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SFM Final > IMMUNO > Flashcards

IMMUNO Flashcards

1
Q

In Mature, Naive Tcells at rest
What Cds do they express/are associated with?
What MHC/HLA class?
What TCR complex molecules are associated?
What are the main adhesion molecules?
and the main chemokine receptor?

A 
CD4+, 8+, 28+
Class 1
CD3 and zeta
LFA-1 and VLA-4
CCR7
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2
Q

Where do MN Tcells habit and where are they activated?

and What activates them

A

Blood and lymph organs
Inflammation, DCs, and Bcells+ Macros (+Tmemory)
- CD4+ can in turn + Bs and Macros

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3
Q

What are DCs when they are activated?
What adhesive marker becomes up regulated?
What CD expression is increased?
Where do they then go after +?

A

In the periphery, then they travel to the secondary lymph tissue as they mature via the High endotheliuim venules HEV

  • CCR7–to bind and travel
  • CD80 (B7)
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4
Q 
Tcell Receptors bind to which ligand? and cause what?
L selectin
LFA-1
CCR7
E and P selectin (+)
LFA1 (beta2) and VLA4 (beta1 integrin)
CXCR3
A

L-secectin ligand: weak adhesion of N Tcells in high endothelial venule in lymph node

  • ICAM1: arrest on HEV
  • CCL19 or CCL21: activate integrins and chemotaxis
  • E or P selectin
  • ICAM1 or VCAM1: arrest on endothelium
  • CXCL10
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5
Q

Where do B and Tcells proliferate?

A

Lymph Nodes (why they swell)

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6
Q 
Surface molecules: What function and what ligand if any?
Cd3
zeta
Cd4
8
28
LFA1
CTLA4
PD
A

none: signal transduction
none: signal transduction
MHC II: st
MHC I: st
B7: st on Ag presenters
ICAM1: adhesion/st
B7: inhibition on Ag presenters (such as T reg cells)
PD-L1 /2: Inhibition on Ag presenters, tissue cells, and tumor cells

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7
Q

What type of Tcells do CD 4 and 8 work on

A

Helpers (produce cytokines) and cytotoxic Ts

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8
Q

When a Tcell recognizes an Ag, what happens?

A

Integrin (ICAM) changes conformation increasing affinity and causing clustering

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9
Q

What is the first signal for Tcell Activation, and what gets increased expression?

A

MHC/peptide complex binds to TCR

  • CD40L in Tcells–> CD40 constitutively on APCs
  • B7 on APCs–> CD28 constitutively on T
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10
Q

CD80 is the same as

A

B7

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11
Q

Intracellular signaling involving what two key things, leads to protein synthesis and the production of what major cytokines?

A

ITAM and ZAP70

-NF kappa B, and AP1

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12
Q

What is it called when a non-activated Tcell becomes unresponsive?

A

Anergy (Anergic)

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13
Q 
What is the principle action and cell source for each cytokine?
-IL2
IFN gamma
-IL4
-IL5
-IL17
-IL22
-TGF beta/ IL10
-IL12
A

-Tcell proliferation and Tregulatory survival in +Tcells

-Macro activation in CD4 and 8+ Ts, and in NKs
Also stimulates HLAII and B7 expression

-Bcell switching to IgE, on CD4+ Ts and Mast cells
secreted by Th2

-+ of Eosinophils in CD4+ Ts, Mast, and innate lymphoid cells
secreted by Th2

  • Stimulate acute inflammation in CD4 Ts and others
  • Maintain Epithelial barrier function in CD4 Ts, NKs, and innate lymph cells
  • Inhibit Tcell + and aid the differentiation of reg Ts in CD4/many other types
  • Thelper proliferation
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14
Q

What is the IL2 alpha chain equivalent to, and what does it promote when it binds to IL2 (autocrine signal)?

A

CD25

-Tcell proliferation and differentiation

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15
Q

What binds to S1PR and what happens in result?

A

CD69 (short term) and the binding impairs migration of the Tcell from node–>periphery till about day 5

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16
Q

Once a Tcell is +, CCR7 decreases inversely to what? and where does the Tcell travel to? to meet what?

A

CXCR5 increases

travels to the folicular area from the medulla to meet a Bcell

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17
Q

In T regulatory cells, what cytokines are they influenced by mainly? What do they secrete? and What is their novel transcription factor?

A

IL2 and TGF beta
-IL10 and TGF beta
-FOXp3
(act to suppress immune response and maintain homeostasis)

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18
Q

What kind of Tcell is found mostly in the gut (small number) and must have a Ag while not recognizing many peptides?

A

Gamma Delta Tcells

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19
Q

An effector T cell can bind to an Ag without need of co-stim by what interaction?

A

B7(CD80)—CD28

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20
Q

What do Thelper-1 (bact and viruses) cells respond to? what do they secrete? and what is their novel Transcription factor?

A

IL12 and IFN gamma

  • IL2 and IFN gamma
  • T bet
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21
Q

What do Thelper-2 (helminths/extracell parasites) cells respond to? what do they secrete? and what is their novel Transcription factor?

A

IL4

  • IL4, IL5, IL13
  • GATA3
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22
Q

Key functions of Th2’s?

A 
Stimulate IgE (Ab), mast cells, and eosinophils vs helminths
Also IgA and aboves for atopic disease and mucus production
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23
Q

What Interleukins activate inflammation in Macrophage 1s and which are anti-inflamm in alternatively activated Macro 2s

A

IL1, 12, 23
vs
Il-10, TGF beta

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24
Q

What stimulates proliferation of Th 17, what does it do? What’s its novel TF? what does it secrete?

A

bacteria and fungus/ IL1 and IL6

  • Induces inflamm and leukocytes (neutrophils)
  • ROR gamma t
  • IL-17, and 22
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25
Q

Why won’t every effector T that enteres an area be specific for that Ag?

A

Selectins and Integrins get Tcells interested in an Ag but are not specific

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26
Q

What are the two cytotoxic T ways of killing?

A

1: deliver Granular proteins (granzymes-that +caspases and Perforin) to the surface of infected cell
2: Use FasL-on T and Fas- on target (CD95) induction of apoptosis

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27
Q

What type of cells produce IFN alpha and beta (associated with apoptosis)

A

Type 1 IFNs: NKs and DCs

viruses

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28
Q 
NKs
What kinds of cells do they try and kill? Using What?
What are they enhanced by?
What inhibits them?
What are their surface markers?
A

Tumor and viral infected using granzymes and perforin

  • IFN alpha and beta, and IL12
  • MHC class I
  • CD 56 and 16
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29
Q

What are the two types of Mature, Naive Bcells?

A

B1: in Mucosa- have limited Ag specifity

B2:
Follicular: re-circulating (the majority)
Marginal: in the spleen: blood-borne polysacc Ags

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30
Q

What BCRs are present on M,N Bcells?
Which HLA class?
Other important CDs

A

IgM, D, Alpha, and Beta

CD: 19, 81, 21(CR2)

Class II and I (nucleated)

CD 40 and 20

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31
Q

What presents Ags to the B cells in the Follicle?

A

follicular Dendritic cells

-without an Ag, B cell will die in weeks

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32
Q

How many signals does a B cell need to activate (or a T)?

A

2 signals

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33
Q

During the First Bcell activation signal, what gets phosphorylated? and what is the whole process similar to?

A

SyK (would be zeta in T)

Similar to T cell activation

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34
Q

What triggers the biochemical signals that are converted by receptor-associated signal moleucles by cross linking 2 or more BCRs

A

Ag-induced clustering of membrane bound Ig receptors
–Which have an alpha and beta proteins linked to ITAM (immunoreceptor tyrosine activation motif) that actually signals
(1st is not sufficient to activate fully)

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35
Q

What complement protein binds to … receptor that is attached to CD 19 and 81 that help deliver activation signals to the B cell?

A

C3-d

the CR2 receptor (this provides cross linkage for signaling)

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36
Q

The first B cell act signal:
What is secreted?
What are the consequences?

A

IgM in low levels

Increased survival/proliferation (mitosis and clonal expansion

interaction with helper Ts (if Ag is a protein);

responsiveness to cytokines;

migrations from follicle to T cell areas (edge of follicular zone where they meet the Ts- the pheripheral lymph organs)

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37
Q

What are the two ways the second B cell activation signal can happen?

A

By Ag independence

or Ag Dependence: Ag is presented on B cell surface and binds to Tcell receptor…
B7 and CD40 on B- associate with CD28 and CD40L on the Helper T—-all 3 must occur before the cytokine signals released by T (activation of B)–> proliferation

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38
Q

After activation of B cell–> what do the cytokines from Ts modulate? what enzyme becomes expressed? and what is induced?

A

They modulate class switching (Abs of different heavy chain isotypes)

  • enzyme AID (act induced deaminase)-makes nucleotides susceptible to cleavage/recombination
  • ->CD40 signal induced AID… so VDJ moves to a C region and a new heavy chain is produced

-Affinity maturation aka: somatic hypermutation-a cellular mechanism by which the immune system adapts to the new foreign elements that confront it

SH and switching happen at the same time

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39
Q

What cytokines produce what immunoglobins in the germinal center after Bcell Activation (class switch)

A

IgM forms without anything–activates the complement system

IgG subclasses can form from INF gamma and others– tagging and phagocytosis, complement activation, and neonatal immunity

IgE and IgG4 form from the cytokine IL4—-immunity against helminths and mast cell degranulation

IgA from mucosal cytokines (TGF beta etc)–mucosal immunity

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40
Q

Which type of T Ags do we see class switching/ switch recombination?

A

only T-dependent

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41
Q

What is Affinity Maturation?
Where does it occur?
What does it result from?
Why is Ig mutation called somatic hypermutation?

A
  • the process where affinity of Abs production increases in response to prolonged or repeated exposure to an Ag
  • occurs in the germinal centers of lymphoid follicles
  • somatic hypermutation of Ig genes in dividing Bcells followed by the selection of high aff Bs by an Ag

-Very high frequency in Ig mutations
AID turns random Cs to Us

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42
Q

What is cut out of the Naive Bcell chain during class switching?

A

the mu and delta segments

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43
Q

What kind of Tcell is a T Follicular Helper?
What holds the Activated Bcell and Tfh together and is important for the germ center reaction?
What is secreted by the TFh and what cytokines are released (common)

A
  • CD4+ with low levels of CD25
  • the associated btw ICOS-S (tfh) and ICOS-L (bcell)

IL21 is secreted–faciliates differentiation
IFNgamma and IL4

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44
Q

Plasma cells
-the markers: which are decreased and increased

Where do they migrate from the germ center?

A

Increased: CD27

Decreased: CD19, 20, and HLA Class II

to the bone marrow

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45
Q

B1 (Ag independent) cells respond to what kinds of Ags?

Where are the Bcells located that contribute to T-independent Ab responses to … ?

A

Non-proteins…lipids, polysaccharides, etc

the Marginal zone in spleen
respond to blood-borne Ags (polysaccharides)

46
Q

What do Memory Bs express that contributes to their long life span?

What are the surface markers for mBs

A

anti-apoptotic protein Bcl-2

CD27 and CD45r

47
Q

What is antibody feedback?

A

process where Ab being bound to an Ag inhibits further Ab production
-The Fc ‘tail’ on IgG is recognized by Fc receptor on Bcells (FcgammaRII)
Uses ITIMs

-a control mech dealing only with IgG

48
Q

What is humoral immunity?

A

Branch of adaptive immunity mediated by Abs made by Bs and Plasmas. Main defense vs extracellular pathogens

49
Q

All Ab effector functions are mediated by what region and what are it’s two functions?
All the functions are triggered by the binding of the Ag to what region?

A

Fc’

  1. Delivers Abs to inaccessible anatomical sites
  2. Links bound Ag to molecules that effect destruction

Fab’ (variable region)

50
Q 
What is the function of the main Ab isotypes?
IgG
IgM
IgA
IgE
A 
G: neutralize microbes and toxins
Opsonize Ags for phago by Macros and NPhils
Classical Comp activation
Ab-dependent cytotoxicity by NK cells
Neonatal immunity (Ab across placenta)
Feedback - of Bcell Activation

M: +classical complement path

A: Mucosal immunity: secreted into GI lumens and respiratory tract
Neutralize microbes and toxins

E: Helminth defense
Mast cell degranulation

51
Q

Which Abs bound to Ags can activate the complement system?

What component of complement binds to the Fc region of the Ab/Ag complex?

A

IgM or 2x IgG

the C1 component (q associates to two r’s and s’s

52
Q

What are the effector functions of the Ig Abs?

A
  • Activate complement
  • Neutralize infectivity of microbes and the toxin interaction w/ host cells

-Opsonize for phagocytosis
-plays role of waste manager
CR1 on erythocytes binds with C3b and C4b to transport to liver and spleen

Using Fcgamma (CD16), NK (and other leuks) cells are activated to Ab-coated cells for killing 
"Ab Dependent cellular cytotoxicity" ADCC

Therapeutics: ie IV-IG after exposure for rapid protection

  • inflamm diseases/autoimmune
  • uses inhibitory FcR on Bcells to suppress immune response
  • Use IgM and IgG to cross-react with blood alloAgs
  • Use IgE for Eosinophil/Mast cells reactions vs Helminths and Allergies

Use IgA and IgM for mucosal immunity

53
Q

Which Abs are found in the placental fetus and in the breastmilk

A

IgG

IgA

54
Q

What transports IgG from maternal circulation across the placental barrier, and across the intestine?
Where is it found?

A

FcRn found on the surface of endothelial cells, Macros, and other cell types

55
Q

When is a baby most vunerable to immune compromise?

A

between about months 3-12 when maternal IgG decreases and new IgG, IgA is still being formed

56
Q

What is passive immunization and what are examples?

A
  • Uses preformed Abs…short term but immediate

- snake bites, mother to child Ig, Ebola?

57
Q

Active Immunization

A

vaccine and natural pathogen exposure
-long term (memory) but delayed in working

Can have combined immunizations with both passive and active
-tetanus and rabies

58
Q

Evasion of Humoral Immunity

By Antigenic variations
Inhibition of complement activation
and
Blocking hyaluronic acid capsule

A

–viruses and bact (HIV…Neisseria Gonorrhae)

–Many bact like N Gono

–Streptococcus

59
Q

What is the epitope?

A

The part of an Ag that is recognized–contains Ag binding site of Ab

60
Q

What is the difference between T-dependent and non-dependent Ags?

A

D: proteins—need Th and Bs to stimulate Ab response

N: non proteins (lipids, polysaccs)

61
Q

What is a haptin?

A

a small molecule that cannot induce an immune response alone

62
Q

Which Tcells do MHC class 1 and 2s present to?

A

1: CD8+ cytotoxic Ts
2: CD4+ helper Ts

63
Q

HLA-DM is associated with which MHC class?

and what does it do?

A

Class II

Faciliates the removal of CLIP (from Ii) and the addition of peptides

64
Q

HLA Class II: Ii chain enters with the protein Ag in vesicles and combines with what cell component?
What does Ii do?
What important molecule is formed from the degradation of Ii?

A

Lysosomes/endosomes

stabilizes and blocks peptides from binding groove

CLIP

65
Q 
What MHC class pathway is TAP associated with?
What does it do and where does it do it?
A

HLA Class I

Transports peptides from cytosol to interior ER where it is trimmed and loaded onto Class I molecule

66
Q

In class I HLA path, how is the protein Ag broken down (whether viral or in phagosome)?

A

It is ubiquinated, then peptides are chopped by proteosome–> then enters the TAP (using tapasin) into the ER

67
Q

What allele is expressed in most Ankylosing Spondylitis cases?

A

HLA-B27

68
Q

What do BCRs contain?

A

Immunoglobin with alpha and beta (making invarient chain) =ITAM on bottom

69
Q

What structures are involved with TCR signaling?

A

CD3 complex and zeta

70
Q

What is allelic Exclusion?

A

Where one allele is silenced (only one antigenic epitope)

71
Q

The production of the Heavy chain Bcell correlates to which Tcell chain?
Light chain B?
What does not happen in Tcr’s that does in BCRs?

A

Heavy B=== Beta T

Light B=== Alpha T

Somatic hypermutation (adapting to viruses etc… class switching)

72
Q

Which genes lead to junctional diversity in Chains?
What inserts nucleotides randomly after the cutting?
Which nucleotide adding type is not in light chains?

A

RAG 1 and 2

TdT

N is not in light chains. P is in both (templated)
–all leads to diversity in the hypervariable region

73
Q

Which cytokine acts on B and Ts altering the protein express requirements?

A

IL-7

74
Q

What adhesion molecules are used in B-cells/stem cells initially?

A

VCAM1 and VLA4

75
Q

The Pre-BCR contains a surrogate light chain that allows the Pre-BCR to signal what?

A

Proliferation (largest expansion during Bcell development)

Irreversible inhibition of Lg Heavy chain–leading to allelic exclusion, maintaining clonal specificity

76
Q

What stage of Bcell development has the heavy chain recombined?
Where is Rag and Tdt expressed?

A

Pre-B stage

Between Pro and Pre-B stages

77
Q

Which stage does the Bcell move from the Bone Marrow to the pheriphery (and spleen)?

A

Immature B phase (where is undergoes negative selection and receptor editing)
IgM is shown as a surface marker

78
Q

Where are surface markers IgM, IgD, and Cd19 all expressed? (what Bcell stage)

A

Mature Naive B

where it gets activated (prolif and differentiate)

79
Q

Does the self-reactive rescue mechanism happen in Tcells?

How does it work?

A

NO! just Bs

RAG proteins stay and keep rearranging for a second round, if the new light chain is not reactive, then it will mature and migrate to periphery, if it is recognized after the receptor editing, then it dies.

80
Q

How does a mature T lymph leave the Thymus?

A

The blood

81
Q

What stage of Tcell maturation does it leave the bone marrow and enter the Cortex of thymus?
When does it enter the medulla?
When does it go to the periphery?

A

Stem cell–> proT

PreT–>Double Positive T

Single positive (immature) –> Mature Naive T

82
Q

T regs are a small population of which T lymphs?
What is their function?
What surface markers?
What unique transcription factor is present?

A

self-reactive CD4+s that undergo differentiation

To inhibit self-reactive Thelper1s in the periphery (suppression)

CD4 and CD25**-from IL2

FoxP3

83
Q

Defensins definition:

A 
small, cysteine-rich cationic proteins which active vs bact. fungi, and enveloped/nonenv viruses
In granules (neurtrophils)
84
Q

Left shift is seen when?

A

acute infection– bone marrow dishing out WBCs and releasing before they are mature**

85
Q

What makes up a neutrophil NET?

A

core DNA element which histones, proteins (cathepsins) and enzymes are released from granules

They continue functioning/chemotaxis after it’s release

86
Q 
What is a macrophage called in the 
Bone
CNS
Lung
Liver
Connective tissue
Spleen
A 
Osteoclast
Microglial
Alveolar
Kupffer cell
Histiocyte
White/Red pulp; marginal zone; metallophilic
87
Q

What kind of cell is a Langerhans, and where is it?

A

DC (fetal stage development)

in the epidermis

88
Q

Major difference btw Mast and Basophiles?

A

Mast: tissue fixed

Baso: circulating

parasites and allergies

granules w/ hist, sero, heparin, cytokines/chemos

89
Q

What makes up the Sentinel cells?

A

DCs, tissue Macros, Mast cells

90
Q

What is unique about Eosinophils?

A

Large secondary granules w/ 4 basic proteins

Small granules have Major Basic Protein

anti-parasitic, exfoliation, brochospasm

91
Q

Bcells can develop where?

A

Bone marrow

Spleen

92
Q

Cell Mediated Im is comprised of what?

A

Tcells in concert many times w/ Ag presenters and Phagocytes

viruses and bact that aren’t accessible to circulating Abs

93
Q

What is sebum consisted of?

A

lactic acid and fatty acids

-reduce skin pH

94
Q

What are the pyrogenic cytokines?

What do they activate?

A

TNF
IL-1 and 6 in Macros
Potent fever inducers

Hypothalamus

95
Q

What terminal glycan is not found in humans?

A 
Mannose
Mannose Receptor (Pattern Recognition Receptor)
96
Q

What TLRs are extracellular, which are intracellular

A

1-6, not 3
3, 7-9

ff: 2,4,9 for Neisseria meningitidis

97
Q

Which Toll Like Receptor does not signal to MyD88?

A

TLR3

MyD88 stimulates IRAK–> MAPK–> NFkB
or Interferon Reg Factor IRF

98
Q

What do many PAMPs activate?

What do they do?

A

Inflammosomes containing NOD-like Receptors–

  • Scaffolding proteins: assemble platforms that trigger NFkB and MAPK signaling paths
  • Inflammosomes + protease caspase 1: process IL-1beta and IL-18—-POTENT PROINFLAM cytokines
99
Q

What is fMet and what is unique about it’s location?

A

in Prokaryotes only

It’s a PAMP: phagocytes use it to distinguish self from non-self
-initiates phago by Phag cells

100
Q

Where are mast cells located? and why is it important?

A

Near sites exposed to external env- like skin….near blood vessels- to regulate vascular perm and recruitment of blood cells

Can be activated by IgE+Ag, cytokines, C3 and C5a’s, temp/pressure change

101
Q

What is special about activated C1 in classical complement path?
What is the classical C3 Convertase?
What is the role of C3b?

A

One can cleave many C2 and C4 molecules

C4bC2a

either Phagocytosis (opson) activation or formation of C5con

102
Q

What are c-reactive protein and Mannose binding protein considered?
What do they do?

Which of those two is a marker along with Serum Amyloid P for diagnosis of ….?

A

Acute Phase Proteins

Fix complement, opsonization

CRP and SAA used for inflammation diagnosis (up to 100 fold increase w/in 24-48 hours)

103
Q

Where do Neutros and Monocytes ender tissue?

A

Post-capillary venules—-caps in parenchymal tissue (kidney, lungs, liver)

104
Q

What are key activities helping neutrophils enter Endothelial cells ECs (after activation by TNFalpha and IL1 from Mast and Macros)?

A

Increased expression of adhesion molecules E and P selectin (PSGL1 and ESL1 on neutrophils)

LFA1 and VLA1 are on neutrophils and activated by chemokine signals, then bind to ICAM1 and VCAM1 before being brought in (diapedesis)

105
Q

What is the difference between classically activated M1 Macros and Alternatively activated M2 Macros?

A

M1: induced by microb products binding to TLRs/cytokines (IFNgamma)—–proinflammatory

M2: induced by IL-4 and IL-13—–Anti-inflammatory; tissue repair and fibrosis

106
Q

What is the order of the respiratory burst in Macros?

A

O2 consumption
Superoxide anion production
H2O2 production (potent ox agent–broken down by catalase)
Singlet Ox production
Hydorxyl radicals produced (react w/ most organics)
Myeloperoxidase can cat toxic peroxidation of hydroxy rad or Hypochlorite (very antimicrobial)

107
Q

What are the two methods of Anti-viral innate immunity?

A
  1. NK cells
  2. Type 1 IFNs alpha/beta
  • PKR blocks viral rna translation
  • IFNs + ribonuclease –> rna degrade
  • IFNs also + NKs

-NKs kill and release IFNgamma to stim Macros Phagocytosis

108
Q

Important Receptors of NKs

A

Activating: KIR (killer Ig like rec)- recognize stress molecules MICA and B
–trigger PTK

Inhibitory: recognize class I MHC and activate PTP

If sufficient KIR binding to MHCI (PTP) occurs, cell walks away with its life

109
Q

How might Neisseria Meningitidis and Steptococci resist innate immunity?

A

Blocking C3 and C5 convertases or C3b binding to complement receptors

110
Q

What is the bridge between Innate and Adaptive Responses?

A

Pathogen recognition by PRRs—causing + of APCs—> Ag presentation to naive Ts—> secreted cytokines assist development and maturation

SFM Final (4 decks)

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