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IMMUNOLOGY VDMP817 > lecture 6 exam 2 > Flashcards

lecture 6 exam 2 Flashcards

1
Q

T cell differentiation by

A

TCR
accessory molecules
functions of specific Tcell (alpha beta, gamma delta, innate lymphoid)

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2
Q

alpha beta t cells

A

CD4+ & CD8+

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3
Q

CD4+ t cell example

A

type of alpha beta
T helper 1, TH2, TH17, Treg
memory T cell

with 2 of something

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4
Q

CD8+ t cell example

A

type of alpha beta
cytotoxic t cell
memory

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5
Q

innate lymphoid cells

A

type of tcell subpopulation
NK cell
NK T cell

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6
Q

CD8+ t cell function

A

defend against INTRACELLULAR PATHOGENS
immune defense against VIRUSES & INTRACELLULAR BACTERIA
kill infected cells to prevent pathogen replication and spread to adjacent healthy cells
recognizes MHC 1 (displays peptide from pathogen - on B cell?)

also known as CTL!! cytotoxic t lymphocytes

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7
Q

t cell activation and proliferation signals

A
  1. antigen specific
  2. costimulatory
  3. cytokines
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8
Q

antigen specific signal for t cell activation/proliferation

A

TCR & CD3 (TCR complex)

CD4 & CD8 (co receptor)

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9
Q

costimulatory signal for t cell activation/proliferation

A

CD28 binds to B7 (CD80/CD86)

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10
Q

cytokines signal for t cell activation/proliferation

A

IL2 for proliferation

others for differentiation of Th cells (IL6, IL12, TGFbeta, IL4)

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11
Q

CD8+/CDL activation

A

must be activated to become cytotoxic effector cell!
activated in 2 lymphoid tissue
requires stronger costimulatory activity than CD4+ t cells for activation
only virus infected DCs upregulate sufficient B7 for co stimulation and CD8+ tcell activation
activated CD8+ T cell synthesizes own IL2 & IL2R which drives own proliferation and differentiation
need CD4s to become CTLs when APCs have weak costimulation
CD4 Tcells provide CYTOKINES for proliferation, increase MHC1 expression and costimulation

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12
Q

CD8+/CTL effector phase

A

CTLs kill in 2-10 minutes if TCR of CTLs recognize the MHC 1 peptide on target cell through CYTOTOXINS and CYTOKINES
perforin pathway - adhesion phase & lethal hit

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13
Q

cytotoxins

A

used by CTLs when antigen recgonized by MHC1
specialized products contained within lytic granules of cytotoxic cells
perforins
granzymes
granulysin

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14
Q

perforins

A

cytotoxin from CTL when effector phase activated

PRODUCE PORES! in target cell to kill

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15
Q

granzymes

A 
cytotoxin from CTL when effector phase activated
INDUCE APOPTOSIS (through serine proteases)
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16
Q

granulysin

A 
cytotoxin from CTL when effector phase activated
INDUCE APOPTOSIS (through antimicrobial peptide)
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17
Q

cytokines

A

used by CTLs when antigen recognized by MHC1

TNF - tumor necrosis factor family members (CD95L) INDUCE APOPTOSIS

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18
Q

adhesion phase of effector phase of CD8+

A 
perforin pathway (produce pores!)
IMMUNOLOGICAL SYNAPSE (MHC1 + peptide + TCRs on CTL)
site of Tcell APC contact formed by CLUSTERING of the TCR complex upon binding to MHC peptide complex on APC
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19
Q

immunological synapse

A

TCRs CTLs + peptide MHC1 complex on target cell during adhesion phase of effector phase of CD8+
site of TcellAPC contact

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20
Q

adhesion phase of effector phase CD8+ function

A

helps overcome low affinity of TCRs for peptide-MHC ligands
facilitates prolonged T cell signaling
ensures specific delivery of signals

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21
Q

lethal hit of effector phase CD8+

A

perforin pathway
CTLS will orient golgi and granules toward target cell
cytoplasmic granules migrate to the center of the synapse
fusion with T cell membrane and cytolytic granules are inserted into target cell

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22
Q

perforins

A

pore forming glycoproteins produced by CTLs and NK cells
insert themselves into the target membrane and oligomerize to form tubular transmembrane channels
granzymes -> caspase3 go through and cause DNA fragmentation then apoptosis

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23
Q

granzyme

A

perforin pathway w CD8+
serine proteases that enter the target cell via the perforin pores and trigger apoptosis through caspase 3

CTLs have granzyme inhibitors so they themselves are not damaged during this process (snake and venom - have vescicles)

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24
Q

Fas/FasL effector phase of CD8+

A

death receptors
T cell surface molecule - FasL (CD95L) binds to cell death receptor Fas on target cell
CD95L expressed on an activated CTL and NK cell -> apoptosis!
creates DISC

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25
Q

DISC

A

death inducing signaling complex
initiates apoptosis
engagement of CD95L (CTL/NK cell) and CD95 (target cell) draws 3 CD95’s together to make this disc for Cas8 -> Cas3 -> apoptosis

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26
Q

apoptosis process

A

normal cell -> clumping of chromatin, blebbing, loss of organelles -> nuclear fragmentation, apoptotic bodies -> apoptotic bodies
release debris that contain content and are cleaned up by macrophage and other phagocytes

results from DISC, granzymes, perforins, FasL, cas8,9,3,6,7

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27
Q

apoptosis

A 
active
energy dependent
tightly regulated type of cell death 
normal function
NUCLEAR DISSOLUTION WITHOUT COMPLETE LOSS OF MEMBRANE INTEGRITY

eaten by macrophages and phagocytes

28
Q

necrosis

A

major pathway of cell death in many common injuries
severe damage to cell results in enzymes leaking out of lysosomes, entering the cytoplasm, digesting the cell

pathologic process

29
Q

CTLs kill infected cells in succession

A
  1. recognition of peptide MHC1 complexes on an infected cell by CTL programs the infected cell to die
  2. CTL detaches from its target cell and synthesizes a new set of lytic granules
  3. CTL seeks out and kills another target
30
Q

CTL targets

A
  1. any cell that expresses foreign peptide in MHC1
  2. often cytosolic infections (viral/protozoal/bacteria)
  3. tumors
  4. exception: cells that lack MHC1 expression require NK cells to kill

tumor cells downregulate MHC1 (CD8)
RBC dont have MHC1`

31
Q

CD4 & CD8 synergy

A

eradicates intracellular infections

IFNgamma w CD4 -> killing of microbes in phagolysosomes -> CD8 binds to target cell -> infected cell killed

32
Q

Immunological memory

A

key feature of adaptive immunity formed during primary immune response
-longterm immunity
-ensures host will generate more potent immune response upon re-encounter with same antigen
-induced in both B and T cells
- generally last lifetime of host
-second infections are usually celared before symptoms produced
-generated in all secondary lymphoid organs
-generated from natural infection or immunization
memory B and T cells

33
Q

memory B cells

A

respond quickly to antigen after previous encounter
have undergone affinity maturation and isotype switching
more sensitive to infection
more easily activated

34
Q

memory CD4 and CD8 T cells

A

respond more quickly to antigen after previous encounter
CD4 memory have undergone differentiation to TH1,2,17,Tfh or Treg
more sensitive to activation upon infection
quicker activation
less costimulation required

35
Q

antigen experienced memory T cells

A

can be most abundant T cell population in body -> accumulate throughout life

36
Q

memory t cells

A

antigen experienced
created by asymmetric division of T cell after activation
apoptosis resistant
long lived (self renewing & half life is 8-12 yrs)
resting until interact w APC a second time
activated w/in 48-72 hrs of reexposure (QUICKER THAN NAIVE T CELLS)
enter tissue sites other than lymphoid
LESS COSTIMULATION NEEDED THAN NAIVE
ACTIVATED BY MACROPHAGES, DC, B CELLS

37
Q

what cells activate memory t cells

A

macrophages, DC, B cell - second time to exposure

38
Q

types of memory T cells

A
  1. central memory
  2. effector memory
  3. tissue memory
39
Q

central memory Tcells

A

circulate through secondary lymphoid tissues
high CCR7 expression on T cell
LACK IMMEDIATE EFFECTOR FUNCTIONS (until stimulated)
rapid recall responses
rapidly express CD40L to interact w CD40 on B cells

40
Q

effector memory Tcells

A

constitutively express integrins and receptors for INFLAMMATORY cytokines, enabling them to go to inflammed tissues
nearly IMMEDIATE EFFECTOR FUNCTION upon reencounter to antigen
secrete HIGH LEVELS OF CYTOKINES

41
Q

tissue memory Tcells

A

OCCUPY TISSUES (dont move)
provide FIRST RESPONSE to pathogens
reside under BODY SURFACES (CD8) or throughout body in small clusters (CD4) of memory cells
RAPIDLY PRODUCE CYTOKINES after infections
dont circulate in peripheral blood

42
Q

microbes evade cell mediated immunity through

A

inhibiting antigen presentation, transporters, proteasomal activity, removing MHC1 (herpes simplex virus, cytomegalovirus, epstein-barr)

43
Q

what cells bridge innate and adaptive immunity

A

NK
gamma delta
NKT cells

critical components of body’s defenses as are able to respond to foreign (external) antigens or destroy abnormal cells (internal) immediately

44
Q

alpha beta TCR lymphocytes

A

Thelper (CD4)

CD8 (CTL)

45
Q

B cells in adaptive immunity

A

IgG, A, E

classical pathway

46
Q

NK cells

A

produced by bone marrow stem cells
found in peripheral blood, lymph nodes, spleen, bone marrow (NOT THYMUS)
dont express T cell receptor (TCR)
not antigen specific

triggered by:

  1. antibody mediated cellular cytotoxicity (ADCC)
  2. recognition of altered surface molecues
47
Q

NK cell triggering mechanicsm

A

ADCC
recognition of altered surface molecules:
-MHC 1 prevents NKcell killing
-NK cells recognize receptors that are only upregulated in stressed cells (ex: infected w viruses or intracellular bacteria)

48
Q

MHC 1 say what to NK

A

dont kill me!!! not on RBC

49
Q

ADCC

A

triggering mechanism of NK

  1. antibody binds antigens on surface of target cell
  2. Fc (BCR) receptors on NK cells recognize bound antibody
  3. cross linking of FC receptors signals the NK cell to kill the target cell that antibodies bound to
  4. target cell apoptosis

NK cells recognize IgG antibodies bound to cellular targets via CD16
NK cell cytotoxicity can only occur at a late stage in primary immune response or during a secondary immune response

50
Q

NK cells respond to inhibitory receptors

A

specific for various MHC1 molecules

KIR (killer inhibitory receptor) engagement of MHC 1 inhibit cytotoxic activity

51
Q

NK cells respond to activing receptors

A

specific for cellular proteins (MICA MICB) expressed on stressed cell

52
Q

NK cell effector (killing) mechanisms

A

perforin
granzymes
CD95/CD95L mediated apoptosis (pore!)

also produce IFN gamma - inflammatory cytokine

53
Q

gamma delta T cells

A

derived from same precursor as alphabeta T cells
express gamma delta TCR
BRIDGE INNATE AND ADAPTIVE IMMUNITY
NOT MHC RESTRICTED: do not undergo +/- selection in THYMUS
prominent in mucosal tissues/skin
-lack CCR7 so no enter LN - instead enter inflammed tissues
PROMINENT IN NEONATAL ANIMALS, decline w age
increased in ruminents and pigs, low in humans and mice

54
Q

CCR7 allows/invites cells to enter

A

lymph node

not in gammadelta
in NK

55
Q

gammadelta T cell link to innate immunity

A

respond to PAMPS - recognize conserved antigens & phosphoproteins
rapid response to PAMPS and DAMPS (like B1 cells)
high density at epithelial borders

56
Q

gammadelta T cell link to adaptive immunity

A

rearrange TCR genes w junctional diversity
present antigen via MHC 2
directly cytotoxic
can differentiate into memory cells

57
Q

gammadelta T cell functions

A

immunity against pathogens
drive or down regulate adaptive immunity
kill targets directly (cytotoxicity)
tissue surveillance and healing

58
Q

immunity against pathogen function for gammadelta T cells

A

cytokine help to activate other immune cells (IFNgamma (inflammation), IL4, IL10, IL13, TNFalpha)
chemokines released to recruit immune cells

59
Q

drive or down regulate adaptive immunity function for gammadelta T cells

A

cytokines help call memory T cells to site of infection

down-regulatory cytokines (TGFbeta, IL10 - B10 cells)

60
Q

kills targets directly (cytotoxicity) function for gammadelta t cells

A

cytolytic via FasL or degranulation of perforin and granzyme

pathogen destruction via granulysin

61
Q

tissue surveillance and healing function of gamma delta t cells

A

recognize stressed epithelial cells for apoptosis

express tissue growth factors

62
Q

NK T cells

A

heterogenous population of cells
share traits of both NK cells and T cells
-express TCR of limited diversity and classical NK cell antigens
respond to glycolipids and foreign lipids presented by CD1 (a MHC1 like molecule)
most common in liver, but also in bone marrow, adipose tissue, thymus, spleen and blood

63
Q

NK cells antigen recognition/mechanism of activation & location in body

A

CD16 (ADCC)
activating/inhibitory receptors

blood, spleen, mucosal, tissues

64
Q

gammadelta T cells antigen recognition/mechanism of activation & location in body

A

phosphoproteins
PRR
gammadelta TCR

blood, skin, mucosal tissues

65
Q

NKT cells antigen recognition/mechanism of activation & location in body

A

alphabeta TCR of limited diversity
CD1 restricted glycolipids (need CD1 to activate for antigen directly)

liver, adipose tissue, bone marrow

IMMUNOLOGY VDMP817 (22 decks)

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