Inflammation, Innate and Adaptive Immunity

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  • Created by: Sarah
  • Created on: 16-05-17 09:28
what do monocytes do?
migrate to tissues and differentiate
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what are monocytes function?
phagocytosis, antigen presentation and cytokine production
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what Immune system cells are part of the granulyte series
mast cells, basophils, eoisoniphil, neutrophil
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what is the least common WBC?
basophils
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what do basophils release? why?
prostanglandin, histamines, increase permeability of capillaries and dilation
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what is the key role of mast cells in?
anaphalyxis and allergy
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what do mast cells contain granules of? (3)
1)histamine 2) heparin 3) cytokines such as TNFalpha,IL4
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mast cells release cytokines such as?
IL4 and TNFalpha
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what percentage of circulating WBC is neutrophils?
50-60%
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what do neutrophils form at the site of injury?
puss as they die
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what is the function of neutrophils?
1) pagocytyose microbes 2~) release anti-microbials 3) generate extracellular neutrophil traps 4) release cytokines to recruit macs
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an anti parasitic response responds to what cell?
eosinophils
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what is the function of eosinophils?
1) present antigen to adaptive IS 2) generate cytokines 3) kill cancer cells
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what are released in acute inflammation?
neutrophils
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what can cause an impact in permeability (vascular)?
histamines
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what does the reduction in blood velocity promote?
margination and diapedesis
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what is diapedsis?
passage of blood cells through intact walls of the capillary
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what is margination?
process in which free flowing leukocytes exit the blood stream and initiate leukocyte and endothelial cells interactions (cells move to outside of vessel and interact with endothelial cells)
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what is the sequence of events in diapedesis?
rolling, activation, adhesion, locomotion, diapedesis
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what is the definition of inflammation?
the innate response to infectionj (real or perceived)
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what allows the polymorphs to undergo diapesis, what do the endothelial cells have that polymorphs stick to?
integrins (ICAM-1)
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how do polymorphs know how to get to the site of inflammation?
move down a chemotaxic gradient set by chemokines
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how do they manage to break the basement membrane to get through?
dissolve it with proteases
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what does the chronic inflammation response involve?
lymphocytes, plasma cells and macs
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if there's extreme positive feedback of cytokines on WBCs what can it turn into
systemic cytokine storm. Fatal consequences- anaphalyxis, septicemia
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what are some early inflammation responses inhibited by?
anti-histamines
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what is affected in an immediate transient response?
small blood vessels- damage by histamine, bradykinin, NO, complement, leukotins, platelet activating factor
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what is released from intact endothelial cells?
nitric oxide
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what can cause an immediate transient response?
nettle sting, insect bite
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what would cause an immediate persistent response?
burns, endothelial cell injury
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characteristics of immediate persistent response?
any vessel involved, endothelial cell damage, injury due to bradykinins, NO, complemtn, leukotriens, platelet activating factor and potentiated by prostaglandins
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what is a delayed persistent response likely to be from?
radiation damage to endothelial cells, sunburn, DXT (radiotherapy), bacterial toxins
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what are affected in a delayed persistent response?
capillaries and venules
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what can early responses depend on (2)?
1) extent of damage 2) site of damage
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what are arachidonic acid derivaties usually?
cell derived chemical mediators
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which pathway makes prostaglandin form arachidonic acid?
cyclo-oxygenase pathway
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what pathway makes leukotrienes from arachidonic acid?
lipo-oxygenase pathway
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what inhibits cyclo-oxygenase pathway (prostaglandin)?
aspirin
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what 3 things indicate an infection?
1)C-reactive protein 2)neutrophils, eosinophils and lymphocytes (NEL) 3) HPA hormones
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what would indicate a viral infection?
lymphocytes
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what are HPA hormones?
hypothalamic pituitary, adrenal
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what kind of HPA hormones indicates an infection?
growth hormone, ACTH (adrenocorticotropic hormone)
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what does ACTH cause?
is a consequence of biological stress that causes increased production of cortisol
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what would indicate a allergy or parasitic infection?
eosinophils
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what would show a bacterial infection?
neutrophils
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chronic inflammation results in what?
fibrosis (loss of function)
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what shows chronic inflammation?
angiogenesis (dev of new blood vessels),, monoculear cell infitrate, fibrosis
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what would cause acute inflammation?
infarction, bac infections, toxins or trauma
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what would cause chronic inflammation?
vira infections, chronic infections, autoimmune disease, persistent injury
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what could be resolutions to acute inflammation?
healing, pus formation, fibrosis, clearance of injurous stimuli, clearance of mdiators and inflammatory cells, replacement of injured cells
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what diseases can have chronic inflammation?
TB, symphillis, leprosy and arthiritis
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what might not have an acute inflammotory phase before going chronic?
abcess, rheumatoid arthiritis
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what is osteomyelitis?
chronic infection of the bone, chronic inflammation, poor vascularisation means poor recovery
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inflammatgion involes cells and mediators that are also involved in what?
immune responses, blood clotting and repair
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characteristics of inflammation?
rubor (redness) dolor (pain, swelling (tumour), calor (heat)
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what are the features of arachidonic acid?
produced locally and degraded quickly, various responses eg vasodilation
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what is granulomata?
encloses infected cells with immune cells
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2 types of chemical mediators?
plasma derived and cell derived
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what are the cell derived chemical mediators?
lysosomes, kines family (sig molecules), arachidonic acid
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what are plasma derived chemical mediators?
kinin family -) reinforce vascular changes
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what causes heat and overrides the hypothalamus?
pyrogens
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what are sinuosoids?
type of blood vesel large intercellular gaps and intracellular basement M
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where are sinusoids found?
bone marorw, lymph nodes and liver
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what do continous blood vessel allow through?
only small molecules like water
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where are continous blood vessels found?
muscles, gonads, fingers, CNS
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what do fenestrated blood vessels allow through?
some small molecules and proteins
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what makes lots of chemical mediators?
the liver
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difference between cytokines and chemokines?
chemokines chemical based, cytokines-pro based
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what is the main features of the adaptive IS?
memory, tolerance, specificity
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where do B cells differentiate?
in the bone marrow
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where do T cells differentiate?
in the thymus
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what kind of response do T cells give?
cell-mediated immunity
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what response do B cells give?
antibody-mediated immunity+ immunological surveillance
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what do both T and B cells start from?
hemocytoblasts -> lymphoid stem cells then differentiate to b or t cells
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from lymphoid stem cells what are the 2 types of B cells produced?
natural killer clels or B cells
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what are major histocompatibility complex proteins?
cell surface glycoproteins that bind antigens and present them to passing cells of the immune system
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MHC I activates what cells?
cytotoxic T cells
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what cells have MHC I's?
all nucleated cells = constitutive
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what are the major players in adaptive immunity?
lymphoid tissue, APCs, follicular dendritic cells, T+B lymphocytes
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where are the T cells in the lymph node?
In the paracortex/interfolliclar zone
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where are B cells in the lymph node?
cortex/follicular zone
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what is in the Cortex with B cells in the lymph nodes?
follicular dendritic cells
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what surrounds the lymph gland?
marginal sinus
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what do APCs do?
display fragment of invading pathogens on their surface + presnt them to other IS cells- esp T lymphocytes
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what APC are there?
fixed and free mac (kupffe rcells, monocytes, microglia), epithelia+endothelia, B lymphocytes
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what do lymph nodes do?
drain the excess fluid from the body in through afferent lymphatic out through efferent lymphatic
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in each follicle in lymoh nodes is what?
a germinal centre
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what do follicular dendritic cells do?
help B cells with differentation, make antiboidy reasonable fit for antigen
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what do MHC I do?
present antigen synthesised by cell, viral rna enters which synthesis RNA put on surface
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what does MHC II activate?
T helper cells
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what are MHC IIs in?
APCs ut inducble in many cells
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what does MHC IIs do?
lysosomal digestion of antigen present
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what do cytoxic T cells do?
perforin (perphorate membrane), lymphotoxin, apoptosis
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t helpper cells activate/ form what?
cytotoxic T cells, memory T cels
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what do memory T cells produce
a reserve and rapid response
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what evokes t helper cell activation and division?
a receptor binding of MHC II (APC) to CD4
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what populate and/or circulate through lymphoid tissue?
T cells, B cells and APCs
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what happens to cells in the lymphoid tissues when antigens are presented?
they divide, leave and migrate to infection attracted by chemokines
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what is lymphocyte mobilization for?
taking antigens to lymph nodes to activate cells to respond
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what is the most common form of antibody in the blood?
IgG
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what is the most common antibody in the body overall? why?
IgA, abundant secretion by mucous membranes
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5 types of Igs?
MADGE
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each mature cell produces what (Igs)?
one variant and recognises one epitope
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what makes up the tail region of an antiboy?
heavy chains
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what is the hypervariable region?
antigen binding site (5-10 aa's)
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how long is clonal expansion?
2000s-1
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what are Fc receptors on?
macrophages
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what binds to Fc receptor on macs?
Fc region of IgG antibody
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what do antibodies coat?
bacterium, bound to surface activate complement
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what are Igs recognised by?
phagocytes
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what is there a loss of in development in clonal deletion?
self-reactive lymphocytes in the thymus
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what autoimmune diseases are there?
myasthenia gravis, crones disease, rheumatoid arithiris, psoriasis
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what is the constant region of the antibody
the tail region
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what happens in a secondary response to an antigen?
many more antibodies produced, quicker response
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what are immunoglobins
antiboyds, glycoproteins produced by B plasma cells, recognise and bind specific antigens
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what happens in myasthenia gravis?
autoimmune disease antibodies and IS cells attack Ach receptors in muscle
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