Immune-2 Flashcards by Emily Liu

what are cells that express CD4

helper T cells

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what happens when naive helper T cells interact with DCs

they differentiate into TH1, TH2, TH17, THreg

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what does the type of TH cell depend on

the specific type of cytokine released from the DCs

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what determines the the specific type of cytokine released from the DCs

the specific type of pathogen

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what 2 things characterize each TH cell

the cytokines that they produce, the innate immune effector mechanism that is activated

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what are the three phases in CD4 T cell activation

recognition, activation, effector

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what happens in recognition phase

macrophages display foreign antigens on their surface in a form that can be recognized by antigen-specific TH lymphocytes.

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what happens in activation phase

TH cells produce cytokines that promote the proliferation and differentiation of the T cells as well as other cells, including macrophages

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what happens in effector phase

activated macrophages carry out phagocytosis and cytolysis

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what is a super important thing that is released during T cell activation (CD4+)

the release of IL-2

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what is the role of IL-2 + how do they work

These are essential to allow maturation of t cells

It works in autocrine mechanism, they start proliferating, dividing - clonal expansion

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what is the 3 signals in CD8+ T Cell activation

TCR-MHC class interaction
co-stimulation
pro-inflammatory cytokines

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what is the early outcome of CD8+ T Cell activation

no cytokine secretion

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what is the late outcome of CD8+ T Cell activation

clonal expansion and cytotoxicity

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what are the 3 mechanisms of CD8 killing

granzymes
Fas ligand on their surface (death receptor)
make cytokines, like TNF-alpha

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what happens to T cells with T cell activation + how

increased T-cell survival and differentiation through production of cytokines like IL-2

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what happens to metabolism with T cell activation

increased

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what happens to cell survival genes with T cell activation

upregulated

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what happens to cell division with T cell activation

upregulated

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what happens to cytotoxic cells with T cell activation

they are activated (killer functions)

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what happens to memory cells with T cell activation

they become activated

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why do you have death of t cells as a consequence with t cell activation

because you need to down regulate the immune response

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what are the 2 transcription factors that are activated once the t cell receptor is activated

NFAT and mTOR

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what is the role of NFAT

the activation of T cells, increases IL 2 production and also more proliferation and differentiation

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what is the role of mTOR

activation, differentiation and migration

what activates mTOR

IL2 and TCR

is t cell activation regulated

yes highly

what are the 2 checkpoints for the immune pathway

CTLA-4 and PD1

what is the point of checkpoints for t cell activation

to balance protective immunity and immunopathology

what is a bad thing about the immune checkpoints

during responses to chronic pathogens, they can limit protective immunity

which is the leader of the immune checkpoint inhibitors

CTLA-4

what causes CTLA-4 to be upregulated

stimulatory signals from both TCR and CD28(B7) binding induces upregulation of CLTA-4 on cell surface

what is CTLA-4 similar to (explain)

CD28 homolog with much higher affinity for CD80/86 (B7)

what is b7

another name for CD80/86

what competes for binding of CD80/86 (immune checkpoint)

CLTA-4 and CD28

where does CTLA-4 work

at the lymph node (starting location of immune response/ naive T cell activation)

what happens once CTLA-4 binds to CD80/86 (2 things)

- can prevent the costimulatory signal by CD28 | - produces inhibitory signals

what happens to t cell activation when CTLA-4 and B7 bind

full activation is prevented

how is full activation of t cells by CTLA-4 inhibited

by inhibiting IL-2 production and inhibits cell cycle progression

what can CTLA-4 do for autoreactive t cells

stops then at the initial stage of activation

what is PD-1

a member of the B7/CD28 family of costimulatory receptors

which cells does PD-1 regulate/ effect + where

previously activated T cells in peripheral tissues

how does PD-1 regulate t cell activation

PD-L1 and PD-L2 (programmed death ligand 1 and 2)

what is PD-1 a hallmark of

exhausted T cells

when does T cell exhaustion occur

during chronic infections and cancer

what does PD-1 binding do generally

reduce activation of T cells

what are the 3 signals that PD-1 binding do

- inhibits T cell proliferation - inhibits cytokine production - reduces T cell survival

what are the 2 main differences between CTLA-4 and PD-1

- anatomic locations and timing of immune inhibition | - signalling mechanisms

where is CTLA-4 expressed (which cells)

only on T cells

where is PD-1 expressed (which cells)

on activated T cells, B cells and myeloid cells | and in lots of tissue too?

what are 2 things that B cells express

antigen specific B cell receptors (BCR) | germ-line encoded, pattern recognizing toll like receptors (TLRs)

what is responsible for fine tuning functional B cell responses

dual BCR and TLR engagement

what does dual BCR and TLR engagement link

innate and adaptive immune functions

what are the 2 types of naive mature B cells

- innate like B cells | - Adaptive follicular B cells

what are 2 types of innate like B cells

B-1 and marginal zone B cells

where do most of the marginal zone b cells stay

in the spleen

what kind of receptors do B-1 and marginal zone cells have

toll like receptors

what happens with ligation of TLRs with B-1 and marginal zone cells

they redistribute to the blood, lymph and spleen follicles

where are b-1 cells (lots of them at least)

in the peritoneal cavity

what are 4 direct functional responses of b-1 and marginal zone b cell

- proliferation - secrete Ig and cytokines - upregulate survival pathways - increase expression of co-stimulatory molecules to function like APCs

what does BAFF do

leads to prolonged survival

how can you get the 5 direct functional responses of b-1 and marginal zone b cell

likely require BCR and TLR engagement

why can you call the direct function of b-1 and marginal zone b cell innate

because you dont need t cells to activate

what can innate like b cells generate independently

antibody responses (independently of t cell help)

how can b cells recognize pathogens and self ligands

using b cells TLRs

what plays a crucial role in autoimmune pathogenesis

activation of autoreactive b cells by dual BCR and TLR engagement

how are b cells activated t-cell-dependently

via BCR engagement and interaction with cognate CD4+ T cells

what is required for maximum activation (t-cell-dependently)

combination of BCR engagement, T cell help via CD40 signalling and TLR stimulation

what do TH cells release that help B cells + what does it cause

cytokines to promote proliferation and differentiation of B cells into plasma cells and memory cells

what do plasma cells do

product high affinity antibodies

what do memory cells do

respond more rapidly and efficiently to subsequent encounters with the antigen

do plasma cells divide

what are 5 functions of antibodies

- neutralize pathogens/ toxins - complement activation - opsonization and phagocytosis - degranulation - cytotoxicity

what kind of cells do antibodies help degranulate

mast cells, basophils, eosinophils

how do antibodies neutralize pathogens/ toxins

prevent interactions with host cell receptors, bring it to barriers (like mucus)

what are 3 examples of antibody mediated complement activation

- phagocyte recruitment, make inflammatory mediators - opsonization - membrane attack complex

how do antibodies cause cytotoxicity

activation of natural killer cell degranulation to kill infected cells

what kind of cells degranulate because of antibodies

mast cells, basophils, eosinophils

what do mast cells, basophils, eosinophils release with degranulation

vasoactive substances, chemoattractants, cytokines

which cell expresses PD1

T B and myeloid cells

which cell expresses PDL1

tissue (peripheral)