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IMM2011 > T CELLS AND ADAPTIVE > Flashcards

T CELLS AND ADAPTIVE Flashcards

1
Q

What is cell mediated immunity?

A

Defense against intracellular microbes –> needed when pathogens resist the antimicrobial activities of pathogens

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2
Q

What stimulates the ability of macrophages to kill ingested phagocytes?

A
  • T cells
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3
Q

What are 3 functions of T cells?

A
  1. ACTIVATION of phagocytes
  2. KILLING of infected cells
  3. HELP for B cells
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4
Q

Do naive T cells have effector functions??

A

NO! only effector T cells. Naive T cells must first be activated

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5
Q

What happens once naive T cells recognise antigen in the peripheri?

A
  • Proliferation of T cells and differentiation into effector T cells and memory T cells is INITIATED
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6
Q

What are the GENERAL steps for T cell activation and where does it occur?

A

Naive T cells recognise MHC: peptide on professional APC

  • Lymph node
  • T cells produce IL-2 cytokine and also have IL-2 receptor (thus autocrine signalling)
  • IL-2 binding causes T cell proliferation
  • Differentiates into effector T cells and memory T cells and goes out into peripheri
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7
Q

Do ALL T cells go into effector organs/tissues?

A
  • NO! Some T cells stay in lymph nodes

- Eradicate infected cells OR give signals to B cells –> antibody

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8
Q

Where do naive T lymphocytes travel and what do they do?

A
  • Constantly circulate through peripheral lymphoid organs to FIND ANTIGENS matching their receptor
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9
Q

What are the 5 different factors (general) needed on T cells to recongise the ligands on APCs and allow for activation of T cells?

A
  • TCR
  • CD4/CD8 coreceptor molecules
  • Adhesion molecules
  • Costimulator molecule binding to costimulatory receptor on naive T cell
  • Cytokines to amplify T cell response
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10
Q

What recognises both complexes of peptide antigen and MHC on APCs? (signal 1)?

A
  • TCR + CD4/CD8 coreceptor
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11
Q

Do the TCR alpha and beta chain both take part in atnigen recognition?

A
  • YES!
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12
Q

Where do the CD4/CD8 coreceptors recosgnise the class I/II MHC?

A
  • At a site DIFFERENT to the peptide binding cleft
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13
Q

Which T cell surface molecule does signal transduction by TCR complex?

A
  • CD3 (x3) + zeta chain

- Transmits the biochemical signals

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14
Q

Do CD3 and zeta proteins stay the same or different in different T cells?

A
  • Stay the SAME (invariant)
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15
Q

What is the role of adhesion molecules in T cell responses?

A
  • Recognise their specific ligands and STABILISE binding of T cells to APC (DC)
  • Bc. T cells usually bind with low affinity so adhesion molecules allow there to be time for signalling interaction to occur. E.g. integrins (LFA-1) –> APC ligand —> iCAM-1
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16
Q

What does ‘costimulator’ mean?

A
  • Molecules that provide stimuli to T cells that function together with antigen’
    e. g. CD80 and CD86 (B7 molecules) (APCs express this and increases expression with microbe detection)
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17
Q

Which receptor on T cells recognises CD80 and CD86 (B7) molecules?

A

CD28 receptor which is essential for naive T cell activation

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18
Q

What would occur without CD28:CD80/86 ?

A

NOTHING

- No activation–> anitgen recognition by TCR would not be enough for T Cell activation

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19
Q

What does costimulation ensure?

A
  • Makes sure T cells aren’t activated by random substances that are not harmful (autoreactivity)
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20
Q

Where is the CD40L (ligand) present?

A
  • ACTIVATED T CELLS

`

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21
Q

Where is CD40 present and what does it do?

A
  • Present on APCs (e.g. Dendritic Cells)

- Makes APCs ‘better’ at stimulating T cells

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22
Q

Do the CD40 ligand/CD40 directly enhance T cell activation?

A
  • NO
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23
Q

What happens when CD40L on T cells binds to CD40 on APCs?

A
  • Causes the APC to express MORE CD80 (B7) costimulators + secrete cytokines (IL-12)–> Enhances T cell differentiation
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24
Q

What do Adjuvants do?

A
  • They are products of microbes sometimes and induce expression of costimlators (APCs)–> stimulate APCs to secrete cytokines
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25
Q

What are the inhibitory receptors of T cells?

A
  • CTLA-4

- PP-1

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26
Q

What does CTLA-4 recognise?

A
  • CD80 and CD86 (B71 and 2) on APCs
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27
Q

What do the inhibitory receptors of T cells (CTLA-4 and PP1 do?

A
  • Induced in activated T cells and terminate responsiveness of T cells
  • Evolved to PREVENT immune responses against SELF antigens
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28
Q

What does the activation of CD8 T cells require?

A
  • Class I MHC
  • Costimulation
  • CD4+ T cells (Helper)
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29
Q

What does the differentiation of T (CD8) cells into active T cells + memory cells require?

A
  • CD4 T cells –> can produce cytokines or membrane molecules to help activate CD8T cells
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30
Q

What level of protein synthesis do proteins have?

A

LOW

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31
Q

Which 3 biochem processes does antigen recognition involve?

A

Activation of enzymes
Adaptor protein recruitment
Production of transcription factors

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32
Q

When are the biochem pathways activated?

A

When TCR complexes + coreceptor are brought together by binding to mhc:peptide complex

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33
Q

Do the proteins come together with cell-cell contact?

A

YES! TCR complex, CD4/CD8 coreceptors, CD28 come together to form the PERIPHERAL RING

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34
Q

What is required for optimal induction of activating signals in T cell?

A

Redistribution of signalling and adhesion molecules

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35
Q

What is the immune synapse?

A

Region of contact b/w APC and T cell (including redistributed proteins

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36
Q

What is CD69?

A

Marker of T cell activation (cell migration)

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37
Q

What does IL-2 do?

A
  • Promote T cell survival signal and proliferation
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38
Q

What does CTLA-4 do?

A

Inhibits immune responses

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39
Q

What is cFos?

A
  • Transcription factor involved in expression of the naive T cell
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40
Q

Which protein kinase does CD4 and CD8 coreceptors facilitate signalling through?

A
  • Lck
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41
Q

What are ITAMs found on and what are they critical for?

A
  • Immunoreceptor Tyrosine Based Activation Motif
  • critical for signalling
  • CD3 + zeta chain contain these
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42
Q

What contains the ITAMs?

A

CD3 and zeta chain

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43
Q

What is Lck brought near the TCR by?

A
  • CD4/CD8 molecules
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44
Q

What are the 4 major signalling pathways linked to the zeta chain and phosphorylated ZAP70?

A
  1. Calcium-NFAT pathway
  2. Ras/Rac-MAPK pathway
  3. PKCtheta-NF-kappa B pathway
  4. PI3K pathway
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45
Q

What is NFAT?

A
  • Transcription factor inactive when phosphorylated in resting T cells
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46
Q

What does NFAT activation and nuclear translocation depend on?

A
  • Ca2+ ions in cytosol
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47
Q

What is the calcium NFAT-pathway iniitated by ?

A
  • ZAP70 and activation of phospholipase C
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48
Q

What does activation of transcription factors in T cells lead to and what are the transcription factors?

A
  • NFAT
  • AP-1
  • NF-kappaB
  • Activation of TFs in T cells leads to stimulation of transcription and cytokines, cytokine receptors, cell cycle inducers, effector molecules like CD40 ligand
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49
Q

Which general metabolic changes occur when T Cell are activated?

A
  • INCREASE in glucose uptake, increase in amino acid synthesis, + building blocks for organelles
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50
Q

Which type of T cell secretes IL-2 in response to antigens and costimulators?

A
  • CD4+ T cells
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51
Q

What happens after CD4 T cells secrete IL-2?

A
  • Increase in the expression of high affinity Il-2 receptor

- So T cells can respond and bind to Il-2 receptor

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52
Q

What is the structure of the Il-2 receptor and which cells excpress it/in what form?

A
  • 3 chain molecule

- Naive T cells express LOW AFFINITY complex (2 chains )

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53
Q

How does activation of T cells by antigens and costimulaotrs change the structure and thus function of the IL-2 receptor?

A
  • Allows third chain of Il-2R to be made

- Il-2R can now bind to Il-2 strognly

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54
Q

Why are so many CD8 T cells made compared to CD4+ T cells?

A
  • CD8 T cells have effector functions that kill infected cells DIRECTLY (so is needed to kill large numbers of infected cells)
  • CD4 T cells secrete cytokines to HELP other T cells
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55
Q

What are the CD4+ T cell subtypes?-

A

Th1, Th2, Th17, Treg
- migrate from peripheral lymphoid organs to the site of infection –> cytokines then RECRUIT OTHER LEUKOCYTES –> destroy infectious agent

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56
Q

When is CD40L transcribed?

A
  • In response to antigen recogition and costimulation
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57
Q

What do the T cells that stay in the lymph nodes and migrate to lymph follicles do?

A
  • Help B cells produce antibodies
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58
Q

What does the CD40L bind to?

A
  • CD40 receptor on MACROPHAGES, B cells, and DCs

- These cells are stimulated from CD40L:CD40R interaction

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59
Q

Which two cytokines have an effect in keeping Memory T cells alive after infection has gone?

A
  • IL-7 (via upregulation of Bcl2) and Il-15
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60
Q

Where can memory T cells be found?

A 
Lymphoid organs (central memory cells--> RAPID clonal expansion) 
Peripheral tissues (mucosa and skin--> effector memory cells) 
Circulation
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61
Q

where are T cell responses primarily inititated?-

A
  • In secondary lymphoid organs (lymph node and spleen)
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62
Q

Where is the effector T cell phase mainly?

A
  • In peripheral tissue at sites of infection
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63
Q

Where do naive T cells circulate before encountering DCs in lymph organ?

A

-Between blood and secondary lymph organs

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64
Q

Which 3 families of proteins control T cell migration (naive and effector) ?

A
  • Selectins
  • Integrins
  • Chemokines
  • These regulate migration of ALL leukocytes
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65
Q

Which adhesion molecule and chemokine receptor does a naive T cell express?-

A
  • L-selectin (CD 62L)

- CCR7 receptor

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66
Q

Which strucutre do naive T cells migrate to the lymph nodes via?

A
  • HEV
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67
Q

What do HEVs do in lymph node?

A
  • Have endothelial cells that express carb ligands –> bind to L-selectin
  • Display chemokines only recognised by CCR7
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68
Q

What is the process of naive T cell migration?

A
  • Naive T cells in blood (L-selectin rolling interactions with HEV)
  • Chemokines can bind to CCR7 on T cells –> intracellular signals
  • LFA-1 gets activated on naive T cell
  • Increased binding affinity of integrin to ICAM-1
  • Increased adhesion of T cells (so they slow down)
  • T cells EXIT through endothelial junctions and retained in lymph node
  • Goes to T cell zone of stroma (lymph node)
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69
Q

Do effector T cells express CCR7 or L-selectin?

A

NO! Hence don’t get drawn to lymph node

70
Q

Is the migration of activated T cells controlled by the same factors as in leykocyte migration?

A
  • YES
71
Q

What do activated T cells epxress a lot of?

A
  • Glycoprotein ligands –> E and P selectins + integrins LFA-1 and VLA-4
72
Q

In T cell migration, what do TNF-alpha and IL-1 act on endothelial cells to increase?

A
  • Act on endothelial cells to INCREASE E, P selectins + ligands for integrins like ICAM1, VCAM-1 (Vascular cell adhesion molecule)
73
Q

Does effector T cells migrating to the infection site (homing of effector T cells) depend on antigen recognition?

A
  • NO!!
  • It depends on adhesion molecules and chemokines
    (BUT lymphocytes that recognise antigens are preferentially retained at this site )
74
Q

Can any effector T cell in blood enter any site of infection?

A
  • YES!

- To maximise chances that effector T cells will happen to recognise antigen and help with infection

75
Q

Can any effector T cell be REACTIVATED from ANY host cell displaying peptide:MHC?

A
  • YES! (but not the same for naive T cells)
76
Q

What is expressed on lymphocytes that determines specificity and diversity?

A
  • Antigen recepotrs generated via VDJ recombination
77
Q

What is the clonal selection theory?

A

one cell-one antibody

  • after exposure to a microbe, antigen specific clone “selected” and then proliferates
  • Immune response SPECIFIC to that antigen occurs
78
Q

What is clonal expansion?

A
  • Lymphocytes proliferate after activation generating army of clones with a SINGLE SPECIFICITY
79
Q

What is specialisation?

A
  • Tailored responses for effective elimination of specific pathogen
80
Q

What is the contraction of homeostasis?

A
  • The decline of the immune response from apoptosis of lymphocytes AFTER pathogen is elminated
  • Homeostasis settled with memory cells
81
Q

Why do we need two types of adaptive immunity?

A
  • Because certain antigens are important for SOME pathogens and not others
    e. g. Cholera needs the adaptive immune system
  • Bacteria has flagella which innate immune system will recognise BUT won’t work because it is the toxin the bacteria secretes that does damage
  • SO adaptive response needed to PRODUCE ANTIBODIES TO NEUTRALISE TOXIN
82
Q

Can antibodies block infections from occuring in the first place?

A
  • YES!

- Can bind to virus infected cell

83
Q

A combination of ___ and _____ activates DCs:

A

A combination of PRRs and CYTOKINES will activate DCs

84
Q

Why do DCs and T cells BOTH express CCR7?

A
  • So they can MIGRATE to lymph node and come into contact at T cell zone –> adaptive immune response generated
85
Q

What is T cell priming?

A
  • Where the T cell meets the CORRECT/MATCHING DC with peptide
86
Q

What is the role of adaptor proteins such as SH2 and SH3?

A
  • LINK receptors to COMMON signalling pathways in cell

- mediate protein-protein interactions

87
Q

What is signal 1 for T cell activation?

A
  • Antigen recognition
88
Q

Is signal 1 (Antigen recognition) sufficient for activation of a T cell?

A

No! (Well technically it is sufficient and not necessary)

- need signal 2

89
Q

`Can TCR induce signals and why?

A
  • NO

- Small cytoplasmic domains

90
Q

What does ITAM stand for?

A
  • Immunoreceptor Tyrosine based Activation Motif
91
Q

What is the advantage of CD4/CD8 domains interacting with MHC?

A
  • Coreceptor can be in close proximity to TCR complex
92
Q

What is the function of Lck?

A
  • Interacts with the large cytoplasmic tails of CD4 + CD8

- Lck phosphorylates ITAMs and creates docking sites

93
Q

What are the 3 parts of signalling?

A
  1. MEMBRANE PROXIMAL EVENTS (Tyrosine is phosphorylated–> activates enzymes–> creates docking sites for adaptor proteins
  2. COMMON BIOCHEMICAL SIGNALLING PATHWAYS (Enzymes + 2nd messengers amplify the cell surface signal and transduce signals)
  3. TRANSCRIPTION FACTORS ACTIVATED
94
Q

What is the generalised pathway for TCR: peptide recognition/signalling?

A

TCR recognises peptide: MHC

  • CD4/CD8 interacts with MHC in a PEPTIDE INDEPENDENT WAY
  • Lck comes into CLOSE PROXIMITY with TCR complex AND phosphorylates tyrosines in ITAMs of CD3 and zeta chains
  • ZAP70 (tyrosine K) binds to phosphorylated tyrosines on CD3 and zeta chains which ACTIVATED ZAP70–> proteins phosphorylated–> adaptor proteins + enzymes go into signalling pathway –> 2nd messengers made and TFs activated – > ACTIVATED T CELL TURNS ON NUMBER OF GENES
95
Q

What does LFA-1 on a T cell bind to?

A
  • ICAM-1 on APC
96
Q

What is signal 2 for T cell activation?

A
  • B7 molecules (CD80 and CD86) on DC

and CD28 on T cell

97
Q

What is LFA-1 LOW AFFINITY on?

A
  • Naive T cell BEFORE antigen recognition
98
Q

If DC is presenting self MHC: peptide then there is no:

A

No costimulatory signal

99
Q

What do microbes cause the expression of?

A
  • Costimulatory molecules

- Signal 2 –> CD28 on T cell is confirming that there is a threat

100
Q

Which 4 things must occur for T cell activation to be SUCCESSFUL?

A
  • Antigen recognition (TCR and peptide: MHC)
  • Signal transduction (TCR complex + CD4/CD8 coreceptor)
  • ADHESION—> Stabilises T cell-APC interaction (LFA-1 and ICAM1)
  • Costimulatory signals (signal transduction via CD28 (T cell) binding to CD80 (DC)
101
Q

which genes are transcribed from signalling pathways?-

A
  • Cell cycle proteins e.g. c-Fos
  • Molecules important for effector functions e.g. CD40L
  • Molecules that regulate immune response e..g CTLA-4
  • Cytokines like IL-2
102
Q

Without IL-2 expression, what DON’T you have?

A
  • No clonal expansion
103
Q

What occurs in T cell activation in terms of IL-2 expression?

A
  • Increased expression of Il-2R alpha chain
  • Causes Il-2 to bind with HIGH AFFINITY to IL-2R
  • Leads to PROLIFERATION AND SURVIVAL
104
Q

What is the function of CTLA-4?

A
  • Binds to CD80/CD86 (on DC) which leads to DECREASED costimulation, decreased IL-2 expression and decreased proliferation
105
Q

What additional help do CD8 T cells need to be activated?

A
  • Cross presentation

- Present class II to MHC then class I

106
Q

What does it mean if a T cell becomes anergic?

A
  • Lack of a reaction

- only requires one instead of 2 signals

107
Q

DO CD4 T cells get activated in close proximity to CD8 T cells?-

A

YES!

- So CD4+ helper T cells can Secrete Il-2 which stimulates CD8 T cells

108
Q

How does CD4 T cell help CD8? (2 reasons)

A
  1. Secretes Il-2 (allows CD8 T cell to proliferate more)

2. Sends signals to DC to INCREASE costimulators on surface to activate CD8 T cells)

109
Q

What activation in migration are chemokines involved in?

A
  • integrin activation
  • Integrin goes from low affinity–> high affintiy
  • Also chemotaxis
110
Q

What are integrins important for?

A
  • Stable adhesion of leukocytes to endothelial cells (LFA-1) –> has multiple adhesion functions
111
Q

What is selectin?

A
  • ‘A naive T cell home-in molecule’

- Gets the naive T cell into lymph node

112
Q

Do activated helper T cells differentiate into any type of cell to eliminate a microbe?

A
  • NO! The one that BEST eliminates the pathogen is selected –> e.g. either Th1, Th2, Th17 cells
113
Q

What are CD4+ T helper cells involved with in general?

A
  • intracell (phagocytosed) and EXTRACELLULAR bacteria

- MHC II presents it CD4+ T cells recognise it –> macroophages and B cells activated –> INFLAMMATION (in general)

114
Q

What are the 3 signals that DCs give to naive T cells?

A

signal 1: Antigen recognitiopn (TCR recognition of peptide:MHC)
Signal 2: Costimulation signal CD28 (T cell) with CD80/CD86 (B7) proteins on activated DCs
SIgnal 3: Cytokines–> diffrerentiation of helper T cells

115
Q

What do cytokines allow T cells to do?

A
  • Differentiate into various helper T cells
116
Q

`What happens when flagella on microbes is detected? (what PRRS, what cytokine secreted etc)

A

TLR5 (flagella) and TLR-4 (LPS) activated

  • DC recognises it–> secretes IL-12
  • STAT 4 and STAT1 (TFs) ACTIVATED
  • Th1 cells formed
117
Q

In basic terms what is Th1 responsible for?

A
  • Intracellular microbes
118
Q

In basic terms what is Th2 responsible for?

A
  • Helminths
119
Q

In basic terms what is Th17 responsible for?

A
  • Extracellular fungi and bacteria
120
Q

What is a T0 cell?

A
  • AN ACTIVATED T cell but not differentiated
121
Q

Which cytokine does Th1 secrete, what does it act on (target), which host is it defending and what role does it have in the disease?

A
  • Cytokine: IFN-gamma
  • Target cell: Macrophage (paracrine signalling)
  • Host defense: intracellular pathogen
  • Role in disease is autoimmune diseases and CHRONIC inflammation
122
Q

Which cytokines does Th2 secrete, what is its target cell, which host is it defending, and what role does it play in disease?

A
  • Cytokine: IL-4, Il-5, IL-13
  • Target cell: Eosinophils
  • Defense: Parasites
  • Role in disease : Allergy
123
Q

Which cytokines does Th17 secrete. what is the target cell the cytokines act on, what is the host defense and what role does it play in disease?

A
  • Cytokines: Il-17, IL-22
  • Target cell: Neutrophils
  • Defense: Extracellular fungi
  • Role in disease: Autoimmunity
124
Q

Are T cell cytokines produced all the time?

A
  • NO! Only produced when needed
125
Q

What does it mean when we say T cells and cytokines exhibit pleiotropy?

A
  • That each cell has multiple biological actions
126
Q

What does it mean when we say T cell cytokines are redundant?

A

MULTIPLE cytokines share the SAME activity

127
Q

What does IL-2 cause?

A
  • T cell activation (via autocrine signalling) and proliferation
128
Q

What does IFN-gamma cause?

A
  • Activation of macrophages

- from CD4+ CD8+ and NK cells

129
Q

What does IL-5 cause?

A
  • Activation of eosinophils

- from CD4+ T cells, mast cells, innate lymphoid cells

130
Q

What does IL-4 cause?

A
  • B cell switches–> IgE

- from CD4T cells and mast cells

131
Q

What does Il-17 cause?***

A
  • Stimulates ACUTE inflammation
  • Promotes production of antimicrobial peptides
  • from CD4 T cells, and other cells
    (not sure what other cells)
132
Q

What does IL-22 cause?

A
  • Maintains epithelial barrier
  • Increased barrier integrity
  • Promotes the production of antimicrobial peptides
  • From CD4+ T cell, NK cells, innate lymphoid cells
133
Q

What does TGF-beta cause?

A
  • Inhibits T cell activation
  • Differentiation of Treg cells
  • from CD4+ T cells and other cells
134
Q

What are 3 examples of intracellular microbes (ones that evade killing in phagolysosome-not viruses) rthat Th1 cells will work against?

A
  • Leishmania
  • TB
  • Protozoa
  • Lysteria (food borne)
135
Q

For a T0 cell to differentiate into a Th1 cell, which two cytokines does it need to be exposed to and what isthe process?

A
  • IL-12 and INF-gamma
  • Intacellular microbes cause DCs and macrophages to secrete IL-12 + NK cells secrete IFN-gamma
  • Th1 cell produced
136
Q

Is INF-gamma produced by other Th1 cells?

A
  • YES! Later in the immune response
137
Q

What is the Th1 cell effector function?

A
  • Secretes IFN-gamma –> activates macrophages (classical macrophage activation) —> makes macrophages BETTER killers of microbes
  • Complement activation (opsonisation and phagocytosis)
138
Q

Do CTLs work with Th1 cells sometimes to fight infection?

A
  • YES!
  • Th1 cells aren’t always on their own e.g. those that escape into the cytosol following phagocytosis
  • Th1 cells ACTIVATE macrophages to BETTER kill microbes and CTLs KILL infected macrophages
139
Q

Which cytokines does Th2 secrete?

A

Il-4, Il-5, IL-13 , acts on parasites like helminths and acts on eosinophils

140
Q

Which cytokine do you need for differentiation T0 cells to Th2 cells?-

A
  • IL-4 secreted by ILC2 and NKT cells (natural killer T cells), and mast and eosinophils
  • IL-4 also acts on B cells for IgE production
141
Q

Which cytokines do you need for the differention of T0 cells to Th17 cells ?

A
  • Il-1
  • IL-6
  • IL-23
  • TGF-beta
  • These then cause differentiation to Th17 which then secretes IL-22 and IL-17
142
Q

Which Th2 cell cytokines are involved in intestinal mucus secretion and peristalsis (weep and sweep response) ?

A
  • IL-4 and IL-13 (weep-mucus and sweep response)
143
Q

What role do the cytokines IL-4 and IL-13 have with macrophages?

A
  • They ALTERNATIVELY activate macrophages –> M2 macrophages -antiinflammatory
144
Q

Are M2 macrophages inflammatory or antiinflammaotry?

A
  • Antiinflammatory
145
Q

Which cytokine is involved in antobody production and mast cell degranulation (Th2) ?

A
  • IL-4
146
Q

Which Th2 cytokine activates eosinophils?

A
  • Il-5
147
Q

What does Eosinophil activation result from?

A
  • Crosslinking of FceRs by IgE + IL-5 (Th2 cells)
148
Q

What is the Th1/Th2 paradigm?

A
  • There must be a balance between Th1 and Th2 responses
149
Q

In terms of the Th1/Th2 paradigm, what does a strogner Th1 cell response mean?

A
  • There will be a weaker Th2 response

- TH1 cytokines will INHIBIT Th2 differentiation via IFN-gamma

150
Q

What do Th1 cells inhibit the Th2 differentiation with ?

A
  • IFN-gamma
151
Q

What do Th2 cells inhibit the Th1 cell response with (cytokine)?

A

Il-4 at the developmental level

152
Q

What are M1 macrophages?

A
  • Proinflammatory

- Dangerous cells (lots of chemokines, cytokines and lysosomal enzymes)

153
Q

What are M2 macropohges and which cytokine inihibits the M1 macrophage?

A
  • Antiinflammatory

- IL-10 and TGF-beta inhibit inflammation and IL-4 and Il-13 (Th2) inhibit M1 macrophage activation

154
Q

Is the Th1/Th2 balance affected by both environmental and genetic factors?

A
  • YES! e.g. high or low fibre diet and UV
155
Q

What are the effects of Th1 cells causing pathology?

A
  • Chronic inflammation will occur
  • Activation of M1 and pro inflammatory cytokines
    e. g. Inflammatory bowel disease (autoimmune disease)
  • tH CELLS, CTL and B cells involved
156
Q

What happens when Th2 cells go bad?

A
  • Asthma, anaphylaxis, allergic rhinitis
  • Reexposure to allergen = mast cell degranulation, histamine release and cytokine production
  • IgE binds to the Fc receptor on mast cell
157
Q

What are Treg cells important in?

A
  • Regulation of balance between Th1/Th2 cells

- Secrete TGF-beta to suppress differentiation and proliferation of Th1 and Th2 cells

158
Q

What are three examples of conditions that Th17 cells work against?

A
  • Staph aureus
  • Pneumoniae (klebsiella pnemoniae)
  • Candida albicans (thrush)
159
Q

Which 4 cytokines drive the differentiation of T cells?

A
  • IL-1
  • IL-6
  • IL-23
  • TGF-beta
    These switch on RORy + STAT 3 : T0–> Th17
160
Q

What does IL-17 do?

A
  • INDIRECTLY attracts neutrophil to site of infection

- Acts on other cells and induces them to secrete pro inflammatory cytokines and chemokines to INCREASE inflammation

161
Q

What does IL-22 do?

A
  • Acts on endothelial cells to enhance integrity of epithelial barriers
162
Q

What do IL-17 and IL-22 act together to do?

A
  • Promote the production of antimicrobial peptides =DEFENSINS (Cause microbe to lyse)
163
Q

What are 3 exmaples og conditions that CTL try to eliminate?

A
  • Cytosolic microbes (Influenza and ebola)

- Tumor cells (melanoma)

164
Q

Which cytokine is needed to help CD8 T cells to activate and differentiate?

A
  • IL-2 needed
165
Q

What are the CD8 T cell effector functions?

A

-Perforin and granzymes in CTL granules

166
Q

When do CTLs become activated?

A
  • After recognition of peptide:MHC on target cells (immune synapse forms)
167
Q

What does perforin do?

A
  • Pokes pores in target cell membrane and vesicle membrane
  • Allows GRANZYME B to enter
  • GRANZYME B activates caspases –> APOPTOSIS
168
Q

What is an effector funcion of CD8 T cells ?

A
  • Can secrete IFN-gamma –> upregulates MHC class I expression (more likely CD8 T cell will recognise)
  • inhibit viral replication
169
Q

What does IFN-gamm cause for Th1 differentiation andf macrophages?

A
  • Increases Th1 differentiation (intracellular microbes)

- Increases Macrophage activation (become better killers)

170
Q

Do CTLs, Igs and Th1 cells all cooperate in viral infections?

A
  • YES!
  • Antibodies work to neutralise virus (prevents entry in cells)
  • CTLs KILL viral cells
  • Th1 cells result in CTL differentiation and HELP B cells prosduce neutralising Igs

IMM2011 (7 decks)

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