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immuno: tolerance and autoimmune disease Flashcards

1
Q

tolerance

A

process by which body ensures immune responses are directed against foreign Ags or altered self (tumors) NOT against normal self tissues/cells

  • specific unresponsiveness of individual to an Ag
  • need Ag-sp rec. to be tolerant
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2
Q

T and B lympho: Ag binding rec

A

TCR (T)
Ig (B)
generated at random, potential for self rxn

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3
Q

tolerance that occurs early in lymphocyte development

A

central tolerance

peripheral tolerance catches “escapees” (from both is rare)

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4
Q

central B cell tolerance: once B cells express IgM on surface in BM–>tolerance induced via

A

clonal anergy: (soluble Ags) become “tolerant” OR

clonal deletion: (particulate, cell-assoc. Ags) dev. arrested–>apoptosis

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5
Q

peripheral B cell tolerance

A

constant low level stim. of BCR but no secondary sigs (T cell, inflamm) maintains B cell in anergic/unresp. state

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6
Q

central T cell tolerance

A

in thymus
cell clones that strongly recog. self-peptides pres. in MHC molecules–>apoptosis
(almost always self peps in thymus)

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7
Q

peripheral T cell tolerance

A

primary stim of T cells (MHC/peptide-TCR) w.out secondary stim (B7-CD28)–>no IL-2 prod–>clonal anergy
B7-CD28 interaction needed to stabilize IL-2 mRNA
cannot become activated
if repeatedly stim–>apoptosis
more rapid and prolonged than B cell tolerance
reg. T cells can inhibit activation of T cells by self peptide/MHC

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8
Q

regulatory T cells (Tregs/T suppressor cells)
+??
cytokines??
lysis of ??

A

typ. CD4+, FoxP3+
produce inhib. cytokines:
IL-10 (Th2) inhibits Th1 response
TGF-B suppresses T lymphocyte prolif (w.out: uncontrolled inflamm. response)
lysis/apotosis of B/T cells expr. peptides w. HLA (via CD8+)
specific suppression

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9
Q

regulatory B cells (Bregs)

A

produce IL-10: inhib Th1 CD4+ and CD8+ cells, can dampen auto reactive responses
(dec. in MS, SLE)

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10
Q

individuals that may be anergic to TB skin test

A

MMR vaccine, have measles

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11
Q

immune response depends on inherited HLA types, i.e.

A

HLA-B27 in ank spond and reactive arthritis

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12
Q

immunogen factors

A

dosage over time may induce tolerance
self-Ags may be hidden–>exposed by trauma–>IR (lens prot. of eye, synovial chondrocytes, sperm. Ags)-sympathetic opthlamia
weak immunogens induce tolerance

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13
Q

etiology of AIs

A

genetics (HLA)
molecular mimicry of IDs–>cross-reacting IR
environ. triggers (celiac)
impaired immunoreg mechs (T cell defects, imm. deficiency)
hormonal/gender (F>M, estrogen)

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14
Q

exs of molecular mimicry

A

S. pharyngitis: RF and heart valve destruction
H. pylori: gastric ca
Campylobacter jejuni: Guillain-Barre (IR agains LPS, cross reacts with motor nerves–>sev. paralysis, polyneuritis)
Klebsiella: ank spond (chr. inflamm, fibrosis, ossification of spine articulations, 90% HLA-B27+, HLA classI)
pathogens that can polyclonally activate lymphos

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15
Q

celiac disease (CD)

A

malnutrition, diarrhea, abd pain from intestinal inflamm. from gluten
-bowel mucosa changes: villus atrophy, T cell infiltration (CMI)
>95% have autoAgs agains tissue transglutaminase (anti-TG)
>90% have HLA-DQ2, the rest 10% HLA-DQ8
-assoc. with IgA deficiency

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16
Q

Myasthenia gravis

A

organ-specific: anti-ACh receptor Abs at NM junctions, organ specific
blocks nerve impulses–>sev. musc wkness
eyelid drooping, diff chew/swall/breathe–>resp fail
assoc. w/ HLA-DR3

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17
Q

autoimmune hemolytic anemia (AIHA)

A

org-sp: Abs agains Rh antigen or “I” Ags, target RBCs for destruction via compl. med lysis or phago by macros (spleen)
primary or sec. to another illness

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18
Q

AIHA dx

A

anemia, hemolysis, reticulocytosis, low haptoglobin, inc. LD, elev. ind. bilirubin, + direct antiglobulin test (Coombs test)

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19
Q

AIHA caused by…

A

hemagluttinins:
warm (IgG, find RBC at 37d, sp. for Rh Ag) or
cold (IgM, attach RBC when seen up to 30% of pts w. Mycoplasma pneumonia)

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20
Q

SLE

A

systemic, multi organ: Abs against ds-DNA (ANAs)–>form soluble ICs–>trapped in BM of kidneys, arteriolar walls, synovium–>activate complement, attract PMNs and other granulos–>local, acute inflammation–>fever, jt pain, malar face rash (butterfly) CNS, heart, kidney damage

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21
Q

80% of individuals with ??? will have SLE

A

complement deficiency: C1, C4, C2

due to lack of C3b production (opsonizer for phagos)

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22
Q

SLE: spontaneous ??
loss of control of ???
M or W??
presenting age??

A

remissions and exacerbations
B cell system (lack of C3b)
10x more freq. in women
15-45 yrs

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23
Q

SLE genetically linked to HLA…

A

HLA-DR3 and -DR2 (MHC Class II)

24
Q

SLE dx

A

presence of ANA by ind. fluorescent Ab staining on Hep-2

type/pattern helps w. dx, px, classification

25
Q

scleroderma

A

systemic: fibrosis, arthritis, hair loss, arteritis, GIT, kidneys, lungs, Raynaud’s
more EC matrix molecules (collagen) produced
ANAs against topoisomerase-1 and RNA polymerase I (sometimes centromere Ags) (synthesis enzs. vs DNA, RNA)
diff. staining patter than SLE
W>M, pres. 30-50 yrs

26
Q

Sjogren’s syndrome

A

systemic: inflamm./destruction of exocrine glands (sal, lacrimal)–>dry mouth, dry eyes
50% have coex. AI
Abs against SS-A (Ro) and SS-B (La) (cytoplasmic prot-RNA complex Ags)
Abs agains muscarinic ACh rec (M3R) responsible???

27
Q

Sjogen’s dx

A

ELISA, western blot

NOT IFA

28
Q

Graves’ disease

A

hyperthyroidism
TSI (TS Ig) mimics TSH and binds/activates TSH receptor
W>M 4:1
HLA-DR3
passive, natural acq. Ab in neonate–>transient hyperthy.

29
Q

TBIIs

A

thyroid binding inhibitory IgGs: block TSH rec–>hypothyroidism (diff. epitope)
NOT Grave’s

30
Q

Goodpasture’s syndrome

type ?? hypersn

A

type II hypersn-med
Abs agains a3chain of BM collagen (type IV), bind BM in renal glomeruli–>dec. Ur output, inc. BUN, Cr
sometimes pulm alveoli–>hemoptysis, diff breathing
Fc portion of Ab ligates Gcy rec on monos, neutros, tissue basos, mast cells–>activation, complement activation, tissue injury

31
Q

MS

A

T cell mediated, demyelination of CNS tissue, loss in nerve transmission
gen. susc, environ. exposure
CD4+, CD8+ involved, MHC class II present–>DTH response

32
Q

relapsing-remitting MS

A

myelin destroyed, inc. in density of Na+ channels to overcome loss of AP–>neurological function restored

33
Q

chronic progressive MS

A

myelin AND AXONS destroyed–>preventing function return

34
Q

MS links

A

EBV
Adenovirus 2
Hep B
HLA-DR2

35
Q

DM type 1

A

T cell-mediated, CD8+ CTLs destroy insulin-prod. Beta cells of pancr. islets of Langerhans (Abs play minor role)
CD8+ T cells sp. for insulin pres. in HLA-A2–>Beta cell destruction
“reverse vaccine” in making, dec. CD8+ response against pro-insulin

36
Q

RA

A

BOTH Ab and T cell mediated
initiated by IC deposits–>sustained by chronic inflamm. infilt of synovial mem: macros, T cells, plasma cells–>aff. cells rel. cytokines, enz, granular components–>create “pannus” (fibrovasc tissue)–>destroys cartilage, exposes chondrocytes to imm. damage

37
Q

RA markers

A

ACPAs : anti-citrullinated peptide Abs (2/3 RA pts), 90-95% likelihood, early marker
RF (IgM agains IgG Fc) titer do not always correlate with occurrence/severity

both form ICs deposited in synovium–>complement–>rel. chemotactic factors

  • 20-30% RA pts have no RF, other conditions have RF (SLE)
  • RA may be ANA+
38
Q

RA may happen in ?? pts, showing Ab response is not essential to pathogen of disease

A

agammaglobulinemic

39
Q

Hashimoto’s thyroiditis

A

T cell mediated (mono infiltrate, DTH, Type 4 hypersn. rxn)
Abs against thyroid peroxidase and thyroglobulin
dry skins, puffy face, brittle hair/nails, cold feeling
HLA-DR5, -DR8, -B8

40
Q

myasthenia gravis tx

A

cholinesterase inhibitors

41
Q

SLE lupus nephritis tx

A

organ transplant/renal dialysis (IC formation)

42
Q

IC mediated AI disease can be tx w.

A

plasmaphoresis

43
Q

immunosuppressive tx

A

anti-mitotics and cyclosporine (bad SEs! like infection)
anti-inflammatory (steroids, NSAIDs-PUD)
these do not reverse cause, tx end-stage

44
Q

new, radical tx for life-threatening SLE, scleroderma

A

BM ablation

45
Q

cytokine tx for MS

A

INF-B 1a

46
Q

Ab tx: RA, ank spond, psoriasis

A

TNF-a or TNF-a rec blockade

Infliximab, Etanercept, Adalimumab, Golimumab, Certolizumab pegol

47
Q

Ab tx w. costim modulation of T cell activation for RA

A

abatacept (CTLA-4-IgG fusion protein)

48
Q

targeting B- cell using anti-CD20 Ab tx

A

Rituximab

49
Q

IL-6 rec blocking for RA

A

Rocilizumab

50
Q

???: humanized Abs against ??? for MS

A

Natalizumab

a4 integrins

51
Q

???: human MoAb against BAFF cytokine (dec. B cells) used for ???

A

Belimumab, Benlysta

SLE

52
Q

give low dose Ag….

A

“oral tolerance”

53
Q

another tx: activation of Ag-sp. Th3 following low oral doses of Ag, how it works

A

CD4+ T cells (in Peyer’s patches, LP of intestine) cause isotype switching of B cells to produce IgA
if low dose Ag, T cells
–>Th2–>IL-4 and IL-10 (suppr. Th1) OR new phenotype:
–>Th3–>only TGF-B (suppr. Th1 and Th2 activation, inhib. inflamm. cytokine production)

54
Q

if large dose Ag admin..

A

CD4+ T cells clonally exhausted, anergic (unknown)

55
Q

clin. trials for MS

A

oral bovine myelin–>appearance of myeline basic protein-sp. Th3 in blood

56
Q

clin. trials for RA

A

oral type II collagen, improvements

57
Q

clin. trials for preventing allograft rejections

A

oral feeding of HLA molecules

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