Innate Immune System Flashcards
What are the six routes of entry?
airway GI tract GU tract External surface Wounds and abrasions Insect bites
what is the first phase of response to initial infection
innate immunity:
- immediate response
- 0-4 hours
What is the second phase of response to initial infection
early induced response:
- 4-96 hours
what is the third phase of response to initial infection
adaptive immune response:
>96 hours
what are the three barrier to infection
chemical
mechanical
microbiological
chemical barriers
- fatty acids not he skin
- enzymes (lysozyme) in the saliva, sweat and tears.
- low pH in the stomach
- antibacterial peptides such as defensives (skin and gut) and cryptidins (gut)
mechanical barriers
- tight junctions between cells which prevents access
- air and fluid flow across the epithelium
- movement of mucus by cilia
microbiological barriers
normal flora compete for nutrients and attachment (biofilms), and also produce antibacterial substances (colicins)
what kind of receptors help to enhance the function of macrophages and monocytes
- mannose receptor
- glucan receptor
- scavenger receptor
- CD14 (LPS)
- CD11b/CD14 (CR3)
What are all cells derived from
hematopoietic cells
monocyte
bilobed
large cells approximately 10 microns
becomes a macrophage when it enters the tissue
- phagocytosis and activation of T cells and initiation of immune response
what is another name for granulocytes
polymorphonuclear (PMN) leucocytes
neutrophils
70% of all WBC
multinucleated (lots of lobes)
- phagocytosis and killing of microorganisms
short time spent in circulation
eosinophils
2% of all white blood cells filled with granules and is bilobed - killing of antibody-coated parasites through release of granule contents histamine, peroxidase, lipase circulate for 12 hours
neutropenia
low number of neutrophils
may be genetic or the result of medication including chemotherapy
Chronic Granulomatous disease
failure in respiratory burst, superoxide production limited, antibacterial activity impaired
alpha 1-antitrypsin deficency
elastase from neutrophils not adequately inhibited, excessive tissue damage during inflammation-pulmonary emphysema
eosinophilia
increase in eosinophils, seen in parasitic infection of the gut, some vascular diseases, Hoskins disease, Addisons disease
eosinopenia
often seen when glutocorticoids used
basophils
function similar to mask cells and eosinophils - dark purple granules
mast cells
lots of granules appear very dark with light nucleus
- when activated they release alot of substances that effect vascular systems
- expulsion of parasites from the body through the release of granules containing histamine and other active agents
what are within the two divisions of lymphocytes
B AND T cells the adaptive immune response: - B cells producing antibodies - T cells becoming helper T cells (CD4) - T cells becoming cytotoxic T cells (CD8)
Natural killer cells
recognise virally infected cells non-specifically
dendritic cells
bridges the innate immune system and adaptive immune responses.
- specialised in antigen uptake and antigen presentation
What do NK cells produce and what are the actions
- induce resistance in viral replication in all cells
- increase MHC class 1 expression and antigen presentation in all cell s
- activates NK cells to kill virus-infected cells
The key difference between NK and CD8 T cells
NK cells are not antigen specific. Also they do not require to undergo the lengthy clonal expansion of T cells in lymph nodes when virus is detected
What happens if a cell presents a MHC class1 receptor?
it send a NO KILL signal and therefore the NK cell leaves it alone and continues to monitor elsewhere
what happens there is no MHC receptor presented (therefore is a virus infected cell)
Sends a KILL ME signal and therefore the NK cells is activated to degrade the cell
What are the two different types of complement pathway
classical pathway = antigen binds to specific antigen on pathogen surface
alternative pathway = pathogen surface creates local environment conclusive to complement activation
What are the further pathways of the these complement pathways
- recruitment of inflammatory cells
- opsonisation of pathogens, facilitating uptake and killing by phagocytic cells
- lysis and death of pathogens
what is protein 3b
membran -binding protein and opsonin
what are proteins C5a and C3a
they are peptide mediators of inflammation
how is the classical pathway initiated
by activation of the c1 complex
what causes the alternative pathway
caused by spontaneous hydrolysis (tickover) of serum C3, which then bind factor B allowing cleavage by factor D into Ba and Bb. The resulting soluble C3 convertase cleaves C3 to C3b, which binds to membranes.
role of C5a
C5a assists in the phagocytosis of C3b covered bacteria
What proteins form the membrane attack complex
- C5b binds C6 and C7
- C5b, 6, 7, complexes bind to the membrane via
- C8 then binds to this complex and inserts into the cell membrane
- C9 molecules then bind to the complec and polymerise
this punches a hole in the bacterial surface therefore resulting in the spilling out of its contents which inevitably leads to death
What are some examples of proteins which inhibit the membrane attack complex formation
DAF: Decay accelerating factor
MCP: membrane cofactor protein
CR1: complement receptor 1
