Primary defences
- These prevent the pathogen from entering the body
- These mechanisms have evolved through selection and are considered as adaptations
Barriers to entry
- The skin
- the skin covers the body surface providing a physical barrier that most pathogens find hard to penetrate
- Keratinocytes
- cells produced by mitosis at the base of the epidermis
- they migrate to the skins surface
- they dry out and the cytoplasm is replaced by keratin = keratinisastion
- this prcess take about 30 days
- by the time they reach the surface they are dead and everntally slough off
- Mucous membrane
- produced by the epithelial layer traps pathogens
- epithelial layer contains goblet cells
- these produce mucus that lines the airways trapping pathogens
- ciliated cells move the mucus up the oesophagus so it can be swallowed
- pathogens are killed by the acidity of the stomach (pH 1-2) which denatures their enzyme
- Mucus membranes are also found in the gut, ears and nose
- Hydrochloric acid in the stomach provides a low pH that the enzymes of most pathogens are denatured and therefore the organisms are killed
Secondary Defence
- Phagocytes (non-specific)
- Neutrophils - most common
- have multi-lobed nucleus and are produce in the bone marrow
- they are found in the blood and tissue fluid and may also be found on epithelial surfaces such as the lungs
- short lied but are released in large numbers
- Macrophage - larger than neutrophils
- manufactures in the bone marrow
- travels in the blood as monocytes
- they tend to settle in the body organs particularly the lymph nodes
- here they develop into macrophages
- they plan an important part in specific response to pathogens
- The role of macrophages
- infected cells release histamine
- this attract neutrophils
- it also causes capillaries to become more leaky
- as a result more fluid leaves the capillaries in the area of infection
- so more fluid passes the lymphatic system
- this leads the pathogen towards the macrophages in the lymph nodes
- How phagocytes work
- they engulf and destroy pathogenic cells
- these have chemical markers on their outer membranes = antigens
- these are recognised as non-self or foreign
- these are specific to pathogen
- Phagocytosis
- once bound the phagocytes envelopes the pathogen by folding its membrane inwards
- the pathogen is trapped within a phagosome
- lysosome fuse with phagosome and release enzymes lysins
- these digest the pathogen producing harmless products that can be absorbed
Specific immune response
T and B lymphocytes
- these have receptors that are complementary to the foreign antigen
- this antigen may be attached to the pathogen or on the surface of the host cell
- when antigen is detected, the lymphocyte is activated
"Describe the changes that occur to T lymphocytes during an immune response. Explain the roles of T lymphocytes in fighting infection by a pathogen, such as a virus"
- reference to antigen presentation - described
- receptors on T cell surface or complementary to the antigen
- reference to specificity in context of T cells
- clonal selection - described
- clonal expansion/T cells divide by mitosis
- T helper cells release cytokines
- stimulates B cells to divide/clone/differentiate
- stimulate macrophage to carry out phagocytosis
- T/Killer cells search and kill infected host cells
- secrete enzymes
- named enzyme
- active immunity
- memory T cells/immunological memory
- secondary response - more rapid
Antigen
- Usually large proteins or glycoproteins
- specific shape
- the antigen is specific to the pathogen
- a foreign antigen stimulates the production of antibodies = an immune response
- there is one type of antibody for one type of antigen
Antibodies
- produced by lymphocytes (WBC)
- are large proteins also known as immunlglobulins
- they have specific shape tat is complementary to particular antigen
- these antibodies are specific to the antigen
- therefore the antibody is specific to the pathogen
- antibodies attach to antigens and render them harmless
Antibody structure
- the constant region is the same on all antibodies
- this allows the attachment of phagocytic cells during phagocytosis
- the variable region has a specific shape and differs from one type of antibody to another
- this is due to its amino acid sequence
- this makes it complementary to a particular antigen
- this allows it to bind to the antigen
- the hinge region allow flexibility
Antigens, antibodies and phagocytosis
- the presence of a foreign antigen can trigger the production of antibodies
- antibodies (proteins) in our blood attach to foreign antigens (antigen-antibody complex)
- phagocytes have membrane bound receptor proteins
- these can bind to the antibody antigen complex
- allows the recognition of the pathogen
How antibodies work - neutralisation
- the antigen in the pathogens cell surface membrane may be used as a binding site
- this would allow it to bind to host cells
- if the antibody blocks this binding site then the pathogen cannot bind to the host cell
- this is called neutralisation
Agglutination
- some antibodies are larger than those previously described
- they resemble several Y shaped molecules attached together with many specific variable region
- each one can bind to an antigen on a pathogen
- the attachment to many pathogens at the same time is called agglutination
- the pathogens cannot enter host cells
Producing antibodies
- Infection = antibody production
- It takes a few days before antibody levels are high enough to successfully combat the infection
- This is the primary immune response
- antibodies do not stay in the blood
- if the body is infected a second time by the same pathogen, the antibodies must be made again
- however, the production is faster and the concentration is higher
- this is the secondary immune response
Communication between cells
Cell signalling
- Communication is achieve through sell surface molecules and through the release of hormone like chemicals called cytokines
- the target cell must have a cell surface receptor
What information is communicated
- Identification - the pathogen carries antigen that identify it as foreign
- Distress signals - these are produce when a cell becomes infected by a pathogen
- lysosomes breaks down the infecting pathogen
- parts of the pathogen end up attached to the host cells plasma membrane (antigen presentation)
- these can act as a distress signal that can be detected by other cells
- or they can act as markers so the infect host cell can be destroyed by T killer cells
- Antigen presentation
- macrophages engulf pathogens by phagocytosis
- they do not fully digest them
- they incorporate the antigen into their cell surface membrane
- they become known as antigen-presenting cells
- its function is to find the lymphocyes that can neutralise that particular antigen
- Instructions
- chemicals called cytokines act as instructions to target cells
- they bind to specific receptors
- this causes the release of second messengers inside the cells
- e.g. macrophages release monokines to attract neutrophils
- macrophages release monokines to stimulate B lymphocytes to release antibodies
- T and B lymphocytes release interleukins which stimulate the proliferation and differentiation of T and B lymphocyte
- Many cells release interferon which can inhibit virus replication and stimulate killer T cells
Cheers ;)
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