chapter 7&8 (antigens, immunity & diseases) Flashcards
self antigens
- located on the surface of cells
- marked as ‘self’ so immune system does not attack
MHCI
- major histocompatibility complex
- expressed on all cells except those without a nucleus (e.g red blood cells)
MHCII
- major histocompatibility complex
- found on specialised cells of the immune system
non-self antigens
- immune system reads as ‘foreign’ and is activated to kill it
cellular pathogens
- have cell structure and are living organisms
BACTERIA: disease through enzymes and toxins effecting functions in cell
FUNGI: yeast and mould organisms
PARASITES: invertebrate (eggs, larval)
PROTOZOA: free living, parasitic, inhibits functions
non-cellular pathogens
VIRUSES: composed of genetic material in protein coat, uses host cells to replicate (unable to itself)
PRIONS: abnormally folded proteins which causes other miss folding, only occurs in mammals and affects the brain
allergies & allergens
ALLERGIES: overreaction to the presence of an allergen
ALLERGEN: a non-pathogenic antigen that triggers an allergic reaction (inflammatory response, breathing issues)
first line of defence plants
(non-specific/innate)
- physical- prevent pathogens from physically entering
(e.g bark, galls, closing of the stomata) - chemical- production of chemicals which are harmful to pathogen
(e.g phenols (repel/kills), defensins(toxic))
first line of defence animals
(non-specific/innate)
- physical - e.g skin, cilla/hair like structures, mucous secretions
- chemical - e.g acidic sweat, stomach acid & antibacterial parts of earwax
- microbiological - prevents growth of pathogenic bacteria
(e.g normal flora on skin and gastrointestinal tract)
second line of defence cellular components
(non-specific/innate)
- natural killer cell: destroys infected/abnormal cells with insufficient MHCI markers
- mast cells: causes inflammation through release of histamine
- eosinophils: releases toxic chemical mediators to destroy invading pathogens
- phagocytes: cells that engage phagocytosis (engulfing via endocytosis)
phagocytes
- neutrophils: phagocytosis of pathogens
macrophage/dendritic cells: phagocytosis of pathogens and the antigen presentation within the adaptive immune system (APC)
second line of defence non-cellular components
(non-specific/innate)
-interferons: causes changes to neighbouring cells that make them less susceptible to infection
-complement proteins: aids in the destruction of pathogens via opsonisation (surrounded), chemotaxis (attraction of phagocytes), lysis (MAC, swell/burst)
-fever: abnormally high body temperature to kill pathogens
inflammatory response
-initiation: damage, introducing pathogens, mast cells degranulate and release histamine
-vasodilation: histamine travels to blood vessels, widens increasing blood flow and causes swelling, redness & warmth
-migration: number of innate immune components leave bloodstream and enter injury site (PUS: is caused by increase blood flow and immune cell activity/dead cells)
- this continues until site is cleared
third line of defence
(specific/adaptive)
- APC take antigen to t-helper cell and t-helper cell is activated
- t-helper cell release cytokines
- cytokines and pathogens(B) active T and B cells
- once activated they remember the pathogen
humoral immunity (external)
- COLONAL SELECTION: a pathogen with complementary antigen to the B cell bind, a t-helper cell also complementary recognise the selected B cell and secrete cytokines
- COLONAL EXPANSION: the B cell replicated and many copes are formed
- DIFFERENTIATION: differentiates into b-memory cells and plasma cells
antibodies (released from plasma cells)
- consists of four polypeptide chains (two heavy chains/long and two light chains/short)
- joined by disulphide bond
- variable and constant region
five types: IgA, IgD, IgE, IgG, IgM
key functions of antibodies
- neutralisation: block site used to attack host cell & block toxins
- agglutination: bind together with antigens of pathogens to make a larger complex for phagocytes to recognise and destroy
- opsonisation: antibody binds to pathogen to easily phagocytose
- activation of complement proteins: antibodies attach to surface and facilitate activation
cell-mediated immunity (internal)
- COLONAL SELECTION: naive T cell complementary to the antigen presented will bind with APC at the same time as the t-helper cell, naive T cell is now selected, t-helper cell releases cytokines
- COLONAL EXPANSION: the cytokines released stimulate the T cells to replicate and form copies
DIFFERENTIATION: differentiates into t-memory cells and cytotoxic-t-cells
cytotoxic-t-cells
- arrives at site of infection
- cytotoxic-t-cells contains receptor specific to foreign antigen
- finds the abnormal cell and binds the complementary MCHI complex
- chemicals (perforin) are secreted by the cytotoxic-t-cells and induce apoptosis
immunological cell memory
- b-memory cells form new antibody producing plasma cells when antigens match their receptors
- t-memory cells rapidly turn into t-helper cells and cytotoxic-t-cells from stimulation from the APC
primary lymphoid tissue
- where it is produced and matured
BONE MARROW: B lymphocytes remain in bone marrow to mature
THYMUS: T lymphocytes travel to the thymus to mature
secondary lymphoid tissue
- where it is stored
- lymph noes, spleen, tonsils
- when APC travel to the lymph nodes to activate T and B cells results in a large number of cells and therefore swelling of lymph nodes
lymphatic system as transport network
- DRAINAGE: after injury liquid from blood vessels can leak, the fluid is drained by the lymphatic capillaries
- FLOW: capillaries join together to form vessel that re full of lymph and get pushed towards lymph nodes
- SURVEILLANCE: fluid arrives at lymph nodes via afferent vessel, antibodies and cytotoxic-t-cells exit via efferent vessels
natural active immunity
- own immune system creating antibodies and memory cells specific to that pathogen
- antibodies from individual immune system
e.g getting chickenpox and then being immune afterwards
natural passive immunity
- acquires antibodies from natural, non medical sources
- external source of antibodies
e.g antibodies from placenta/breast milk
artificial active immunity
- own adaptive immune system produces antibodies and memory cells due to medical intervention
- antibodies from individual immune system
e.g vaccines
artificial passive immunity
- acquires antibodies from external source via medical intervention
- external source of antibodies
e.g anti-venom
primary and secondary vaccination
- PRIMARY: antibodies and memory cells formed, diminishes quickly
- SECONDARY: memory cells recognise the vaccine, large immune response, resulting in large long-lasting immunity
herd immunity
- protection against disease when a high percent of population (approx. 70%) is immune to the disease
- often achieved through vaccination
- helps prevent the spread
contagious & virulent
- contagious: how easily it is transmitted between people
- virulent: how severe is the disease the pathogen causes
emerging & re-emerging
- emerging: diseases that have no occurred in humans before
e.g COVID-19, influenza - re-emerging: once were major public health problems and then declined but once again are becoming a problem
e.g ebola, measles, malaria
epidemic & pandemic
- epidemic: specific population and specific location
- pandemic: spread to different countries and/or continents
(endemic - one specific area)
factors contributing to emergence and re-emergence of diseases
- evolution of organisms
- globalisation and travel
- exposure of humans to animals
- increasing human population
- changing technology
- insufficient vaccination
lack of immunity in indigenous population
- europeans would have encountered the disease in their childhood, some form of natural active/passive immunity
- Indigenous Australian’s had no immunity and therefore were more likely to severely contract the disease
lack of knowledge and experience
- Indigenous understood how to treat their own diseases but not the new european diseases
- medicine was often prevented and therefore there was no treatment
disruption due to colonisation
- access to food was redistricted and denied
- forced into camps, and infection where heightened due to close proximity
methods of identifying pathogens
- physical: microscopes
- phenotypic: selective media
- immunological: serology (presence of antibodies or antigens
- molecular: whole genome sequencing (provides info)
modes of disease transmission
- airborne transmission
- droplet transmission
- direct physical contact
- indirect physical contact (food/mosquitoes)
- faecal-oral transmission
controlling disease transmission
- prevention (hygiene, PPE, vaccination, lockdown)
- screening (routine testing)
- quarantine and isolation
- identification (identify pathogen)
- control transmission (mitigate)
- treating the infected (use of medication such as antiviral)
immunotherapy
- a form of medical treatment that modulates the functioning of the immune system in order to treat disease
- ACTIVATION IMMUNOTHERAPIES: induce or amplify an immune response
- SUPPRESSION IMMUMOTHERAPIES:
prevent or reduce an immune response
examples of immunotherapies
- CAR-T therapy: modification of t cells to destroy cancer cells
- dendritic cell therapy: activation of lymphocytes kill any tumour antigens
monoclonal antibodies and production
- laboratory-made proteins that can be used to treat a number of different diseases
STEPS: - cancer cell antigen identified
- vaccination/injection of mouse
- cells/extraction of mouse cells
- fuse of cells with myeloma cells to form hybridomas cells
- selection of hybridomas cells
- collection and purification of antibodies
two types of monoclonal antibodies
- naked monoclonal antibodies (nothing attached)
- conjugated monoclonal antibodies (drugs/material attached)
monoclonal antibodies against cancer and autoimmune disease
CANCER
- antibody-dependent cell-mediated cytotoxicity: (bind to cancer cells and use NK cells)
AUTOIMMUNE DISEASE
- cytokine inhibition: (bind and inhibit cytokines to reduce immune response)
traditional cancer treatment
- chemotherapy and radiotherapy
- many other cells are suffered by these treatments causing hair loss, and nausea
article info
- smallpox was a pandemic
- infected the lymphatic system
- was spread through contact with scabs or contamination
- using inoculation (deliberately infected with scabs) if they survived they gained immunity
- smallpox pus was injected under the skin if they survived they gained immunity
- smallpox disease could withstand most and stayed viable
- with the cowpox virus the vaccine was created (less symptoms compared to smallpox, then gain immunity)
- smallpox was eradicated in 1977
