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EXAM 5 > Immuno for Exam 5 > Flashcards

Immuno for Exam 5 Flashcards

1
Q

obligate parasites

A

viruses capable of reproducing only within a living host cells

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2
Q

Universal features of all viruses

A
  1. one or more viral genome segments (RNA or DNA)
  2. capsid
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3
Q

capsomeres

A

each face of virus has a triad of identically placed proteins

larger viruses simply have more subunits

various rotational symmetries

most economical way of buildoing a shell - change volume!

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4
Q

Baltimore Classification scheme

A

classification based on how protein is made and how virus generates mRNA.

how do you get to RNA?

has to be readable my machinery

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5
Q

Group I - dsDNA

A

make mRNA from cell machinery

papovavirus, papillomaviruses, herpesviruses, adenoviruses

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6
Q

Group II - + ssDNA

A

make second strand of DNA and then make a lot of RNA

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7
Q

Group III - dsRNA

A

make single strand mRNA

has own RNA pol which copies negative strand to make a lot of positive strand that gets translated and packaged

once in a new capsid, positive strand is copied to make a negative strand and make dsRNA

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8
Q

Group IV - ssRNA +

A

i.e. polio

can be read by ribosomes - usually make neg strand to make more pos strand

make template of self and then make more and more

Most positive-strand viruses (Group IV) often make a negative strand copy of themselves: this serves as (a) the template for making more viral genomes and (b) a way to make MORE copies of the positive strand to be translated into proteins.

the RNA is ‘infectious’ in the experimental sense because if introduced directly into a cell without any viral proteins being present it can be translated into the replication proteins including an RNA-dependent RNA polymerase and amplification will follow….

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9
Q

Group V - ss RNA -

A

i.e. flu

have to make + strand to make mRNA

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10
Q

Group VI - ssRNA +

A

i.e. HIV

use RT to make ssRNA into dsDNA

then make mRNA

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11
Q

Group VII ds DNA

A

make ssRNA then rt to make ds DNA

dsDNA-RT virus

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12
Q

+ RNA

A

can make peptide right from the strand

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13
Q

RNA-dep RNA polymerase

A

used to make negative (antisense) RNA into positive (sense) RNA so it can be translated

cells don’t have, viruses bring it

often an amplifying step to make more RNA/protein

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14
Q

positive strand ssRNA

A

no RNA-dep RNA pol, translate immediately, infectious

in reality - makes a lot of negative sense ssRNA too as a template to make more + ssRNA - some to be packaged and some to be translated

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15
Q

negative strand ssRNA

A

RNA-dep polymerase, transcription first, non-infectious

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16
Q

dsRNA

A

RNA-dep pol

transcription first, non infectious

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17
Q

structural proteins

A

components of capsid and envelope

protection btwn cells - some stable, some sensitive

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18
Q

virion-associated enzymes

A

polyemerase, integraze, enzymes needed to integate into chromosomes

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19
Q

budding

A

how enveloped viruses are releaesd

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20
Q

cell lysis

A

how non-enveloped viruses are released

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21
Q

zoonosis

A

jump from animals to humans

i.e. ebola

from wild and domesticated animals creates a changing landscape of viral disease

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22
Q

virus sensing system

A

virus has things that activate it

TLRs - rec RNA and DNA

RLRs - rec viral RNA

CDRs- rec viral DNA

stim production of IFN alpha and beta

secete to nearby cells

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23
Q

IFN a/b signaling

A

bind to IFNAR (same cell or new cell)

TYK2/JAK

STAT/STAT/IRF

stim ISGs - IFN stim genes

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24
Q

PAMPS

A

general indicators of viruses and ther pathogens

dsRNA

cytDNA

nakedDNA (no chromatin)

viral genome replication intermediates

capsid proteins/env glycoproteins

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25
Q

PRRs

A

TLRs - endosomes and PM

RIG-I (RLRs) - cytoplasm (mt anchored)

NOD-like Receptors (NLRs) - cytoplasm

CDRs - cytoplasmic DNA receptors

C-type lectin receptors - plasma membrane

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26
Q

TLRs

A

in plasma membrane, rec PAMPs

either send signal to transcribe pro-inflammatory cytokines OR endoctyosed and then signal to transcribe Type I IFNs

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27
Q

OAS

A

oligoadenylate synthase

activated by viral dsRNA and makes a 2’-5’ linked oligoadenylates from ATP

that activates RNAse L dimers which degrades RNA

inhibits viral propagation and induces apoptosis

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28
Q

cGAS

A

activated by cytoplasmic dsDNA

produces cGMP from ATP and GTP which can travel and alert nearby cells OR
bind to STING receptor which leads to a cascade that results in cytokine expression

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29
Q

Type I IFN

A

a/b

front line defense from cells that contact a lot of pathogens! fibroblasts, epithelial cells, macrophages, monocytes pDCs

mostly viruses, some microbial products

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30
Q

Type II IFN

A

ifn gamma

T cells and NK cells

immune activation stimulates them

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31
Q

Type III IFN

A

IFN-lamda

pDCs, endothelial cells

mostly viruses

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32
Q

IFN signaling

A

bind IFNAR (Type I) or IFNGR (type II)

kinases attract JAK/TYK2 and activate and P STAT

STAT 1/2 bind when P and usually bind to IRF9

goes into nucleus, binds to promoter, transcription of ISGs

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33
Q

IRF9

A

binds to STAT complex for TF function

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34
Q

herpes simplex Us11

A

how HSV evades immune system

OAS responds to viral dsRNA

Us11 binds to OAS 11 so it can’t activate RNAse L so viral replication can happen and RNA isn’t degraded!

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35
Q

herpes simplex virus ICP34.5

A

PRK detects viral dsRNA and when activated it P on EIF2A so it turns off protein synthesis

ICP is a phosphatase that removes the P so protein synthesis and viral replication can happen

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36
Q

Aicardi-Goutieres syndrome (AGS

A

clinical features mimic in utero acquired infections/systemic lupus

linked to 7 mutations

inhereted mutations lead to inappropriate accumulation of self-derived nucleic acids that induce a sustained Type I IFN response

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37
Q

systemic lupus erythematosus (SLE)

A

pDCs produce IFN-a in a sustained faschion

stimulate autoreactive B cells to differentiate into plasma cells and produce autoabs, stim autoreactive t cells

DNA and RNA containing immune complexes further activate pDCs, loop!

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38
Q

Defensins

A

cationic, amphipathic effector peptides of the innate immune system with broad antimicrobial activity

active against enveloped and non-enveloped viruses

alpha-defensins - neutrophils, epithelial cells in the gut

beta-defensins - epithelial cells of skin and mucosal surfaces

don’t understand how they work

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39
Q

secondary immune response

A
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40
Q

memory B and T cell formation

A
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41
Q

primary response abs

A

IgM, IgG, IgA, IgE

tiny fraction respond to given ag

low affinity, low somatic hypermutation

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42
Q

secondary response abs

A

IgG, IgA, IgE (no M)

many more abs

high affinity, high somatic hypermutations

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43
Q

immuno memory points

A

resluts from ag exposure

follows primary immune response

more rapid, greater, more effective

innate respoinses help direct memory resoinse

duration of memory varies

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44
Q

how do vaccines induce immunity?

A

inject into muscle

inflammation - cells to area, acquire ag, exposed to adjuvent

cells migrate to LN, present ag - T cells and maybe B cells – immune response

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45
Q

live attenuated vaccine

A

organism is alive and can replicate but mutated so can’t cause serious illness

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46
Q

killed vaccine

A

chemical treatment to kill pathogen so it can’t replicate

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47
Q

subunit vaccine

A

most antigenic part of vaccine

purified in vector - 1 proein expressed, covalently coupled to carrier

purified secreted protein - toxin

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48
Q

polysaccharide conjugates

A

immunogenic in infant

polysaccharides bring in T cell help so b cells make better abs against ag

use T cell help for higher affinity abs and longer lived memory

can prevent mucosal colonization - not just disease

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49
Q

adjuvants

A

stimulate APCs through innate immune receptors

induce:

DC maturation (increase MHC II and costim molecule expression)

dendritic cytokine secreteion to direct differentiation of stim cells

LA vaccines don’t need - still have PAMPS!

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50
Q

immunodeficiency

A

impaired immune response resulting in increased susceptibility to infections with obligate and opportunistic pathogens

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51
Q

primary immunodeficiencies

A

resulting from specific genetic defects in a component of the immune system

manifest in infancy or childhood

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52
Q

secondary immunodeficiencies

A

acquired as a result of disease, treatment, infection

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53
Q

physological immunodeficiencies

A

newborn/elderly

newborn (low IgG between maternal and own IgG)

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54
Q

glucocorticoids

A

cause immunosuppression

inhibition of T cells

inhibition of macrophages

apoptosis of immune cells

inhibition of TF needed to activate cells

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55
Q

cyclosporin A

A

immunosuppressive drug

organ transplant/autoimmune

T cell - rec ag —-> Ca 2+ –> calcineurin –> deP NFAT –> TF activates cytokines

cyclosporin A inhibits calcineurin

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56
Q

metabolic disorders

A

diabetes, kidney failure

hyperglycemia - suppress immune function and leukocyte igration (vasculopathy)

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57
Q

malnutrition

A

insufficient uptake of protein –> decreased production of immune cells - need to constantly replenish

zinc = cofactor

decreased number and funcition of T cells and ab roduction by B cells

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58
Q

SCID

A

T cell defect - from mutations in genes that inhibit lymphocyte development

“bubble boy”

B and T cell defect, impaired ab production

frequent infection with obligate and opportunistic pathogens

candidiasis

failure to thrive

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59
Q

ADA

A

mutation - build up of nt - toxic

T, B, NK cells

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60
Q

RAG1/2

A

mutation for scid, no vdj, no b or t cells

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61
Q

AK2

A

mutation for scid

no b, t, nk - in becoming lymphoid stem cell

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62
Q

IL-2R gamma chain

A

SCID

no T or NK cellspart of ck receptor for IL7

most common cause of SCID

gene therapy: select CD34+ Stem cells, gene transfer IL2R gamma chain, expand, infuse stem cells

leukemia in 2/9 patients

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63
Q

Omenn syndrome

A

mutations in Rag 1/2

impaired but not completely absent VDJ

T cell numbers are normal but very restricted and autoreactive

no B cells - decreased IgG

opportunistic infection

looks like GVHD

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64
Q

SCID therapy

A

avoid infections (bubble boy)

abx

IVIG

bone marrow transplant

somatic gene therapy - IL-2R gamma chain gene transfer

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65
Q
A
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66
Q

DiGeorge Syndrome

A

no thymus

reduced number of T cells

increased infection

deletion in part of Ch 22

heart problems

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67
Q

Wiskott-Aldrich Syndrome

A

mutations in the gene for WAS protein - defects in actin polyerzation and signal transduction in T cells

severe eczema

bleeding (abnormal platelets)

bacterial infections (defect in T cell function)

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68
Q

Agammaglobulinemia

A

X-linked

no antibodies at all

No B cells

mutations in B cell tyrosine kinase - no signaling

many bacterial infections

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69
Q

hyper IgM Syndrome

A

B ell numbers are normal but imapired class switching

  1. B cell intrinsic - AID and UNG - class switch and somatic hypermutation
  2. mutation in CD40L so T cells can’t signal to B cells to class switch

lots of IgM but no others

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70
Q

CVID

A

most common, mostly young adults

antibody deficiency but normal B cell numbers

usually genes important for terminal B cell diffeentation into plasma cells

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71
Q

IgA defieicency

A

infections with encapsulated bacteria!

can develop into CVID with time

72
Q

neutropenias

A

chronic severe infections with pyogenic pacteria

mutations in neutrophil elastase (ELA2) required for neutrophil maturation

73
Q

LADI, II, III

A

impaired neutrophil migration from blood to sites of infection

chronic serious infections (innate)

74
Q

Macrophage defects

A

mutations in IL-12/IFN-g axis which is required for macrophage and T cell cooperation

increased susceptibility to mycobacterial infections

75
Q

how do you know it’s a T cell defect?

A

viruses, fungi, and parasites

76
Q

how do you know its a neutrophil disorder?

A

pyogenic bacteria

77
Q

How do you know it’s a B cell disorder?

A

encapsulated bacteria (also for complement disorder)

78
Q

elimination

A

developing tumor is recognized and destroyed by immune system - immune system is looking

79
Q

equilibrium

A

tumor dormancy by immune system - not eradicated but kept in check

80
Q

editing and escape

A

tumors are no longer recognized by immune system and develop immune suppressive enviromnent

response shapes what kind of cancer can escape

81
Q

checkpoint blockade drugs

A

CTLA-4, PD-1

82
Q

neoantigens

A

novel proteins due to tumor specific mutations

ag never seen in that person! foreign

i.e. lung and melanoma because of mutational burden –> clinical efficacy

toxins and mutagens

83
Q

CARs

A

1 molecule that rec ag like a B cell (no MHC) but activated/signals like a T cell

giving signal 2 = breakthrough

84
Q

CD19

A

expressed on all B cells except plasma cells

CD19 CARs that rec CD19 for myeloma

possibly Breg with CD19 and suppress T cells

85
Q

HP SC transplant

A

high dose therapy with HP stem cell rescue

only established SC therapy

immunotherapy of cancer (GVT)

personalized/precision med

adoptive cell therapy

86
Q

autogenic

A

self - harvest marrow, gie high dose therapy, use own marrow as rescue

87
Q

allogenic

A

someone else

gvt

88
Q

GVT

A

T cells in allograft rec ags of host origin on tumor cells and kill

lower relapse if there is GVHD

89
Q

GVHD

A

immune cells from allo transplant recognize host body cells as foreign and attack

certain organs more

none in heart or kidney

APCs in host may be activated by innate pways - start to show allo-ag rec by donor T cells, activate Tcells in graft to mediate GVHD

90
Q

top cause of death after BMTP

A
  1. primary disease
  2. GVHD
  3. Infection
91
Q
A
92
Q

infections following BMT

A

first - decrease t cell count, bacterial –> sepsis immediately

later - parasites and viruses, opportunistic, slow rebound of T cells, like AIDS

93
Q

CD34 T Cell BMT

A

less GVHD

BUT

no T cells (decreased GVHD and GVT)

many more infections

94
Q
A
95
Q

Prep for BMT

A

decrease tumor loads as much as possible wiht chemo

2nd therapy to increase tolerance to host

96
Q

haplotransfer

A

from father or mother

share one set of chromosomes 50% - dangerous because GVHD

give chemo at peak alloactivation - GVHD is relatively low

97
Q

BMT and microbiota

A

decreased diversity after transplant - turn into a monoculture - really bad!

decreased survival with decreased diversity of microbiota

fecal transplant

98
Q

Type I Hypersensitivity

A

Allergies, anaphylaxis, atopic asthma

IgE antibodies and mast cells

immediate (minutes)

99
Q

Type II Hypersensitivity

A

autoimmune disease

transfsion and drug rxns

IgG antibodies binding to:

cells –> cytotoxicity

extracellular matrix –> inflammation

100
Q

Type III Hypersensitivity

A

serum sickness

arthus rxn

HS pneumonitis

autoimmune disease (SLE)

IgG form immune complexes with soluble ags

101
Q

Type IV Hypersensitivity

A

contact dermitits

autoimmunity

transplant rejection

Delayed (2-3 days)

CD4 and CD8 T cells

102
Q

Type I Hypersensitivity phases

A
  1. sensitization
  2. immediate response
  3. late phase reponse
103
Q

Sensitization

A

Type I hypersensitivity

allergen uptake and presentation by APCs, activate CD4+ T cells and diff to TH2, activate B cells to make IgE, bind mast cells, 2nd exposure

104
Q

Th2

A

produce IL-4, become TH2 due to IL-4

105
Q

IL-4

A

T cells

B cell class switching to IgE plasma cells

106
Q

IL-5

A

TH2 make

eosinophil maturation/activation (phase 3)

107
Q

TH2 bias

A

CD4 cells turn into TH2 in response to allergic stimuli

IL-4

108
Q

Mast Cells

A

IgE (b cells) bind to FcE receptors on mast cells

filled with antimicrobial

binding of antigen causes mast cell activation and degranulation in seconds

109
Q

atopy

A

exaggerated tendency to mount IgE responses to allergens

elevaed serum IgE and eosinphils

genetic, pollution, hygeine

110
Q

Hygiene hypothesis

A

because no infections in early childhood, TH1 response is not used so TH2 predominates

111
Q

Type I Immediate response

A

phase 2

primary and secondary mediators released

112
Q

Type I Primary mediators

A

histamine

proteases

vasodilation/permeability

smooth muscle spasm

tissue damage

mucus secretion

113
Q

Type I Secondary Mediators

A

hours: RNA –> protein

IL-4, 1, 5, TNFa

IgE production, chemotaxis of eosinophils, macrophages

15 min-hours:

leukotrienes, prostaglandins, PAF (from PPL –> arachadonic acid)

vasodilation and permeability

smooth muscle spasm

chemotaxis of neutro-baso-eosinophils

114
Q

Type I late response

A

eosinophils n blood recruited to inflamation

by eotaxin, leukotriene B4 (mast cells)

115
Q

eosinophils

A

Type I

Late phase

release granules with inflammatory mediators, proteins that destroy epithelial cells

activated by IL-5 (TH2 and mast cells)

recruited by leukotriene B4 (mast cells), eotaxin (lung, fibroblasts, smooth muscle)

116
Q

acute uticaria

A

wheel and flare

ag uptae through skin or systemic

mast cell activation in upper dermis

local - vascular permability, edema, inflammation

117
Q

angioedema

A

ag uptake through mucosal surfaces/sytemic

mast cell activation in dermis/mucosa

edema and inflammation

118
Q

allergic asthma

A

type I hypersensitivity

elevated IgE, eosinophil

mast cell activation in lung

triggered by specific allergens

(like immdiate phase of type I)

119
Q
A
120
Q

anaphylaxis

A

systemic allergen uptake (iv, oral)

acute

shock - systemic vasodilation, slow hearth

121
Q

anaphylaxis treatments

A

epinephrine - cardio

b2 receptor agonist, methylprednisone - bronchospasm

antihistimine - hives

122
Q

damange from Type II Hypersensitivity

A
  1. phagocytosis/lysis of ab coated cells
  2. recruitment of neutrophils causing inflammation
123
Q

abs for type II hypersensitivity

A

IgG

124
Q

Transfusion reactions

A

Type II Hypersensitivity

donor is O, give to A, abs attack RBCs –> anemia

125
Q

erythroblastosis fetalis

A

Type II hypersensitivity

transplacental tranfer of maternal anti-RBC abs from mom to fetus

lysis of fetal red blood cells

during pregnancy - circulating abs from mom

126
Q

drug allergies

A

type II hypersensitivity

some drugs alter cell surface molecules that can be targets for ab responses

127
Q

acutre rheumatic fever

A

autoimmune

type II hypersensitivity

strep abs bind to cardiac glycoproteins

128
Q

Complement and Type II Hypersensitivity

A

abs bind to membrane protein –? complememnt activated –> C5a recruits neutrophils –> release reactive oxygen and enzymes to degrade ECM proteins

129
Q

goodpasture syndrome

A

ab to collagen of basement membrane –> complememnt

130
Q

immune complexes

A

Type III hypersensitivity

between soluble ag and IgG abs

ICs are deposited in the wall of blood vessels –> vasculitis (inflammation)

131
Q

Phases of Type III Hypersensitivity

A
  1. IgG production (about 1 wk after infection)
  2. IC form and deposit
  3. IC mediated inflammation
132
Q

serum sickness

A

IV application of protein (serum components)

drugs

systemic IC disease

rashes (IC in skin)

arthritis (IC in joints)

glomerulonephritis (IC in kidney)

delayed onset after first ag exposure

133
Q

arthus rxn

A

type III hpersensitivity

local IC vasculitis

subcutaneously deposited ag diffuses into walls of blood vessels and forms large ICs with preformed abs

edema, swelling

hours after injection

134
Q

Farmer’s Lung

A

Type III hypersensitivity

not infection - immune response

bacteria causes ab response

abs and bacteria form immune complex in lungs

135
Q

Stages of Type IV Hypersensitivity

A
  1. memory TH1 cells rec ag on apc
  2. T cell releases cks
  3. recruitment and activation of macrophages 48-72h - tissue damage by macrophages
136
Q

cytokines in Type IV hypersensitivity

A

IFNg - activates macrophages

TNFa - local tissue destruction

IL-8 - recruit macrophages

137
Q

Poison Ivy

A

Type IV hypersensitivity

urushol in skin

modify intracellular (CD8), modify extracellular (CD4)

138
Q

contact dermatitis

A

type 4 hypersensitivity

nickel, poison ivy

139
Q

Autoimmune adrenalitis

A

most common cause of adrenocortial insufficiency

destruction of steroidogenic cells that generate glucocorticoids 0 abs against it

isolated or part of APECED

140
Q

negative selection

A

in bone marrowor thymus

clonal deletion of all self reactive T and B cells

141
Q

AIRE

A

transcriptional regulator

tissue specific in thymus

proteins from body

T cells see self ag expressed by aire - preview of peripheray

negative selection

142
Q

APECED

A

disease due to mutation in AIRE

autoimmune against peripheral things

143
Q

immune privileged sites

A

no lymphocyte access to some sites

bloo, eye, testes

limited lymph drainage

low MHC I

inhibit complement

Fas ligan - apoptosis in Fas-expressing lymphoid cells

144
Q

Treg

A

suppression of autoimmune

kill auto effector T

145
Q

IPEX

A

no Treg - peripheral tolerance

146
Q

anergy

A

lymphocyte is unresponsive bc insufficient stimulation

147
Q

Fas

A

CTLs have contraction phase - cells all kill each other

Fas/FasL all stim each other for cell death

get rid so don’t damage

148
Q

ALPS

A

mutation in Fas expression on CD8 T cells - can’t get rid of them after infection

149
Q

C1q

A

complement, required for clearance of IC

if mutated –> SLE

150
Q

T1D + HLA

A

mutation in specific HLA

failure of autoantigen presentation in thymus and lack of negative selection of autoreactive T cell clonse

151
Q

inducing costimulation

A

APCs have self ag and are triggered to activate by bacteria

able to give costimulation to auto CD4 T cell - rec self ag in person

effector T - only need 1 signal!

152
Q

molecular mimicry

A

cross activation of autoreactive T or B cells by structurally similar peptides from infective pathogens

153
Q

rheumatic fever

A

molecular mimicry

abs to strep proeins cross react with glycoprotein ags of heart and joints

154
Q

MS

A

Type IV hypersensitivity and autoimmune

demyelinating CNS inflammation

CD4T cells in CNS –> rec myelin –> secrete inflam cks –> recruit macrophages –> destroy myelin sheath –> neuro disease with motor and sensory deficits

155
Q

T1D

A

type IV hypersensitivity

T cell mediated autoimmune destruction of pancreatic beta cells - absolute insulin deficiency

CD4 - activate macrophages (cks from T cells and macrophages induce apoptosis)

CD8 - directly kill beta cells

156
Q

autoimmune hemolytic anemia

A

type II hypersensitivity

abs to RBCs, platelets

157
Q

goodpasture syndrome

A

type II hypersensitivity

autoabs to type IV collagen in basement membrane of kidney and lung

activate compliment and neutrophils - severe tissue injury

158
Q

graves disease

A

type II hypersensitivity

abs activate TSH receptor - make a lot of hormormoes without ligand

hyperthyroidism

159
Q

mysthenia gravis

A

type II hypersensitivity

abs to Ach receptors - inhibit receptor, compliment fixation and injury

defect in neuromuscular transmission

muscle weakness

160
Q

Type III hypersensitivity autoimmune

A

immune complexes of soluble DNA and anti-DNA abs - deposited in small blood vessels –> vasculitis

161
Q

SLE

A

Type III hypersensitivity

systemic lupus erythematosus

multiorgan disease

mylar rash and many other criteria

IC deposition

genetic + environmental –> IgG ab productin –> IC formation –> clinical symptoms

162
Q

epitope spreading

A

SLE

tissue damage –> more cells die –> more free proteins –> more complexes

perpetuates autimmune response

self ag can’t be cleared by immune! ubiquitous

163
Q

ANA

A

antinuclear antibodies

directed against ubiquitous intracellular ags

DNA, histones, RNOs

anti-dsDNA and anti-Sm abs are diagnostic for SLE

164
Q

sjogrens

A

immune mediated destruction of lacrimal and salivary glands

dry eye and dry mouth

ANAs

165
Q

systemic sclerosis (scleroderma)

A

chronic disease of unknown etiology characterised by fibrossi of the skin and mutliple organs

ANA

166
Q

Tumor intrinsic factors

A

ag/MHC loss

secretion of immunosuppressive cks

cell surface markers like PD-L1

167
Q

tumor extrinsic factors

A

geographic barriers

suppressive/reg immune cells

Tregs, MDSCs, TAMs

168
Q

checkpoint blockade proteins

A

CTLA-4

PD-1

PD-L1

169
Q

CD28

A

costim molecule - has positive impact on T cell activation

170
Q

CTLA-4

A

inhibits T cell response

binds instead of CD28 costim

171
Q

ipilimumab

A

human mab

IgG

abs block CTLA-4, attenuate neg feedback for T cells, results in more sustained T cell activation

survival benefits

toxicity: autoimmune (colitis)

delayed response (may get worse before better)

172
Q

PD-1

A

from inflammation in tissue

dont regulated expereinced T cell (later than CTLA-4)

173
Q

Nivolumab

A

ab to PD-1

better results than ipi!

PD-L1+ had better response, but both had better than control

174
Q

abscopal effect

A

systemic response to localized inflammation

175
Q

combined nivolumab and ipilumumab

A

much better overall response but also more toxicity

176
Q

PD-L1

A

on tumor cells

binds PD-1 on T cells

EXAM 5 (11 decks)

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