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Chapter 6 Flashcards

1
Q

NK T cells

A

recognize glycolipids displayed by MCH like molecule CD1

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2
Q

CD40

A

expressed on B cells

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3
Q

NK cells

A

express CD16 and CD56

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4
Q

CD16

A

on NK cells
FcR for IgG
Ab dependent cell mediated cytotoxcity (ADCC)

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5
Q

NKG2D

A

family which activates NK cells

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6
Q

CD94 family of lectins

A

inhibit NK cells

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7
Q

cytokines which stimulate NK cell proliferations

A

IL2, 15

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8
Q

cytokines which stimulate NK activation

A

IL12, also stimulated the release of IFN-y

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9
Q

Class I HLA

A

A,B,C
heterodimer of polymorphic alpha (heavy) chain and non-polymorphic beta 2-microglobulin chain
Alpha divided into 1,2,3
alpha 1 and 2 make polymorphic peptide binding cleft
display internal Ags like viruses

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10
Q

Class II HLA

A

P,Q,R
dimer of alpha and beta chains, both polymorphic
alpha 1 and beta 1 create polymorphic peptide binding cleft
present extracellular stuff that has been internalized and processed like bacteria

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11
Q

activated CD4 cells

A

secrete IL2 and express high affinity IL2Rs
IL2 acts as GF in autocrine loop
display CD40L which bind CD40 on B cells and Macrophages

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12
Q

TH1

A

secrete IFN-y

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13
Q

TH2

A

secrete IL4 -> B cells -> IgE plasma cells and IL 5 -> Eos

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14
Q

TH17

A

IL17- neutraphils and monocytes

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15
Q

class switching

A

induced by IFN-y and IL4

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16
Q

Type I hypersensativity reaction

A 
aka immediate hypersensitivity
TH2,IgE -> mast cells -> inflammation
occurs w/in minutes
allergies
systemic or local
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17
Q

initial reaction in type I

A

vasodilation, vascular leakage, smooth m contraction, glandular secretions

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18
Q

late phase reaction in type I

A

begins in 2-24 hours, can last for days
infiltration of Eos, neturophils, basophils, monocytes, and CD4 cells -> tissue damage
IL3,5, GM-CSF all promote survival of eos
IL5 most potent stimulator of eos

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19
Q

secretagoges of mast cells

A

IgE, C5a, C3a, codeine, morphine, adenosine, mellitin, heat, cold, sunlight

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20
Q

leukotrienes

A

C4,D4- most potent vasoactive and spasmotic agents

B4-chemotactic for neutrophils, eos, and monocytes

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21
Q

extreme temperature or exercise hypersenativites

A

not mediated by TH2 or IgE

non-atopic allergy

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22
Q

Type II hypersensativity

A

aka Ab mediated

transfusion reactions, hemolytic disease of newborn, autoimmune hemolytic anemia, drug reactions (haptens)

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23
Q

type III hypersensativity

A

aka immune complex mediated
elicit inflammation at site of deposition
systemic immune complex disease
acute serum sickness

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24
Q

morphology of type III

A

acute necrotizing vasculitis
intense neutrophil infiltration
fibrinoid necrosis

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25
type IV
aka T cell mediated
26
APC released IL12
induced CD4 to become TH1
27
What cytokines released from APC induces TH17
IL1,6,23 and TGF beta
28
CD8 mediated type IV
``` autoimmune following viral infections graft rejection tumor rejection kills with perforins and granzymes releases IFN-a tuberculin reaction, contact dermatitis ```
29
3 requirements of autoimmune disease
presence of immune reaction specific for a self Ag or self tissue evidence that reaction is not secondary to tissue damage, but is primary pathology absence of another well defined cause
30
AIRE
critical for negative selection to occur in thymus for central tolerance
31
Treg cells
express CD25
32
FOXp3 mutations
IPEX
33
PTPN-22
tyrosine phosphatase | rheumatoid arthritis and DMI
34
NOD2
chrons disease | cytoplasmic sensor of microbes
35
IL2R-CD25, and IL7R
MS
36
Epitope spreading
when cell injury releases previously immune privileged self Ags
37
SLE
woman 9-1 2-3x higher in black and hispanic arises in early 20s-30s
38
ANAs in SLE
dsDNA histones (drug induced) non-histone proteins bound to RNA Abs to nuclear agents
39
nuclear florescent- homogenous/diffuse
Abs to chromatin, histones, maybe DNA
40
nuclear florescent- rim/peripheral
Abs to DNA
41
nuclear florescent- speckled pattern
most common, least specific | DNA nuclear constituents
42
nuclear florescent- nuclear pattern
RNA Abs
43
Other Abs in SLE
smooth m, RBCs, platelets, lymphocytes | despite Abs to coagulants are in hypercoagulant state
44
genetics of SLE
HLA-DQ deficiencies in C3,4 fail to remove ICs deficiencies in C1q fail to phagocytosis apoptotic cells
45
drugs that induce SLE
hyralazine, procainamide, d-pencillamine, isoniazid HLA-DR4 Abs to histone
46
mechanism of tissue injury in SLE
Type III | nuclei damaged cells exposed to ANAs -> LE bodies -> engulfed by phagocytes -> LE cells
47
morphology of SLE
fibrinoid necrosis
48
type I and II lupus nephritis
minimal mesangial and mesangial proliferative 10-25% mesangial cells proliferate and IC deposition involving glomerular capillaries
49
type III lupus nephritis
``` focal proliferative glomerulonephritis 20-35% less then 50% glomeruli involved glomeruli have crescent formation fibrinoid necrosis proliferation of endothelium and mesangial cells infiltrating leukocytes, eos intercapillary thrombi deposits primarily subendothelial ```
50
type IV lupus nephritis
``` diffuse proliferative glomerulonephritis 35-60% entire glomerulus affected acutely injured and chronically scarred most severe definitely symptomatic deposits primarily subendothelial ```
51
type V lupus nephritis
``` membranous glomerulonephritis diffuse thickening of capillary walls 10-15% severe proteinuria may occur concurrently w/another class deposits primarily subepithelial ```
52
skin SLE
facial erythema in butterfly area uticaria, maculopapular lesions, and ulcers photosensitive vasculitis w/fibrinoid necrosis
53
joints SLE
non-erosive synovitis w/little to no deformity | effusions common
54
CNS SLE
Abs against synaptic membrane proteins | non-inflammatory occlusion of small vessels due to intimal proliferation
55
pericarditis or serosal involvement SLE
acute, subacute, or chronic acute- fibrous exudate chronic- thickened, opaque, shaggy fibrous tissue
56
CV SLE
damage to any layer of the heart pericardial involvement 50% myocarditis less common, but causes resting tachycardia valvular abnormalities (mitral and aortic), thickened on both superior and inferior surface
57
spleen SLE
slenomegaly, capsular thickening, follicular hyperplasia | central penicilliary aa show intimal and smooth mm hyperplasia
58
lungs SLE
pleuritis in 50% and pleural effusions | sometimes chronic interstitial fibrosis and secondary pulmonary HTN
59
chronic discoid lupus erythmatosus
skin maifestations mimic SLE, but systemic manifestations are rare about 35% ANAs, but rarely against DNA
60
subacute cutaneous lupus erythmatosus
``` primarily skin different from discoid b/c: rash widespread superficial, non-scarring mild to systemic symptoms of SLE Abs to SS-A Ag HLA-DR3 ```
61
Sjogren syndrome
``` dry eyes, dry mouth due to destruction of lacrimal and salivary glands when isolated (primary) called sicca syndrome, usually w/other autoimmune conditions (secondary) ```
62
Sjogren syndrome pathogenesis
``` CD4 and some B cells 75% have rheumatoid factor 80% of ANAs Abs against SS-A, SS-B May be triggered by viral infection of salivary gland ```
63
systemic sclerosis/sclerederma
primarily skin, but GI, kidneys, heart, mm, lungs | progressive interstitial and perivascular fibrosis
64
diffuse sclerederma
widespread involvement at onset w/rapid progression
65
limited sclerederma
skin, often confined to finger and extremities | CREST
66
CREST
calcinosis, raynauds phenomenon, esophageal dysmotility, sclerodactyly, and telangiectadia
67
eitology of sclerederma
CD4 response to unknown Ag in skin -> cytokines -> inflammation -> fibroblasts ANAs: DNA topoisomerase (usually have pulmonary fibrosis) Anticentromere Ab (CREST)
68
Sclerederma- skin
``` edema w/CD4 cells eos capillaries and small aa have thickening of BM subcutaneous calcifications (CREST) claw fingers and masked face tips of fingers auto-amputate ```
69
sclerderma GI
90% progressive atrophy and replacement of mm w/collagens most severe in esophagus -> GERD loss of villi -> malnourished
70
sclerederma MSK
inflammation of synovium hypertrophy and hyperplasia of synovial soft tissues rare joint destruction
71
sclerederma kidneys
66% interlobular aa show intimal thickening -> concentric proliferation of intimal cells not always associated w/HTN, if HTN present usually die from renal failure
72
sclerederma lungs
50% | pulmonary HTN and interstitial fibrosis
73
sclerederma heart
pericarditis w/effusions and myocardial fibrosis | thickening of intramyocardial arterioles
74
clinical features of sclerederma
female:male 3:1 50s-60s blacks
75
mixed CT diseases
clinical features mix of SLE, sclerederma, and polymyositis increased Abs to ribonucleoprotein modest renal involvement
76
polyarteritis nodosa
necrotizing inflammation of walls of vessels | non-infectious vasculitis
77
T cell mediated rejection of transplants
destruction of graft cells CD8 | delayed hypersensativity CD4
78
Ab mediated rejection of transplants
humoral rejections must have preformed Abs to graft HLA previous organ rejection, mulitparous women, prior blood transfusions hyperacute reaction, rarely happens b/c check for Abs to donor HLA if does occur usually vascular damage -> rejection vasculitis
79
hyperacute rejection of kidney
w/in min rapidly cyanotic, mollted, flaccid, scant bloody urine Ig and C' on vessel walls neutrophils fibrinoid necrosis of vessles, coagulative necrosis of kidney walls
80
acute rejection of kidney
w/in days or suddenly months/years later due to termination of immunosupressent therapy
81
acute rejection of kidney- cellular reaction
interstitial mononuclear infiltrate and edema renal failure CD4&8 responds well to immunosupression cyclosporine immunosupressent, but nephrotoxic, so must balance
82
acute rejection of kidney- humoral reaction
``` rejection vasculitis anti donor Abs extensive necrosis of renal parenchyma depotstion of CD4 treat w/B cell depleting agents ```
83
chronic kidney injection
progressive renal failure over 4-6 months vascular changes, interstitial fibrosis, tubular atrophy glomeruli scar w/duplication of BM
84
methods increasing graft survival
- HLA matching - immunosupression- cyclosporine blocks NFAT, proteins which bind B7 costimulators (at risk for EBV, lymphomas, HPV, squamous cell carcinoma, KS) - donor specific tolerance therapies
85
transplantation of hematopoietic cells
BM2 specific | GVH disease
86
acute GVH disease
days-weeks immune system, skin, liver, GI generalized rash -> desquamation destruction of small bile ducts -> jaundice GI ulcers infected tissues have decreased lymphocytes
87
chronic GVH disease
extensive cutaneous injury (looks like sclerderma) liver disease and jaundice GI and esophageal constrictions
88
x-linked/brutons gammaglolinemia
failure of pre-B cell to mature b/c cannot form light chain mutation in cytoplasmic tyrosine kinase (Btk) primarily males B cells absent or decreased, germinal centers underdeveloped T cell mediated reactions normal replacement therapy w/Igs may reach adulthood
89
x-linked gammaglolinemia at risk for
recurrent respiratory infections (staph, strep, flu) susceptible to enteroviruses (echovirus, poliovirus, coxsackevirus) and giardia at risk for arthritis, dermatomyositis
90
common variable immunodeficeny
group of disorders hypogammaglobunemia, usually all, sometimes just IgG sporadic and inherited normal B cell number, but cannot become plasma cells BAFF, ICOS weakly implicated both sexes equally onset childhood/adolescence germinal center hyperplastic due to loss of IgG feedback
91
common variable immunodeficiency at risk for
recurrent sinolulomary pyrogenic infections and hypersensativites at risk for autoimmune conditions and gastric cancer
92
isolated IgA deficency
``` 1/600 people of european descent familial or acquired usually asymptomatic mucosal defenses weakened increase in respiratory allergies and at risk for autoimmunity react to IgA as foreign -> shock BAFF ```
93
hyper IgM syndrome
make IgM, but no other Igs T cells cannot deliver signals to B cells and macrophages 70% have x-linked form due to CD40L mutation, the rest autosomal recessive mutations in either CD40L or activation induced deanimase normal # of T and B cells
94
hyper IgM syndrome at risk for
autoimmune hemolyitic anemia, thrombocytopenia, and neutropenia
95
DiGeorge syndrome
T cell deficiency due to failure of 3rd and 4th phayngeal pouches to form thymus and PT tetany, congenital heart defects, abnormal facies, not familial, deletion of 22q11
96
severe combined immunodeficiency syndrome (SCID)
lots of syndromes all have defects in both humoral and cellular immunity prominent thrush in infants failure to thrive maternal IgG attack -> GVH disease -> morbilliform rash with BM transplant will die w/in a year lymphoid tissue hypopastic
97
x linked SCID
50-60% mostly boys mutation in common y-chain of cytokine Rs thymus has lobules of undifferentiated epithelium gene therapy has been successful, but seem to develop T cell leukemias
98
autosomal recessive SCID
deficiency of ADA- accumulations of deoxy-STP -> toxic to dividing lymphocytes -> Hassels corpuscles mutations in recombinase activating gene JAK3- Kinase associated w/T cell AgRs
99
Bare lymphocytes sydrome
occurs in SCID | don't express MCH II
100
Wiskott-Aldrich syndrome/Immunodeficiency w/thrombocytopenia and eczema
x linked recessive, thrombocytopenia, eczema, recurrent infections, early death thymus normal, but progressive depletion of T cells Do not make Abs to polysacharride Ags and respond poorly to protein Ags Low IgM normal IgG high IgE, and IgA at risk for B cell lymphomas WASP gene BM transplant
101
C2,C1,C4 deficincies
ususally no increased risk of infection, but at risk for SLE-like disease
102
deficiencies in alternative C' pathway
rare properdin factor D recurrent pyrogenic infections
103
C3 deficiencies
affect both alternative and classical pathways | severe risk of recurrent pyrogenic infections and increased risk of IC mediatd glomerulonephritits
104
C5-9
loss of MAC at risk for neisserial infections
105
deficiency in C1 inhibitor
herediatary angioedema loss of inhibition of C1, XII, Kallikrein system treated w/C1 inhibitor from human plasma
106
paroxysmal nocturnal hemoglobinuria
cannot form decay accelerating factor of CD59 which regulate C' factor H mutations underlie about 10% of hemolytic uremic syndromes
107
HIV viral core contains
``` major capsid protein p24 nucelocapsid protein p7/p9 2 copied of genomic RNA 3 viral enzymes (protease, reverstranscriptase, integrase) surrounded by p17 ```
108
HIV p24
target for Abs used in early diagnosis
109
HIV viral envelope
gp120, and gp41
110
pathogenesis
binds to CD4R gp120 must bind to coRs CCR5 or CXCR4 binding initiates conformation change so fusion peptide on gp41 can insert into cell membrane and viral core can enter
111
APOBEC3G
found in naive T cells will mutate viral DNA inactivated when T cell matures
112
HIV in macrophages
can replicate in non-dividing macrophages due to HIV1 vpr gene serve as reservoirs have impaired microbicidal activities, decreased chemotaxis, decreased secretion of IL2, inappropriate secretion of TNF and poor APC ability
113
HIV and DCs
present HIV to T cells | follicular- store HIV on surface FcRs sere as reservoir
114
polyclonal activation of B cells
germinal center hyperplasia BM plasmocytosis hyperglobulinemia circulating ICs HIV -> high levels of IL6 -> proliferation of B cells must affect B cells b/c cannot mount T independent B cell immuno response
115
acute retroviral syndrome
40-90% of patients 3-6 weeks after infection resolves in 2-4 weeks number of virons present at this point indicative of prognosis
116
candiasis
most common fungal infection in HIV, may mark transition into AIDs
117
opportunistic infections
candiasis, cytomegalovirus, TB, cyptococcus, toxoplasmagondii, papovirus JC, mycobacteria, herpes, histoplasma capsulatum
118
Kaposi Sarcomas
``` vascular tumor very rare, except in AIDs most common AIDs neoplasm KS herpesvirus increased IL6 and VEGF rare B cell lymphomas caused by KSHV or castelmens disease ```
119
early stage HIV morphology
follicular hyperplasia primary B cell areas HIV particles in germinal center on DC cells viral DNA in CD4 cells B cell hyperplasia in BM -> rouleaux due to hypergammaglobulinemia
120
HIV disease progression morphology
follicles depleted germinal cells hyalinized depletion in spleen and thymus
121
AL
amyeloid light chain derived from Ig light chain produced in B cells lamda light chain or their fragments, sometimes kappa chain plasma cell tumors
122
AA
amyeloid associated derived from unique non-Ig protein from liver cleaved from serum amyloid associated proteins (SSA) associated w/chronic inflammation, therefore called secondary amyoids
123
A beta amyloid
from beta amyloid precursor proteins | alzheimers
124
transthyretin TTR
normal serum protein binds and transports thyroxine and retinol mutant form deposited in familial amyloid polyneuropathies senile systemic amyloidosis- non mutated form in heart of old people
125
beta 2 microglobulin
component of MHC I | amyloid fibril subunit Abeta2m
126
other amyeloids
prions, serum amyloid P, proteoglycans, GAGs
127
primary amyeloidosis
usually AL usually systemic many have plasma cell dyscaria (cancer)
128
Bence-jones proteins
Ig light chains | often excreted in urine in primary amyloidosis
129
reactive systemic ameyloidosis
secondary usually have rheumatoid arthritis heroin users AA
130
Hemodialysis associated amyloids
deposistion of beta 2 microglobulins increased concentration in renal disease, but not filtered by dialysis membranes can cause carpal tunnel
131
familial mediterranean fever
``` heredofamilial amyeloids autoimmune inflammatory disease increased IL1 protein pyrin AA ```
132
other familial amyloids
are usually TTR mutations
133
kidney amyloids
most common and most serious kidneys shrink due to ischemia primary deposits are in glomeruli uneven widening of BM
134
spleen amyloids
2 patterns - deposits limited to splenic follicles -> tapioca like granules -> sago spleen - walls of splenic sinuses and CT framework of red pulp -> lardaceous spleen
135
liver amyloids
hepatomegaly in space of disse, hepatic parenchyma, and sinusoids normal liver function usually preserved
136
heart amyloids
can be enlarged and firm, but usually normal appearance pressure atrophy of myocardium if subendocardial deposits -> electrical issues

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