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SFM > Immuno > Flashcards

Immuno Flashcards

SFM Immuno

1
Q

CD34 is T, P or M?

A

Pluripotent; will give rise to either Myelod progenitor or lymphoid progeitor that are both multipotent

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2
Q

G-CSF

A

Will turn myeloid progenitor to a myeloblast the precursor cell for BEN

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3
Q

M-CSF

A

Will turn myeloid progenitor to a Monoblast the precursor for monocytes and DCs

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4
Q

IL-7

A

Controls bone marrow lymphoid progenitor cells to differentiate into B cells

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5
Q

T cell differntiation

A

When lymphoid progenitor cells migrate from BM to thymus under IL 17 they be T cells son

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6
Q

breakdown of WBC %%

A 
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
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7
Q

CBC

A

complete blood count; a common lab testing; ie increased neutrophils = infection or inc. eosinophils = parasite

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8
Q

DIFF

A

differential leukocyte count

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9
Q

CBC with DIFF

A

complete picture of both tests

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10
Q

Giemsa stain

A

RBCs and especially WBC wont be visible unless stained. GS is basic stain methylene blue and acidic stain eosin

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11
Q

CD markers for T cell

A

CD3, CD4, CD8

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12
Q

CD markets for B cells

A

CD19, CD20

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13
Q

Cd marker for NK cell

A

CD56

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14
Q

Cd marker for Monocyte/MO

A

CD14

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15
Q

4 steps of phagocytic cells action

A

Recruitment, recognition, ingestion, digest that motha; remember active phagocytes also secrete cytokines!!!!

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16
Q

Neutrophil granules

A

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

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17
Q

defenins

A

small cysteine-rich cationic proteins which activate against bacteria, fungi and both enveloped and naked viruses

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18
Q

Leukocytosis

A

elevated WBC, usually neutrophilia, commonly indicative of infection. A 2-3x inc in WBC can be seen in just 4-5 hours.

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19
Q

“left-shift”

A

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

20
Q

Leukopenia

A

reduction of circulating WBCs, often caused by cancer therapy. suspect it if Pt shows frequent or unusual infections

21
Q

3 ways PMNs kill bacteria

A

phagocytosis, degranulation, NETs

22
Q

Monocyte life span

A

usually a few days; can be extended dramatically during inflamation

23
Q

Monocytosis

A

inc monocytes in blood; due to chronic infections, autoimmune disorders, certain cancers, sarcoidosis

24
Q

Mast and bosphils

A

defense against parasites, key role in allergic y anaphylactic reactions, contain bosphilic (purple-black) granules: histamine, serotonin, heparin, cytokines, chemokines

25
Q

Mastocytosis

A

inc of mast cells (in tissues of course); itching, hives, anaphylactic shock (histamine)

Urticaria pigmentosa

26
Q

Eosinophils

A

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

27
Q

NK cell recognition

A

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

28
Q

Inflammatory signs result from biochemical actions of vasoactive mediators:

A

Prostaglandins, leukotrienes, histamine (all from mast cells)

bradykinin

29
Q

Body rxn to inflamtion

A

BV become permeable = warm, red, swelling
tissue and microorganisms debris = pus
inflammatory mediators stimulate nerves = pain
chills, fever, muscle aches

30
Q

Fever

A

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

31
Q

PAMPS

A

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

32
Q

ex. of PAMPs

A

porins, lipoproteins, LPS, lipoteichoic acid, techoic acid, mannoproteins, B-glycans, lipoarabinomannan

33
Q

PRR general properties

A

broad specificity, germ-line encoded, nonclonal distribution (means 2 cells have the same-unlike B/T cells)

ex. mannose receptor

34
Q

Extra-cellular TLRs vs intra

A

1,2,4,5,6 vs 3,7,8,9

35
Q

TLR 3789

A

3-dsRNA-TRIF only, 4 goes to both, rest to MyD88
7-ssRNA
8-ssRNA-NK cells only
9-CpG DNA

36
Q

Why do TLRs exist

A

Entire point of TLRs is to initiate TFs that code for cytokines and other mediators; NF-KB and TRF are major TFs

37
Q

TLR 4 activation

A

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

38
Q

TLR deficiency

A

innate system cant kill microbes leading to recurrent infections, failure of cytokines being produced during bacterial infection, common termed MyD88 and IRAK4 deficiency

39
Q

NLRs

A

scaffolding proteins that assemble signaling platforms that trigger NF-KB and MAPK; make inflammasomes that activate protease caspase-1

40
Q

protease caspase-1

A

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

41
Q

what triggers NLRs to assemble into inflammasomes like the power rangers?

A

bacterial products, crystals, K+ efflux, ROS

42
Q

NON infectious inflamation

A

DAMPs are endogenous released from damaged or dying cells and induce inflammation by activating innate immune system

43
Q

DAMPs

A

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

44
Q

HMGB1

A

nucleolus protein passively released by necrotic cells activating NFKB via TLR2/3 signal

45
Q

examples of DAMPs

A

HMGB1, uric acid, HSP

SFM (4 decks)

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