innate (natural) immunity - week 2 Flashcards
what are the components of innate immunity
the cellular and soluble factors are:
- phagocytic cells - monocytes/macrophages, neutrophils
- natural killer (NK) cells
- cell surface receptors
- complement system
- cytokines
- other soluble factors
where is innate protection found
- lysozyme in tears and other secretions
- commensals
- removal of particles by the rapid passage of air over turbinate bones
- bronchi - mucus, cilia
- gut - acid
- rapid pH change
- flushing of the urinary tract
- skin - the physical barrier, fatty acids and commensals
- low pH and commensal of vignina
how does epithelial barrier against infection
epithelial barriers against infection :
- mechanical
> intact epithelial surface
> longitudinal flow of air or fluid
> movements of mucus by cilia
- chemical
> skin - fatty acids
> enzymes - lysozyme in saliva and tears
> pepsin in the gut
> low pH
> antibacterial peptides - microbiological
> commensal bacteria - competition for nutrients
> blocking off adhesion
> production of anti-microbial substances
what happens when microbes invade
when barriers get broken, microbes invade
Inflammation and tissue injury are caused by white blood cells that leave the blood and go into the skin and kill microbes growing in the wrong place.
what are the mucosal tissues a principal site for and what is the characteristic of mucosal surfaces
mucosal tissues are a principal site for infection and allergic reactions.
mucosal surfaces are:
- absorptive
> absorbs food and oxygen yet defends against dangerous antigens
> barrier against antigen penetration
> responsive to antigen penetration
mucosal surfaces contain 67% B lymphocytes which is 2-3x more than detected in the spleen, bone marrow and lymph nodes
what is the role of mucosal cells in immune defence
roles of the cells in immune defence are:
- slow down the invasion
- signal other areas of the immune system danger
what cells leave the blood and are involved in immune defence at the mucosal surfaces
- lymphocytes
- antigen-presenting cells- Langerhans cells, dendritic cells and macrophages
- neutrophils, natural killer cells
what do commensal bacteria signal and where are they found
main immune stimuli for neonates are signals from the microbial environment/ commensal bacteria in the gut e.g infections in respiratory
they are found on mucosal surfaces and the skin
what prevents commensal bacteria from penetrating into the mucosa
commensal bacteria aren’t always harmless
thus epithelial and immune factors, e,g, antibodies prevent their adherence and penetration into the mucosa
what are neutrophils and how does it indicate megaloblastic anaemia
neutrophils are inflammatory cells and are first on the scene of danger e.g. infection, posttrauma.
normal neutrophils have an average of 3 lobes and always fewer than 5 lobes, a hyper-segmented nucleus (6 or more nuclear lobes) in neutrophils is an indication of megaloblastic anaemia
how do monocytes become macrophages and what are the different types
monocytes become macrophages when they enter tissues
the different types are:
- Kupffer cells in the liver
- Alveolar macrophages in the lungs
- microglial cells in the brain
- osteoclasts in bone
how are macrophages activated
Bone marrow/ stem cell –> blood monocyte –> tissue macrophage –> activation –> activated macrophage
↓
differentiation of macrophage
what is opsonisation and where are they found
opsonisation is a molecule that binds to the surface of a foreign antigen, e,g, immunoglobulin (antibodies) complement protein fragments.
opsonin receptors are found on the surface of phagocytes.
opsonisation cells increase efficiency of phagocytosis
how is killing achieved when a pathogen is marked with opsonin
once a pathogen is marked with opsonin, killing is achieved via 1 or 2 mechanisms:
1-ingested and killed by an immune cell (phagocytosis)
2- killed directly without ingestion
why do macrophages express a range of PRRs and what does it lead to
macrophages express a range of pattern recognition receptors (PRRs) on the cell surface. this is in order to recognise pathogen-associated molecular patterns (PAMPs).
some PAMP-PRR engagement can lead to phagocytosis and other PAMP-PRR engagement can lead to the production of cytokines and chemokines.
