Immuno Flashcards
SFM Immuno
CD34 is T, P or M?
Pluripotent; will give rise to either Myelod progenitor or lymphoid progeitor that are both multipotent
G-CSF
Will turn myeloid progenitor to a myeloblast the precursor cell for BEN
M-CSF
Will turn myeloid progenitor to a Monoblast the precursor for monocytes and DCs
IL-7
Controls bone marrow lymphoid progenitor cells to differentiate into B cells
T cell differntiation
When lymphoid progenitor cells migrate from BM to thymus under IL 17 they be T cells son
breakdown of WBC %%
75% nucleated cells in BM commited to be a leukocyte 50-75% of these will be neutrophils 90% of WBCs remain in Bm for storage 2-3% circulating 7-8% in tissue
CBC
complete blood count; a common lab testing; ie increased neutrophils = infection or inc. eosinophils = parasite
DIFF
differential leukocyte count
CBC with DIFF
complete picture of both tests
Giemsa stain
RBCs and especially WBC wont be visible unless stained. GS is basic stain methylene blue and acidic stain eosin
CD markers for T cell
CD3, CD4, CD8
CD markets for B cells
CD19, CD20
Cd marker for NK cell
CD56
Cd marker for Monocyte/MO
CD14
4 steps of phagocytic cells action
Recruitment, recognition, ingestion, digest that motha; remember active phagocytes also secrete cytokines!!!!
Neutrophil granules
are pre-synthesized so ready to roll asap (unlike MO) they include: peroxidase, lysozyme, defensins, degradative enzymes
can also produce inflammatory mediators: cytokines, prostaglandins, leukotrienes
defenins
small cysteine-rich cationic proteins which activate against bacteria, fungi and both enveloped and naked viruses
Leukocytosis
elevated WBC, usually neutrophilia, commonly indicative of infection. A 2-3x inc in WBC can be seen in just 4-5 hours.
“left-shift”
During serious infection the BM is ejecting Neutrophils faster than they can mature shifting visible N to the left of maturity graph. You see band cells (immature N whose nucleus looks like a band) and during extreme cases you see myelocyte
Leukopenia
reduction of circulating WBCs, often caused by cancer therapy. suspect it if Pt shows frequent or unusual infections
3 ways PMNs kill bacteria
phagocytosis, degranulation, NETs
Monocyte life span
usually a few days; can be extended dramatically during inflamation
Monocytosis
inc monocytes in blood; due to chronic infections, autoimmune disorders, certain cancers, sarcoidosis
Mast and bosphils
defense against parasites, key role in allergic y anaphylactic reactions, contain bosphilic (purple-black) granules: histamine, serotonin, heparin, cytokines, chemokines
Mastocytosis
inc of mast cells (in tissues of course); itching, hives, anaphylactic shock (histamine)
Urticaria pigmentosa
Eosinophils
large secondary granules contain 4 basic proteins, small granules contain histamine, peroxidase, lipase and MBP
basic proteins involved with parasite defense, helminth defense also directly associated w epithelial cell damage, exfoliation and bronchospasm
NK cell recognition
NK cells don’t need prior stimulation or immunization, normally recognize self Ags, if Ags are NOT on a cell the absence of Ag activate
Inflammatory signs result from biochemical actions of vasoactive mediators:
Prostaglandins, leukotrienes, histamine (all from mast cells)
bradykinin
Body rxn to inflamtion
BV become permeable = warm, red, swelling
tissue and microorganisms debris = pus
inflammatory mediators stimulate nerves = pain
chills, fever, muscle aches
Fever
Fever is not related directly to pathogenic factors: rather pyrogenic cytokines IL1, IL6 in MO induce via hypothalamus
most pathogens replicate poorly in elevated temp’s
PAMPS
Allows innate immunity to discern self from non-self; they are unique to classes of pathogens, they are often required for pathogen survival so cannot be altered, suppressed or hidden. They have no similar structure to self Ags
ex. of PAMPs
porins, lipoproteins, LPS, lipoteichoic acid, techoic acid, mannoproteins, B-glycans, lipoarabinomannan
PRR general properties
broad specificity, germ-line encoded, nonclonal distribution (means 2 cells have the same-unlike B/T cells)
ex. mannose receptor
Extra-cellular TLRs vs intra
1,2,4,5,6 vs 3,7,8,9
TLR 3789
3-dsRNA-TRIF only, 4 goes to both, rest to MyD88
7-ssRNA
8-ssRNA-NK cells only
9-CpG DNA
Why do TLRs exist
Entire point of TLRs is to initiate TFs that code for cytokines and other mediators; NF-KB and TRF are major TFs
TLR 4 activation
LPS binds to TLR-4 activating Ap MyD88 which activates IRAK4 which -P TRAF6 which -P IKK which -P IkB which degrades and frees NF-KB which goes into nucleus and does WORK
TLR deficiency
innate system cant kill microbes leading to recurrent infections, failure of cytokines being produced during bacterial infection, common termed MyD88 and IRAK4 deficiency
NLRs
scaffolding proteins that assemble signaling platforms that trigger NF-KB and MAPK; make inflammasomes that activate protease caspase-1
protease caspase-1
process the inactive (zymogen) cytoplasmic precursor (which is there bc of NFKB bc of TLR) into the secreted forms of IL-1B and IL-18 which are both potent proinflammatory
what triggers NLRs to assemble into inflammasomes like the power rangers?
bacterial products, crystals, K+ efflux, ROS
NON infectious inflamation
DAMPs are endogenous released from damaged or dying cells and induce inflammation by activating innate immune system
DAMPs
can originate from diff sources and be EC proteins, IC proteins and plasma proteins
usually recognized by TLRs on MO (CD14) and all will stimulate TNF-a and IL-1
HMGB1
nucleolus protein passively released by necrotic cells activating NFKB via TLR2/3 signal
examples of DAMPs
HMGB1, uric acid, HSP
