Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

IMMUNOLOGY VDMP817 > lecture 6 exam 2 > Flashcards

lecture 6 exam 2 Flashcards

(65 cards)

Start Studying
1
Q

T cell differentiation by

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

alpha beta t cells

A

CD4+ & CD8+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CD4+ t cell example

A

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

with 2 of something

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CD8+ t cell example

A

type of alpha beta
cytotoxic t cell
memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

innate lymphoid cells

A

type of tcell subpopulation
NK cell
NK T cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

t cell activation and proliferation signals

A
  1. antigen specific
  2. costimulatory
  3. cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

antigen specific signal for t cell activation/proliferation

A

TCR & CD3 (TCR complex)

CD4 & CD8 (co receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

costimulatory signal for t cell activation/proliferation

A

CD28 binds to B7 (CD80/CD86)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cytokines signal for t cell activation/proliferation

A

IL2 for proliferation

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cytotoxins

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

perforins

A

cytotoxin from CTL when effector phase activated

PRODUCE PORES! in target cell to kill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

granzymes

A 
cytotoxin from CTL when effector phase activated
INDUCE APOPTOSIS (through serine proteases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

granulysin

A 
cytotoxin from CTL when effector phase activated
INDUCE APOPTOSIS (through antimicrobial peptide)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cytokines

A

used by CTLs when antigen recognized by MHC1

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
DISC
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
26
apoptosis process
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
27
apoptosis
``` 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
necrosis
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
CTLs kill infected cells in succession
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
CTL targets
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
CD4 & CD8 synergy
eradicates intracellular infections | IFNgamma w CD4 -> killing of microbes in phagolysosomes -> CD8 binds to target cell -> infected cell killed
32
Immunological memory
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
memory B cells
respond quickly to antigen after previous encounter have undergone affinity maturation and isotype switching more sensitive to infection more easily activated
34
memory CD4 and CD8 T cells
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
antigen experienced memory T cells
can be most abundant T cell population in body -> accumulate throughout life
36
memory t cells
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
what cells activate memory t cells
macrophages, DC, B cell - second time to exposure
38
types of memory T cells
1. central memory 2. effector memory 3. tissue memory
39
central memory Tcells
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
effector memory Tcells
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
tissue memory Tcells
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
microbes evade cell mediated immunity through
inhibiting antigen presentation, transporters, proteasomal activity, removing MHC1 (herpes simplex virus, cytomegalovirus, epstein-barr)
43
what cells bridge innate and adaptive immunity
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
alpha beta TCR lymphocytes
Thelper (CD4) | CD8 (CTL)
45
B cells in adaptive immunity
IgG, A, E | classical pathway
46
NK cells
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
NK cell triggering mechanicsm
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
MHC 1 say what to NK
dont kill me!!! not on RBC
49
ADCC
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
NK cells respond to inhibitory receptors
specific for various MHC1 molecules | KIR (killer inhibitory receptor) engagement of MHC 1 inhibit cytotoxic activity
51
NK cells respond to activing receptors
specific for cellular proteins (MICA MICB) expressed on stressed cell
52
NK cell effector (killing) mechanisms
perforin granzymes CD95/CD95L mediated apoptosis (pore!) also produce IFN gamma - inflammatory cytokine
53
gamma delta T cells
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
CCR7 allows/invites cells to enter
lymph node not in gammadelta in NK
55
gammadelta T cell link to innate immunity
respond to PAMPS - recognize conserved antigens & phosphoproteins rapid response to PAMPS and DAMPS (like B1 cells) high density at epithelial borders
56
gammadelta T cell link to adaptive immunity
rearrange TCR genes w junctional diversity present antigen via MHC 2 directly cytotoxic can differentiate into memory cells
57
gammadelta T cell functions
immunity against pathogens drive or down regulate adaptive immunity kill targets directly (cytotoxicity) tissue surveillance and healing
58
immunity against pathogen function for gammadelta T cells
cytokine help to activate other immune cells (IFNgamma (inflammation), IL4, IL10, IL13, TNFalpha) chemokines released to recruit immune cells
59
drive or down regulate adaptive immunity function for gammadelta T cells
cytokines help call memory T cells to site of infection | down-regulatory cytokines (TGFbeta, IL10 - B10 cells)
60
kills targets directly (cytotoxicity) function for gammadelta t cells
cytolytic via FasL or degranulation of perforin and granzyme | pathogen destruction via granulysin
61
tissue surveillance and healing function of gamma delta t cells
recognize stressed epithelial cells for apoptosis | express tissue growth factors
62
NK T cells
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
NK cells antigen recognition/mechanism of activation & location in body
CD16 (ADCC) activating/inhibitory receptors blood, spleen, mucosal, tissues
64
gammadelta T cells antigen recognition/mechanism of activation & location in body
phosphoproteins PRR gammadelta TCR blood, skin, mucosal tissues
65
NKT cells antigen recognition/mechanism of activation & location in body
alphabeta TCR of limited diversity CD1 restricted glycolipids (need CD1 to activate for antigen directly) liver, adipose tissue, bone marrow

IMMUNOLOGY VDMP817 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions