Immune system Flashcards
molecules lymphocytes identify
pathogens
cells from other organisms of same species
abnormal body cells
toxins
antigens
proteins on the cell-surface membrane
trigger an immune response when detected by lymphocytes
Antigenic variability
When pathogenic DNA mutates
causing a change in shape of
antigen
previous immunity is no longer effective as memory cells don’t recognise new shape of antigen.
specific antibody no longer
binds to new antigen
physical barriers
skin
stomach acid
lysozymes in tears
phagocytes
non-specific immune response
phagocytes become antigen-presenting cells after destroying pathogen
T lymphocytes
made in bone marrow and mature in thymus gland
involved in cell-mediated immune response
respond to antigen-presenting cells
Antigen-presenting cells
Any cell that presents a non-self antigen on their surface
infected body cells
macrophage after phagocytosis
cells of transplanted organ
cancer cells
role of T helper cells
have receptors on their surface that attach to antigens on ACP
become activated - clonal selection
role of cloned T helper cells
some remain as helper T cells and activate B lymphocytes
stimulate macrophages for phagocytosis
become memory cells for that shaped antigen
become cytotoxic killer T cells
Cytotoxic T cells
destroy abnormal/ infected cells by releasing perforin
so that any substances can enter or leave the cell and this causes cell death
B lymphocytes
made in bone marrow and mature in bone marrow
involved in humoral immune response
involves antibodies
B memory cells
derived from B lymphocytes
remember specific antibody for particular antigen
will rapidly divide by mitosis and differentiate in plasma cells upon secondary encounter
resulting in large numbers of antibodies rapidly
Humoral response
APC activates B cells
B cell undergoes clonal selection and expansion - rapid division by mitosis
differentiate into plasma cells/ memory B cells
plasma cells make antibodies
Antibodies
quaternary structure proteins made of 4 polypeptide chains
different shaped binding sites = variable regions
complementary to a specific antigen
Antibody structure
Antigen binding sites
variable region
constant region
Agglutination
Antibodies have 2 binding sites and are flexible - clumps pathogens together
makes it easier for phagocytes to locate and destroy pathogen
passive immunity
antibodies introduced into body
plasma and memory cells not made as no interaction with antigen
short-term immunity
fast acting
active immunity
immunity created by own immune system - antibodies made
exposure to antigen
Plasma and memory cells made
long term immunity
slower acting
Natural active immunity
after direct contact with pathogen through infection
body creates antibodies and memory cells
Artificial active immunity
creation of antibodies and memory cells following introduction of an attenuated pathogen or antigens
vaccination
Vaccinations
Small amounts of dead of attenuated pathogens injected/ ingested
humoral response activated
memory cells are able to divide rapidly into plasma cells when re-infected
primary vs secondary response
Primary = first exposure to the pathogen
longer time for plasma cell
secretion & memory cell
production
for the secondary response,
memory cells divide rapidly into plasma cells
so a large number of antibodies
made rapidly upon reinfection
Herd immunity
when enough of the population is vaccinated so pathogen is not transmitted and spread easily
provides protection for those without vaccine
monoclonal antibodies
a single type of antibody that can be isolated and cloned
antibodies that are identical - from 1 type of B lymphocyte
complementary to only 1 antigen
uses of monoclonal antibodies
medical treatment - targeting drugs by attaching antibody complementary to tumour cell antigen
medical diagnosis - pregnancy test
pregnancy test
ELISA test which uses 3 monoclonal antibodies and enzymes to test for hCG
purpose of ELISA test
Detect the presence and quantity of antigen
used for medical diagnosis
HIV structure
core = RNA and reverse transcriptase
capsid = protein coat
lipid envelope taken from hosts cell membrane
attachment proteins so it can attach to helper T cells
ethical issues with monoclonal antibodies
requires mice to produce antibodies and tumour cells
requires a full cost-benefit analysis
HIV replication
attaches to CD4 receptor on helper T cells
protein fuses with membrane allowing RNA and enzymes to enter
Auto immunodeficiency syndrome (AIDs)
when HIV has destroyed too many T helper cells, host is unable to produce adequate immune response to other pathogens
host susceptible to opportunistic infection
why vaccines may be unsafe
inactive virus may become active - viral transformation
non-pathogenic virus can mutate and harm cells
side effect of immune response
people may test positive for disease
role of antibodies in ELISA
first antibody added is complementary to antigen in well - attaches
second antibody with enzyme added which attaches to first antibody as complementary.
when substrate solution added enzyme can produce colour change
why do you wash well in ELISA
removes unbound 2nd antibodies
otherwise enzymes may be present = colour change = false positive
why are antibiotics ineffective against viruses?
viruses are inside host cells where antibiotics cannot reach
antibiotics affect parts of bacteria that viruses dont have
pathogen
microorganisms that cause a disease by releasing toxins or killing cells
cytokinesis
Final stage in the cell cycle
when the cytoplasm splits in 2
creates 2 new cells
uncontrolled mitosis
uncontrolled cell division can lead to the formation of tumour and of cancers
many cancer treatments are directed at controlling the rate of cell division
viral replication
following injection of their nucleic acid
the infected host cell replicates the virus particles
cell adaptations for rapid transport across membranes
increase in surface area or membrane
increase in the number of protein channels and carrier molecules in the membrane
Antigen- antibody complex
when a complementary antibody binds to an antigen
this clumps pathogens together
