Chapter 39 Flashcards
pathogens
harmful organisms and viruses that can cause disease
what are the three phases of defence responses?
recognition, activation, effector
recognition phase
the organism must be able to recognise pathogens and discriminate between self and nonself
activation phase
the recognition event leads to a mobilisation of cell sand molecules to fight the invader
effector phase
the mobilised cells and molecules destroy the invader
what are the two general types of defence mechanisms?
innate, adaptive
innate defenses
nonspecific, inherited mechanisms that provide the first line of defense against pathogens
what are some examples of innate defences?
physical barriers such as skin, molecules toxic to invaders, phagocytic cells that ingest invaders
adaptive defenses
aimed at specific pathogens, activated the innate immune system
what are some examples of adaptive defences?
make antibodies to aid in the destruction of pathogens
antibodies
proteins that will recognise, bind to, and aid in the destruction of specific pathogens
immunity
occurs when an organism has sufficient defences to successfully avoid biological invasion by a pathogen
what is the main function of red blood cells?
carry oxygen throughout the body
white blood cells
specialised for various functions in the immune system
phagocytes
large cells that engulf pathogens and other substances by phagocytosis
lymphocytes
B cells and T cells (adaptive), natural killer cells (innate and adaptive)
basophils
release histamine and other molecules involved in inflammation
eosinophils
kill antibody-coated parasites
neutrophils
stimulate inflammation
mast cells
release histamine
monocytes
develop into macrophages and dendritic cells
macrophages
antigen presentation
dendritic cells
present antigens to T cells
B lymphocytes
differentiate to form antibody producing cells and memory
T lymphocytes
kill pathogen infected cells; regulate activities of other white blood cells
natural killer cells
attack and lyse virus-infected or cancerous body cells
physical barrier of the skin
bacteria rarely penetrate intact skin
saltiness of skin
condition is not hospitable to the growth of bacterium
presence of normal flora
bacteria and fungi that normally live on body surfaces will compete with potential pathogens for space and nutrients
mucus
traps microorganisms so they can be removed by the beating of hte cilia
lysozyme
cleaves bonds in the cell walls of many bacteria, causing them to lyse
defensins
insert themselves into the cell membranes of these organisms and make the membranes freely permeable to water and all solutes
internal environment
harsh conditions can kill pathogens
pattern recognition receptors
activates defensive cells by recognising nonself molecules
pathogen associated molecular patterns
unique to large classes of microbes, such as bacterial flagellin and fungal chitin
natural killer cells
initiate apoptosis in target cells that are infected by viruses or have become cancerous
cytokines
signaling proteins that are released by many cell types and can be prpoduced in response to PRR activation
interferons
help increase the resistance of neighbouring cells to infection
inflammation
redness, swelling and heat near the damaged site
mast cells
adhere to the skin and release numerous chemical signals
tumour necrosis factor
cytokine protein that kills target cells and activates immune cells
prostaglandins
fatty acid derivatives that play roles in various responses, including the initiation of inflammation in nearby tissues
histamine
amino acid derivative that increases the permeability of blood vessels to white blood cells and molecules so they can act in nearby tissues
allergic reaction
normally harmless nonself molecule binds to mast cells, causing the release of histamine
autoimmune diseases
immune system fails to distinguish between self and nonself and attacks tissues in the organism’s own body
sepsis
inflammation becomes widespread and blood pressure can greatly drop due to dilation of blood vessels
antigens
nonself substances
antigenic determinants (epitopes)
sites on antigens that the immune system recognises
clonal deletion
immature B or T cell that shows potential to mount a strong immune response against self antigens undergoes apoptosis
autoimmunity
immune response within an individual to self antigens caused by a failure of clonal deletion
immunological memory
after responding to a particular type of pathogen once, the immune system can usually respond more rapidly and powerfully to the same threat in the future
primary immune resonse
takes several days before the adaptive immune system produces specific antibodies and T cells
effector cells
carry out the attack on the antigen
plasma cells (effector B cells)
secrete antibodies
memory cells
start dividing on short notice to produce more effector and more memory cells
secondary immune response
more rapid and powerful response to a repeat antigen exposure
antigen presentation
phagocytic cells display fragments of the pathogen on their cell surfaces for communication purposes
cytotoxic T cells
workhorses of the cellular immune response
B cells that make antibodies
workhorses of the humoral immune response
T helper cell
bears a T cell receptor protein that is specific for the antigen
immunoglobulins
several classes of antibodies
how does a “naive” B cell become a regular B cell?
activated by antigen binding to the receptor from the “naive” B cell
amino acid sequence of the constant region
determines the general structure and function of an immunoglobulin
variable region
this amino acid sequence is different for each specific immunoglobulin
IgG
80% of circuling antibodies
IgD
cell surface receptor on a B cell
IgM
initial surface and circulating antibody released by a B cell
IgA
protects mucous membranes exposed to the environment
IgE
binds to mast cells and is involved with inflammation
Class I MHC proteins
present antigens to Tc cells
Class II MHC proteins
present antigens to Th cells
regulatory T cells
ensure that the immune response does not spiral out of control
