4.1.1 Disease and the immune system Flashcards
What is a non-specific immune response?
-a system that works in the same way for all pathogens, whatever foreign antigen it has
-always present and activated rapidly
Non-specific defence barriers
-the skin
-mucous membranes
-expulsive reflexes
-lysozymes
-blood clotting
The skin
-acts a physical barrier covering the body to prevent entry of pathogens
acts a chemical barrier:
-it has a skin flora of healthy microorganisms that outcompete pathogens for space on the body surface
-produces chemicals that are antimicrobial(help destroy/slow down the growth of microorganisms) and can lower pH, which inhibits growth of pathogens(produces sebum)
-i.e skin cells secrete fatty acids that can kill some bacteria and lower pH so it is harder for pathogens to colonise
-i.e skin cells secrete lysozyme, which catalyses breakdown of carb in the cell walls of some bacteria
Mucous membranes
-many body openings/tracts i.e nose, ears that are exposed to the environment have membranes that can secrete sticky mucus to trap microorganisms
-contain lysozymes which destroy bacterial and fungal cell walls + phagocytes which remove remaining pathogens
-i.e lung epithelium are lined with mucus and have cilia which beat to waft away pathogens(phlegm coughed out through trachea up to throat or swallowed so HCl in stomach breaks it down)
Expulsive reflexes
-coughs and sneezes expel pathogen-laden mucus from gas exchange system after irritation from substance i.e dust
-vomiting and diarrhoea expel contents of gut along with infective pathogens
Lysozymes
-enzymes in tears, urine and stomach acid which help prevent pathogens getting into our bodies
Blood clotting
-Pathogens can enter body through a cut as your skin is breached
-Blood clots are a mesh of protein fibres that seal wounds(prevent pathogen entry and blood loss)
-formed by cascade of chemical reactions when platelets come into contact with collagen in skin or the wall of a damaged blood vessel and begin secreting several substances i.e thromboplastin and serotonin
What do thromboplastin and serotonin do?
- T is an enzyme that triggers cascade of reactions which result in the formation of fibrin
which itself forms a network, trapping platelets
and forming a blood clot - S makes smooth muscle in the walls of blood vessel contract, so they narrow and reduce blood supply to the area
Wound repair
-clot dries out, forming a hard and tough scab that acts as barrier against pathogens
-Epidermis cells below scab divide and migrate to the edges of the wound while damaged blood vessels regrow
-tissue below the wound contracts to bring the edges of the wound closer together + collagen fibres are deposited to give tissue strength(too much collagen= scarring)
-once epidermis reaches normal thickness, the scab comes off and wound is healed
What is the immune response?
-The body’s response to a foreign antigen*/ pathogen that got past primary defences
-it involves a non specific response which is the same for all pathogens and a specific response which is antigen specific
* i.e blood cells reject other blood type
Symptoms of the inflammatory response
(localised response to pathogens)
-pain, heat, redness and swelling of tissue
Steps of the inflammatory response
1) Mast cells(white blood cells) become activated when they detect damaged tissue and release chemicals called cytokines and histamines
2) Histamines causes:
- heat and redness by vasodilation(widening blood vessels) which increases blood flow to affected area(more white blood cells to fight pathogen) + temp increase helps prevent pathogens reproducing
- pain and swelling by making capillaries more ‘leaky’/increasing permeability of blood vessels, to allow specific white blood cells to leave blood plasma and join tissue fluid(then drain into lymphatic system and take pathogen to lymph nodes which become inflamed)
3) Cytokines are cell signalling chemicals that inform + attract phagocytes to the site of pathogen for phagocytosis to occur
How do fevers occur and why are they a good adaptation?
-cytokines stimulate hypothalamus to reset at a higher temp when pathogen invades
-useful because pathogen reproduction is best at 37 degrees or lower so it is inhibited
-specific immune system works better at higher temps
What are phagocytes?
-specialised white blood cells that engulf and destroy pathogens:*neutrophils & macrophages
-build up at a site of infection to attack pathogens(pus consists of dead neutrophils and pathogens)
*first white blood cell to respond to a pathogen inside the body
neutrophil structure
-multilobed nucleus= can squeeze through fenestrations to get to blood and tissue
-lysosome= vesicle with digestive enzymes
Phagocytosis- neutrophils
- role is to digest as many pathogens as possible
1) will recognise an antibody tagged to the pathogen that marks it as foreign(opsonin attach to antigens to aid this)
2) engulf the pathogen by changing the cytoskeleton structure of neutrophil
3) pathogen is enclosed in a vesicle called a phagosome, which then combines with a lysosome to form a phagolysosome
4) enzymes from lysosome digest + destroy pathogen
5) our body will recycle what we can i.e amino acids and the rest is released via exocytosis
Structure of macrophages
-lysosome= vesicle with digestive enzymes
-nucleus
-MHC complex= glycoproteins in the cytoplasm which help form an antigen presenting cell(APC)
Phagocytosis- macrophages
- starts the specific immune response
1) all the same steps as with a neutrophil except that a phagolysosome will not digest the antigen of the pathogen
2) MHC complex combines with the antigen and moves to the cell surface of the macrophage
3) This forms an antigen presenting cell
What are Opsonins?
-chemicals that bind to pathogens and ‘tag’ them so they can be easily recognised by phagocytes
-receptors on phagocyte’s cell membrane bind to common opsonins that act as constant region so phagocyte can then engulf pathogen
The specific immune system
-slower than non specific responses BUT immune memory cells mean secondary responses are very quick
Role of antigens
-on the surface of all cells and the body can recognise the difference between self antigens and non-self antigens(on pathogens)
-some toxins can act as antigens
-trigger immune response involving production of proteins called antibodies
-can bind to antibody to form antigen-antibody complex(similar to lock and key mechanism)
-there is a specific antibody for each antigen
Structure of antibodies
-Y shaped glycoproteins/immunoglobulins (proteins with carbohydrate group attached)
- 4 polypeptide chains= 2 long heavy chains and 2 short light chains
- chains are held together by Disulfide bridges(very strong bonds)
each chain has:
-2 variable regions where the antibody forms antigen-binding sites, shape is specific to complementary antigen, regions DIFFER for antibodies
-constant region which is the same sequence of amino acids in every antibody, allow binding to receptors on immune system
-hinge region gives antibody flexibility, allows it to bind to more than one pathogen
How do antibodies help clear infection?
- act as opsonin so antibody-antigen complex(tag pathogens) is easily identified and digested by phagocytes
- act as agglutinins causing pathogens to clump together, to help prevent them spreading + make it easier for phagocyte to engulf large volume when it binds (specialised with 2 variable regions + hinge region)
- act as anti-toxins= neutralise the toxins produces by pathogens by binding to it and preventing it from affecting human cells–} toxin-antibody complexes are phagocytosed
Primary immune response(specific)
Where do lymphocytes mature?
-B lymphocytes mature in the Bone marrow
-T lymphocytes mature in the Thymus gland
Cell mediated response(T cells)
-Clonal selection: macrophages form antigen-specific cells + receptors of T helper cells(white blood cells with lots of receptors) that are specific to the antigen will bind to APCs and become activated
-Clonal expansion: when activated, Th cells produce interleukins which stimulate more T cells to divide rapidly by mitosis forming clones with the specific antigen
-Differentiation: cloned T cells may:
- develop into T memory cell(rapid 2ndary response)
- T helper cell= produce interleukins(cell signalling proteins, type of cytokine) that detect APCs + stimulate phagocytosis / stimulate B cell division in PLAs
- T regulator(suppress immune system + slow it down to prevent auto-immune diseases)
- T killer cells(destroy pathogen by binding to it and secreting perforin which makes holes in cell membrane + kills cells i.e cancer cells, virus infected cells)
Humoral response
-B lymphocytes(type of white blood cell covered with antibodies, different shape on each membrane complementary to antigen)
-B-cell with complementary antibody engulfs pathogen
-Clonal selection: Activated T helper cells bind to the B-APC with the correct antibody to overcome a specific antigen
-produces more activated T helper cells(release interleukins) activate the B cells
-Clonal expansion: activated B cell divides by mitosis to give clones of B plasma cells and B memory cells
-Differentiation: B effector cells divide to form plasma cells(PLA) which produce lots of antibodies that fit the antigens on the surface of pathogens and form a-a complexes:
could be agglutinins, antitoxins or opsonins
Primary vs Secondary immune response
- primary:
-when the pathogen enters the immune system for the 1st time
-very slow, can take days/weeks to become fully effective against specific pathogen because there aren’t many B lymphocytes that can make specific antibody until memory cells
-activates B and T lymphocytes
-person undergoes symptoms - secondary:
happens if you get exposed to the same pathogen again - the volume of antibodies produced is higher in a shorter amount of time & is a rapid response,(clonal selection happens faster)
-memory B cell produce lots of plasma cells quickly= lots of antibodies quickly
-memory T cells produce lots of T killer cells quickly to kill pathogens quickly
-no symptoms show
What is cell signalling and why is it important?
-it is how cells communicate and it is important because it helps to activate the different types of white blood cells that are needed
-i.e cytokines inform other phagocytes when the body is under attack and stimulate them to move to the site of infection, and can increase body temp
-i.e T helper cells release interleukins which activate B lymphocytes by binding to receptor to signal presence of a pathogen
Blood smears
-sample of blood is smeared over a microscope slide
-stains are added to the sample to make different cells more distinguishable i.e rbcs, wbcs and platelets(tiny fragments involved in blood clotting)
-some wbcs have granules in their cytoplasm so they look grainy
-i.e monocyte is the biggest white blood cell, type of phagocyte, kidney bean shaped nucleus and non grainy cytoplasm
-lymphocyte is smaller than neutrophil, big nucleus, very little cytoplasm, can distinguish between B and T under light microscope
-neutrophil has a multilobed nucleus, grainy cytoplasm
Maintaining immunity
-memory B and T lymphocytes have a limited lifespan and when they die the person becomes susceptible to disease again
-immunity maintained by continuously exposing to pathogen to produce more new memory cells
-i.e areas with high malaria become immune to it
What are the 4 types of pathogens?
-Bacteria
-Viruses
-Protoctista
-Fungi
Bacteria
-prokaryotes(unicellular, no membrane-bound nucleus or organelles)—> naked DNA and plasmids help develop resistant genes
-can be rod shaped(bacilli), spherical(cocci), comma shaped(vibrios), spiralled(spirila) and corkscrew(spirochaetes)
-Gram positive bacteria look purple-blue under a light microscope and Gram negative bacteria appears red–} different types of cell wall which affect how bacteria reacts to antibiotics(kills/inhibits growth of bacteria)
-cause disease predominantly by producing toxins that harm the host(inhibit enzyme action)
Viruses
-non living infectious agents (0.02-0.3 um diameter and around 50x smaller than bacteria)
-some genetic material(DNA/RNA) surrounded by protein
-spread through contacts
-invade living cells by injecting genetic material into host cell and combining it with host cell DNA to make more viruses using host cell’s biochem i.e bacteriophages take over bacteria + use it to replicate while killing it
-reproduce rapidly and develop adaptations to their host
-can cause disease in every other type of organism
-hard to find a cure that won’t damage host cell DNA
