immunology 1,2 Flashcards
describe the main first line defence mechanisms
(physical and anatomical barriers)
respiratory and GI tract- mucous membranes, protective barrier prevents microbes attaching
skin- stratum corneum (outer layer of epithelial cells), contains insoluble keratin, thick layer, waterproof
skin glands- sweat flushes out microbes, temp regulation
tears/blinking- flushes eye surface to clear pathogens, keeps surface moist
nasal hair- traps particles, makes air warm for lungs
saliva- captures/carries microbes to stomach
ciliated epithelium- moves foreign particles from trachea and bronchi to pharynx for removal
reflexes- sneezing, vomiting, coughing, defecation, ejects foreign material
human microbiota- prevents harmful microbes from forming
(non specific chemical defences)
specialised glands- sebaceous glands in skin and meibomian glands secrete sebum with antimicrobial effect
lysosymes and defensins in tears and saliva- hydrolyse peptidoglycan in bacteria, defensins are peptides that damage cell membrane and bacteria/fungi
skins acidic pH and fatty acid content- prevents harmful microbes colonising while good microbes are allowed
sweat- high lactic acid conc, unfavourable to many microbes, temp regulation, maintains pH, allows good microbes
what is the lymphatic system
network of vessels/accessory organs that return extracellular fluid to circulation and carries out immune surveillance via lymphocytes and phagocytes
what does lymph contain
extracellular fluid, WBCs, fats, cell debris
what do lymph vessels do
move fluid from tissue to heart using contractions of surrounding skeletal muscle
name primary and secondary lymphatic organs
primary= thymus gland and bone marrow
secondary= spleen, lymph nodes, MALT, GALT, SALT
what is MALT GALT and SALT
mucosal associated lymphoid tissue
gut
skin
another name for white blood cells
leukocytes
two types of leukocytes
granulocytes- neutrophils, basophils, eosinophils, lobed nuclei, cytoplasmic granules, aid diagnosis, neutrophils most abundant
agranulocytes- monocytes, lymphocytes, globular and non lobed nuclei, lack notable granules, monocyte differentiate into macrophages and dendritic cells
what are PRRs
pattern recognition receptors
displaced on WBC membrane and senses/interacts with pathogens, not microbe specific
what are PAMPs
pathogen associated molecular patterns
shared by pathogens, acts as warning, activates downstream signalling
what is the aim of immune system
prevent harmful microbes and pathogens entering body
what is innate defence
natural defences present at birth, non specific resistance to infection
what is innate defence divided into
first line defence=blocks invasion at entry site (surface barriers like skin, mucous, membranes)
second line defence=non specific phagocytes, internal systems, chemicals (phagocytosis, fevers, inflammation)
what is haematopoiesis
production of RBCs WBCs and platelets in bone marrow
what is inflammation and its characteristics
process to restore homeostasis, after injury or trauma in tissues, after infection or tissue death, symptom of allergy, redness from vasodilation, warmth from increased blood circulation, swelling from increased ECF, pain from stimulated nerves by pressure and chemicals, can cause loss of function
function of inflammation
clear invading microbes and cell debris after immune reactions, attract immune cells and chemical mediators, start repair mechanisms, destroy/block microbes
what are cytokines, what are they produced by, what do they do
complex group of signalling molecules, produced by helper T cells (WBCs), important for downstream actions and communications between innate and acquired immune mechanisms
what are chemokines
type of cytokines that attract cells to infection sites
what is chemotaxis and when does it occur
WBC migration, happens in response to inflammatory chemotactic factors, leaves circulation to reach target tissue
how does chemotaxis occur
- adheres to small blood vessel walls-adhesive receptors line endothelial cells, increased adhesion in response to cytokines
- migrate to tissue via diapedesis-motile circulatory WBC change shape and leave vessel to enter extracellular matrix
name the 3 major stages of phagocytosis
- survey- patrol tissue, investigate foreign invaders/dead cells
- ingest- engulf, eliminate unwanted
- extract- process antigens from pathogens
what is TLR and their functions
toll like receptors
-recognise PAMPs, trap foreign molecules, engulf, release chemical signs
how do TLRs interact with pathogens
TLR joins together in pairs (dimerise) and captures foreign molecules and stimulates phagocytosis, pseudopods extend and encase particle in phagosome, lysosome within cell migrate and fuse with phagolysosome/vacuole, release of antimicrobial chemicals including digestive enzymes form lysosomes
what are iterferons (IFN) and the different types
IFN=cytokine produced by WBC, antiviral and anticancer activity
interferon alpha=from macrophages and lymphocytes
beta=epithelial cells and fibroblasts
gamma=T cells
functions of interferons
stimulate phagocytes/phagocytosis, regulate macrophages and lymphocyte/T and B cells, bind to cell surface and trigger changes in gene expression, inhibits gene tumour suppressor, activate natural killer cells
what is the complement system
(part of immune system that cleans up damaged cells, helps your body heal after an injury or an infection and destroys microscopic organisms like bacteria)
protein cascade triggered by specific recognition molecules and progressing through a series of protein protein interactions that culminate in formation of a cytolytic pore
where are complement proteins produced
liver
name the 3 main complement system pathways and what initiates them
classical- initiated by antibody antigen complexes, connected to acquired third line defence
lectin- initiated by pattern recognition molecules binding to PAMPs
alternative- initiated by microbes in absence of antibody
3 key features of complement system
- membrane attack complex (MAC)-proteins activate reactions, C9 units bind to complex, can kill eukaryotic and bacterial pathogens, C3 converts to C3b and 3a, C5→C5b and C5a, C5b combines with C6,7,8, C3a and 5a stimulate mast cell degranulation, chemotaxis and inflammation
- opsonisation- coating pathogens and labels for phagocytosis
- cytokine release and cell recruitment- promotes further signalling, heightened immune response aide by C3a and C5a
what does PAMP stand for
pathogen associated molecular patterns
