6.7 Flashcards
give 3 non specific respon ses
inflammation, fevers, phagocytosis
what is cell recognition - why is it important?
- ability of body to distinguish bw its own cells + foreign cells/organisms (non self) = KEY TO IMMUNE SYSTEM
- non self glycoproteins = act as antigens - recognised by WBCs - trigger immune response
what is inflammation?
- localised infection (cut yourself - bact enter wound)
- special cells (mast checks) found in connective tissue below skin + around blood vessels
- mast cells + basophils release chemicals known as histamines - cause blood vessels to dilate -> local heat + redness
- locally raised temp - reduces pathogen reproduction
- histamines also make walls of capillary leaky - fluid containing leucocytes and antibodies forced out capillaries
- ABs disable pathogens + leucocytes + neutrophils destroy them (phagocytosis)
fevers?
- when pathogen infects body - hypothalamus increases body temp
1. most pathogens reproduce most quickly at 37 deg or lower, higher temp = less able
2. specific response/ immune system works better at higher temps - too high temp = fatal - denaturing of enzymes
role of neutrophils in phagocytosis?
- NEUTROPHILS (granulocytes) - can only ingest a few pathogens before it dies; cannot renew their lysosomes so once enzyme used up - cant kill more pathogens
- they can change their shape to fit through small spaces = diapedepsis
role of macrophages in phagocytosis?
- MACROPHAGES (agranulocytes) - monocytes migrate to tissues -> macrophages; a v big capacity for ingesting pathogens bc can renew lysosomes; accumulate at site of infection
what is phagocytosis?
- phagocytes engulf pathogens - pathogen enclosed in vesicle called phagosome
- phagosome fuses with a lysosome - enzymes in lysosome break down pathogen
- phagocytes after engulfing pathogen - produce chemicals (cytokines) in surrounding tissue - effective cell signalling molecules - stimulate other phagocytes to move to infection site; also they increase body temp
what are opsonins?
= chemicals that bind to pathogens so more easily recognised by phagocytes
- phagocyte will bind to opsonins
what happens in the T helper activation stage of the humoral response?
- pathogen enters body
- chemicals produced attracting phagocytes (macrophages + neutrophils)
- macrophage engulfs pathogen and separates digested pathogen - combines them with the major histocompatibility complex (MHC)
- MHC moves to surface of macrophage cell outer membrane
- the macrophage is now presenting antigens on membrane -> APC
- then T cell receptors on outer membrane bind to specific antigen on APC
- this binding triggers T cells to reproduce and form clone of cells
- most of these become active T helper cells, some inactive T memory cells
what happens in effector stage?
- B cells have immunoglobulins on surfaces that are specific for antigen
- B cells bind to antigen, engulf pathogen by endocytosis
- vesicle formed fuses w lysosome - enzymes break down pathogen -> fragments of antigen
- fragments are attached to MHC proteins in cell - transported to CSM - B cell becomes APC
- T helper produced from T helper activation stage recognises these specific antigens and binds to it
- triggers release of cytokines from T helper cell
- cytokines stimulate B cells to divide and form clones of identical cells = CLONAL SELECTION
- clones of B effector + B memory cells produced
- B effector cells differentiate -> plasma cells
- plasma cells produce large amount of antibodies identical to immunoglobulin of B cell
- antibody will bind to specific antigen and destroy it in several ways
how can an antibody destroy an antigen? 3
- AGGLUTINATION = ABs bind to antigens on pthogns - MOs clump/agglutinate tg - prevents spread - can more easily be engulfed by phagocytes
- OPSONISATION = AB acts as opsonin - can be recognised by phagocytes
- NEUTRALISATION - ABs neutralise effects of bacterial toxins by binding to it
what are the parts of humoral response?
pathogen -> phagocyte engulfs it -> APC -> T cell binds to antigen -> T cell divides into helper + memory
antigen -> B cell binds to -> APC -> T helper cell binds to antigen -> B cell = clonal selection -> B effector cells + B memory cells -> B effector cells - plasma cells -> release ABs - destroy pathogen
what is the cell-mediated response for?
- when pathogen INSIDE host cell - so humoral response not very effective against it as ABs can’t penetrate cell membranes
what is the cell-mediated response?
- body cell infected w bacterium/virus
- pathogen is digested and surface antigens are bound to MHC and body cell becomes APC
- T killer cells in blood have a wide range of complementary receptor proteins on surface of CSM
- these can bind to matching antigen on APC
- if T cells then exposed to cytokines from active T helper cell (from T helper cell activation in humoral response), the T cells will undergo rapid mitosis -> clone of T killer memory cells and identical active T killer cells
- these can bind to all the infected body cells
- T killer cells release enzymes that make pores in membrane of infected cell - so water + ions enter cell - cell bursts
- any intact pathogens that are released = labelled w ABs + destroyed
role of T and B memory cells in 2ndary immune response?
- B memory cells = long lived so if second invasion, B memory cells help produce antibodies against it
- T m cells = release flood of active T killer cells to engulf + destroy infected cells
what is natural active immunity?
body produces its own antibodies to an antigen encountered naturally
what is natural passive immunity?
antibodies made by the mother are passed to the baby via placenta/breast milk - PASSIVE BC antibodies not made by baby
artificial active immunity?
body produces own antibodies to antigen acquired through vaccination
artificial passive immunity?
antibodies extracted from 1 individual and injected into another
how does a vaccination work?
- attentuated (viable but modified so dont produce disease) antigens introduced into blood system by injection
- immune system produces antibodies against pathogen and appropriate memory cells will be formed
what is herd immunity?
- significant prop of popln vaccinated against disease
- so disease doesnt spread as very few ppl vulnerable to it
- protects those who cannot be vaccinated
pros of vaccination 3
- can be protected against diseases
- societal benefits - herd immunity - those who cant be vaccinated kept safe
- cost of treatment of serious diseases is minimised
cons of vaccination
- side effects/ allergic reactions
