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Immunology (FA+ UW) Flashcards

1
Q

what does the binding of PD1 (Tcell) to PDL1 cause?

A

T cell inhibition/exhaustion

PDL1 is often upregulated by cancer cells

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2
Q

loss of thymic shadow+ diarrhea + oral candidiasis + failure to thrive ( or other severe infections)

A

SCID (loss of both B and T cells)

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3
Q

what types of cells are active during anaphylaxis? what do they release?

A
  • basophils and mast cells

- – tryptase and histamine

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4
Q

explain the process leading to mast/basophil degranulation in anaphylaxis

A
  • surface of mast and basophils have high affinity IgE receptors
    • when the mast and basophils encounter large amounts of IgE, their Fc portion of the IgE receptor binds the IgE, and the receptors aggregate!
  • – the clumping of the receptors leads to degranulation via a pathway with nonreceptor tyrosine kinases
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5
Q

what are the two types of pneumococcal vax? compare and contrast

A
  • polysaccharide and conjugated
  • the polysacch covers more serotypes, but is less “immunogenic”. its not used for kids under 2, because these kiddos lack a robust humoral response
  • the conjugated vax is conugated with diptheria protein, and this allows for Tcell recruitment and formation of memory Bcells
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6
Q

Henoch Schonlein Purpura is what kind of HS rxn

A

Type III

because it is IgA antigen immune complexes

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7
Q

what are the 2 jobs eosinophils do?

A
  1. ) antibody-dependent cell mediated toxicity – kill parasites by binding to IgE’s
  2. ) Type 1 HS— release PGE,Luekotrienes, cytokines in the later phases of Type 1 HS
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8
Q

HIV patients lack

(1) what to prevent superficial Candidiasis
(2) what to prevent disseminated Candidemia

A

(1) TH1

(2) neutrophils

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9
Q

what marker of Hep B indicates that the infection has resolved

A

anti- HBs

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10
Q

CD3 is on?

A

T cells

for signal transduction from the TCR

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11
Q

TCR is on?

A

T cell to bind antigen-MHC

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12
Q

CD28 in on ?

A

T cell, to bind B7 on APC (for costim signal)

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13
Q

CXCR4/CCR5 is on?

A

CD8+ Cytotoxic T cells

its what HIV binds

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14
Q

CD40L is on?

A

CD4+ T cell, to bind CD40 on Bcell and cause isotype switching

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15
Q

what does the Treg cell have?

A

CD25, CD4

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16
Q

CD19, CD20, CS21, CD40 is found on?

what other things are alco found on it?

A

BCell

also: MHCII, and B7 (bc its an APC!), as well as Ig

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17
Q

CD 14 is found on?

what else is found on it?

A

Macrophages ( it is a receptor for PAMPs)
CD40, CCR5
MHCII, B7

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18
Q

NK cells have what?

A

CD56

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19
Q

Hematopoietic cells have what?

A

CD34

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20
Q

what happens when there isnt a co-stimulatory signal (B7- CD28)?

A

Anergy-a mechanism of self tolerance

B and T cells can experience this

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21
Q

How do superantigens work?

A

found in s.aureus and s.pyogenes.
they can cross link the Tcell TCR to the Bcell MHCII
causes overactivation of CD4+— resulting in massive cytokine release

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22
Q

how do gram - bacteria get an immune response?

A

They have endotoxins/LPS that can bind TLR4/CD14 of macrophages (note that T cells are not involved here)

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23
Q

how do intereferon alpha and interferon beta work

A

they are released by cells infected by the virus.. they go tell their neighboring cells (uninfected) to up their viral defense and get ready to degrade viral nucleic acid and protein

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24
Q

what gives sputum its green color?

A

myeloperoxidase

a blue green heme containing pigment

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25
Q

How does oxidative/respiratory burst work?

A

Its first step involves the activation of NADPH oxidase complex.
This gets O2 to become an oxide. From there, SOD and myeloperoxidase make it into HClO radical able to kill bacteria
(note that NADPH also plays a role in neutralizing the radical later)

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26
Q

why are people with CGD at risk for catalase positive infections?

A
  • CGD means no NADPH so no first step of oxidative burst.. BUT bacteria make their own oxygen radicals.. the rest of the steps are intact so the neutrophil/monocyte can use oxide radicals made BY the bacteria to KILL the bacteria
    • note that catalase positive bacteria are able to NEUTRALIZE the oxide radicals they make, so now in patients with CGD no respiratory burst can occur
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27
Q

IL1

A

fever+inflamm
induce chemokine production to recruit WBC
makes endothelin express adhesin

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28
Q

IL2

A

promotes growth of T cells (helper/cytotoxic/reg) + NK cells

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29
Q

IL3

A

stimulates the BONE marrow to grow bone marrow stem cells (acts like GCSF)

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30
Q

IL4

A

IgE isotype swtiching (as well as IgG)
promotes T cells to become TH2
promotes B cell growth

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31
Q

IL5

A

IgA isotype switching
eosinophil growth
B cell growth

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32
Q

IL 6

A

promotes creation of “acute phase reactants”– (like CRP ..)
also causes fever

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33
Q

IL 8

A

chemoattractant for neutrophils

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34
Q

IL12

A

promotes differentiation to TH1 cells

also activates NK cells

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35
Q

TNFalpha

A

activates endothelium– WBC recruitment/vascular leak
cachexia
maintain granuloma in TB

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36
Q

who mediates SEPSIS

A

IL1, IL6, TNFalpha

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37
Q

Interferon y

A

promotes conversion to TH1/ inhibits TH2 differentiation
secreted by NK and T cells in response to IL12 by macorphages
activates NK and macrophages to kill

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38
Q

where is complement made

A

liver

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39
Q

what are the three paths of complement production and what’s unique about each?

A

(1) classic- IgM/IgG mediated— activates C1 first
(2) Alternative- mediated by surface of microbe– activates C3 (terminal complement) first
(3) Lectin (microbe surface that has sugars)- activates C1 like complement first

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40
Q

what is the role of the terminal part of the complement cascade? (aka after C3b is made)

A

after C3b is made— it makes C5a

– it also makes C5b that is joined by C6-C9to make the MAC

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41
Q

name the two primary opsonins?

A

IgG and C3b

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42
Q

what do C3a, C4a, and C5a do?

A

a= anaphylaxis

C5a is also chemoattractant for neutrophil

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43
Q

what is C5b-9

A

MAC complex
important to lyse gram -
especially important in protecting against Nisseria

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44
Q

what inhibits the complements?

A

DAC/ CD55

and C1 esterase inhibitor

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45
Q

c3 deficiency can cause?

A

severe, recurrent pyogenic sinus and respiratory infections

more susceptible to type III HS (bc C3 is what clears the immune complexes!)

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46
Q

C1 esterase inhibitor deficiency

A

angioedema due to unregulated activation of Kallikrein– causing increased bradykinin (so dont use ACEi duhh)

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47
Q

CD55 defieciency

A

PNH.. can cause complement mediated destruction of RBC

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48
Q

what are acute phase reactants?

A

remember they are mediated by IL6
they are factors whose serum concentrations change during inflammation :
CRP, Ferritin, Fibrinogen, Hepcidin, serum Amyloid A, Albumin, Transferrin

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49
Q

what do mature but NAIVE B cells have as surface Ig’s

A

IgM

IgD

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50
Q

whats the most abundant Ig isotype in serum? what’s it do?

A

IgG!

  • main antibody in secondary (delayed response)
  • DOES cross placenta
  • fixes complement, opsonizes bacteria
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51
Q

what does IgA do?

A

prevents attachment of foreign bodies to mucosal membranes (Giardia)
released in secretions like breast milk, saliva, tears
produced the most, but has low serum concentration
does not fix complement

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52
Q

what does IgM do?

A
  • primary (immediate) response
  • doesnt cross placenta
  • pentamer so has avid binding abilities
  • fixes complement
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53
Q

IgD? what does it do?

A

WHO KNOOOOWs

54
Q

IgE?

A

least concentration in serum

  • aggregation causes mast and basophil degranulation
  • helps eosinophils kill parasite
  • type I HS
55
Q

what the FAB region of an antibody?

A

light chain and heavy chain

antigen specificity- 1 antigen per B cell

56
Q

how do you get antibody diversity?
- an antigen independent process (think of it as prepping your antibodies to recognize any antigen at all before there even is one)

A

(1) VJ (light chain) recombination
VDJ (heavy chain) recombination
(2) TdT will randomy add nucleotides during recombination
(3) random combinations of light/heavy chains

57
Q

how do you get antibody specificty? (now that a bad guy has been recognized, how do you expand your cells and make sure that they continue to only recognize him) – antigen dependent

A

(1) variable region- somatic hypermutation and affinity maturation
(2) isotype switching (constant region)

58
Q

kid w/ eczema, recurrent infections, and thrombocytopenia?

A

Wiscott Aldrich Syndrome

59
Q

CD14 is on a?

A

macrophage (/monocyte)

60
Q

anaphylaxis (hives, shortness of breath, and angioedema) upon blood transfusion, what happened?

A
  • selective IgA defeciency (usually the patient will have celiac’s)
  • – there is so little IgA in serum that, they body doesn’t even recognize it. So when pt gets a blood transfusion (that will have trace IgA) it mounts an immune response to it via IgE!
61
Q

nongonococcal urethritis, arthralgia, and conjunctivitis with rash on palm and soles (hyperkeratotic vesicles) is what?

A

reactive arthritis

62
Q

the Rhogam shot is composed of what?

A

IgG anti-D

63
Q

Chronic Granulomatous Disease?

A

XR- mut in NADPH oxidase therefore impaired ox burst
- particularly susceptible to catalase+ bacteria
tests: abnormal (decreased green) on dihihydrorhodamine
nitroblue tetrazolium fails to turn blue

64
Q

Chediak Higashi Disease?

A

AR– microtubule dysfunction causes impaired phago-lysosome fusion
- partial albinism, neuropathy/neurodegeneration, recurrent infections
on blood smear: GIANT granules in platelets and granulocytes

65
Q

Leukocyte Adhesion Deficiency (type 1)

A

AR— mutation in CD18 (LFA-1 integrin involved in tight binding)
causes susceptibility to bacterial infections, lack of pus, and high neutrophil counts
(note: early separation of umbilical cord is often seen)

66
Q

Wiskott-Aldrich Syndrome

A

XR– mutation in WASP gene causing problem in actin cytoskeleton organization in platelets and leukocytes
– thrombocytopenia, Eczema, Recurrent infections
“WATER”
note an increase in IgA and IgE and weird/small platelets

67
Q

Hyper IgM Syndrome

A

XR– mutation in CD40L on TH cells causing problem in isotype switching
severe infections early in live (like CMV, Cryptosporidium)
note: higher IgM levels and very low levels of all other isotypes, can’t make germinal centers

68
Q

Ataxia- Telangectasia

A

AR– defect in ATM gene— can’t repair dsDNA breaks which halts cell cycle
- cerebellar dysfunction, telengectasias, IgA defeciency (3A’s: ataxia, spider Angiomas, low IgA)
note: AFP will be increased, with low IgA, IgE, and IgG.
there is risk of lymphoma/leukemia

69
Q

SCID

A

cause can be XR mutation in IL2r
or a mutation in adenosine deaminase (less common)
symptoms: failure to thrive, diarrhea, and candida
note that thymic shadow will be absent and no germinal centers. TREC will be low.

70
Q

Chronic Mucocut Candidiasis caused by

A

T cell dysfunction

71
Q

Autosomal Dominant Hyper IgE syndrome (Job disease)

A

deficiency of TH17 cells due to STAT3 mutation, causing impaired recruitment of neutrophils
– coarse facies, abcesses, stil have baby teeth, increase IgE, derm problems, easy bone fractures
note IgE and eosinophils will be high, but IFNy will be low

72
Q

DiGeorge’s Syndome

A

22q11 deletion. failure of 3rd+4th pharyngeal pouches to form so lack of thymus and parathyroid gland

  • high viral/fungal infections
  • tetany bc of hypocalcemia
  • conotruncal abnormalities like Tet of Fallot, or truncus arteriosus
73
Q

Defect in B cell differentiation is called?

A

Common Variable Immunodeficiency

presents after 2 yo,with decreased plasma cells ans Igs

74
Q

Selective IgA deficiency

A

unknown causes.
mainly asymptomatic but you can see airway and GI (celiac’s) problems and atopy and autoimmune diseases
can cause anaphylaxis to blood transfusion

75
Q

X-linked (Bruton’s)

A

Agammaglobulinemia
defect in BTK receptor (tyr k)
causing no B cell maturation, after 6mo lots of infections
decrease of ALL Ig’s

76
Q

delayed separation of umbilical cord and omphalitis with recurrent infections are suggestive of

A

LAD1-

CD18

77
Q

whats responsible for clearing immune complexes?

A

C3b

from the classical pathway

78
Q

how can you tell apart Goodpasture’s and Wegener’s Clinically?

A

Wegener’s includes UPPER resp involvement (nasal/oral mucosal ulceration etc), lower resp symptoms (bloody cough),and kidney symptoms (hematuria)

Goodpasture’s will not show that Upper involvmenet usually.

79
Q

MHCII deficiency can look like?

A

SCID

80
Q

what can a defect in IL7 cause?

A

a profound reduction of Tcell numbers.this is because IL7 is part of getting pluripotent stem cells to become T cells

81
Q

drug that targets CD52 and is used for CLL, and MS

A

ALEMtuzumab

82
Q

drug that targets VEGF, is used for CRC, RCC, NSCLC and neovasc macular degen

A

Bevacizumab

83
Q

drug that targets EGFR, used for stage IV CRC and head/neck cancers

A

Cetuximab

84
Q

drug that targets CD20, used for non Hodgekin B cell lymphomas, CLL, RA, TTP

A

Rituximab

85
Q

drug that targets Her2/neu- for breast and gastric ca

A

Trastuzumab

86
Q

drug that targets TNFa- useful in IBD, RA, AS, PA

A

Ada/certo/gol/iflixi MAB

87
Q

drug that targets CD25 for relapsing MS

A

Daclizumab

88
Q

drug that targets a4-integrin for MS and Crohn’s

A

Natalizumab

89
Q

drug that targets c5 for PNH

A

Eculizumab

90
Q

Drug for psoriasis and PA that targets IL12/23?

A

Ustekinumab

91
Q

drug that targets g2b3a for antiplatelet treatment

A

abciximab

92
Q

drug that targets RANKL for osteoporosis

A

Denosumab

93
Q

drug that targets IgE for refractory asthma therapy, and inhibits its binding to mast cells

A

Omalizumab

94
Q

how do Filgrastim and Sargramastim work

A

they are G-CSF and GM-CSF repectively

cause granulocyte stimulation, and granulocyte+monocyte stimulation

95
Q

IFN B can be used for what disease?

IFNy can be used for what disease?

A

B- MS

y- CGD

96
Q

what does cyclosporine do?

A

calcineurin inhibitor via “cyclophilin”

prevents T cells activation by inhibiting IL2 transcription

97
Q

what does tacrolimus do?

A

calcineurin inhibitr via “FK506”

prevents T cell activation by stopping IL2 transcription

98
Q

what does Sirolimus do (Rapamycin)

A

mTOR inhibtor

prevents T cell activation by stopping response to IL2

99
Q

what is Sirolimus used for?

A

kidney transplant rejection prophylaxis

100
Q

what is Basiliximab?

A

monoclonal ab that blocks IL2r

101
Q

how do cortiocsteroids work

A

they inhibit NFkB, suppress B and T cell function, and decrease cytokines, induce T cell apoptosis

102
Q

cyclosporine and tacrolimus have what side-effects

A

both are very nephrotoxic

103
Q

what is a side-effect of sirolimus

A

pancytopenia

104
Q

Hyperacute graft rejection:

  • when
  • who
  • what
A 
within minutes to hours of graft
preformed anitbodies (type IIHS)
widespread thrombosis of graft vessels--> ischemia/necrosis= "white graft"
105
Q

Acute graft rejection

  • when
  • who
  • what
A

weeks-months
- usually CD8+ t cells against donor MHCs (type IV HS)
(note humoral- B cell mediated can occus but simptoms are that of ischemia/necrosis)
- vasculitis of graft vessels with dense lymphocytic infiltrate

106
Q

Chronic graft rejection

  • when
  • who
  • what
A
  • months to years
    -usually CD4+ responding to APC’s presenting donor peptides like MHC
    has both cellular and humoral components (HS4 and HS2)
  • proliferation of vasc sm, parenchymal atrophy, intersitital fibrosis, arteriosclerosis
107
Q

graft vs host disease

A

no time frame
seen when donation is liver or bone marrow
– maculopapular rash, jaundice, hepatosplenomegaly etc.
– Graft T cells attacking host proteins (Type IV)

108
Q

name the two main Xlinked recessive immunodeficiencies

A

Wiscott Aldrich

Bruton’s Agammaglobulinemia

109
Q

what two cells mainly kill tumors?

A

cd8+ Tcells – need to see MHC1

NKcells – kill if they DON”T see MHC1

110
Q

what are the immunoglobulin levels in Wiscott Aldrich Syndrome?

A
  • IgM and IgG are low

- IgA and IgE are higher

111
Q

how does the immune system deal with Step Pneumo

A

IgG mediated opsonization

112
Q

what is an Arthrus reaction?

A
  • its the type III HS rxn response of the body to a vaccine, when it has seen the components of the vaccine before
113
Q

Type IV HS rxn

A

“delayed type” - CD4+ T cells encounter antigen and release cytokine and activate macrophages
“direct cell toxicity” CD8+ Tcells

  • contact dermatitis (poison ivy)
  • graft v host, acute and chronic transplant rejection,
  • TB/ candida injection
114
Q

Type III HS rxn

A

antigen-antibody complexes activate complement
examples include: serum sickness (response to drug) or Arthus reaction (response to vax)

seen in vasculitides
PAN
PSGN
SLE

115
Q

Type II HS rxn

A

antibody mediated- a cell is opsonized by antibodies which leads to either (1) destruction (2) change in cellular function
Direct Coombs +
ex: AIHA, ITP, transfusion reactions (except the IgA def one), hemolytic disease of newborn, Goodpasture, RF, MG, Graves,
Hyperacute Graftrejection

116
Q

Type I HS rxn

A

“atopy or anaphylaxis”
mediated by IgE crosslinking due to antigen.. causes (1) rapid:mast/basophil degranulation of histamines and tryptase
delayed: mast/basophil release of cytokines/inflammation

117
Q

In the lymph node what happens in the:
cortex +follicles
paracortex
medulla

A

cortex/follicles: B cells. isotype switching @ germinal centers

paracortex: T cells + dendrocytes
medulla: communicate w/ efferent lymphatics have reticular cells and macrophages

118
Q

what drains to the cervical lymph nodes?

A

head/neck

119
Q

what drains to the hilar lymph nodes

A

lungs

120
Q

what drains to the mediastinal lymph nodes?

A

trachea and esophagus

121
Q

what drains to the axillary lymh nodes

A

arm/breast

all skin above umbilicus

122
Q

what drains to the celiac lymph nodes?

A 
stomach
liver
gallbladder
spleen 
pancreas
upper duodenum
123
Q

what drains to superior mesenteric lymph nodes?

A

lower duodenum, SI, colon until splenic flecture

124
Q

what drains to the inferior mesentic lymph nodes?

A

splenic flecture to upper rectum

125
Q

what drains the internal iliac nodes

A 
lower rectum till above pectinate line 
bladder
vagina middle third
cervix 
prostate
126
Q

paraaortic lymph nodes drain what

A

kidneys
testis
ovaries
uterus

127
Q

Superficial inguinal nodes drain what?

A

scrotum, labia majora, vulva skin below umbilicus (except popliteal area), anal canal below pectinate lines,

128
Q

Popliteal nodes drain what

A

dorsolateral foot, posterior calf

129
Q

what does the right lymphatic duct vs the thoracic duct drain

A

R lymphatic- R side of body above diaphragm

Thoracic duct- drains everything else :)

130
Q

in the WHITE pulp of the spleen where are the T cells found? where are the B cells found?

A

T cells in PALS (periarteriolar lymphatic sheath)

B cells in follicles

need to knows (31 decks)

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