Search CTL/CD8+ T-Cell Epitope Database

Found 2 matching records:

Displaying record number 59272

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HXB2 Location	Gag(77-85) p17(77-85) DNA(1018..1044)	Gag Epitope Map
Author Location	Gag( NL4-3)
Epitope	SLYNTVATL	Epitope Alignment
Epitope Name	SL9
Subtype	B
Species (MHC/HLA)	human(A*02)
Immunogen	in vitro stimulation or selection
Patient MHC/HLA	285873: A*02:01, A*03:01, B*51:01, C*14:02, C*15:02; controller: A*02:01, A*03:01, B*07:02, B*40:01, C*03:04, C*07:02
Experimental methods	Other
Keywords	kinetics

Notes

• Flourescence videomircoscopy was developed to image CTL migration and immune response for extended-duration (>10h) imaging within a 3D type I collagen matrix. CTL were matured in co-culture with activated HIV-1-infected or cognate peptide (SL9/KK10)-pulsed CD4+ T-cells. Two stages of CTL dynamics were distinguished: An early 'commitment' phase of engagement and killing of the motile infected-CD4+ target of ˜ 15 min, followed by a prolonged 'secretory' phase when the CTL accumulate TCR signals from their killed target, remaining arrested for 3-10 h more, and they secrete cytokines and chemokines. High functional avidity CTL entered both commintment and secretory phases while low avidity CTL permitted target CD4+ cell escape and migration, failing to mount a robust secretory phase.
• The frequency of killing contacts for clone A14 CTLs encountering SL9-pulsed CD4+ target cells was antigen dose dependent.
• CTLs achieved first contact kill efficiencies of >90% in response to cells pulsed with high avidity (i.e. wild type or single mutation) SL9 peptides. Target cells bearing lower avidity SL9 variants required a 100-fold higher concentration to achieve first-contact kill efficiency against migrating targets.

References

Foley2014 Maria Hottelet Foley, Talitha Forcier, Elizabeth McAndrew, Michael Gonzalez, Huabiao Chen, Boris Juelg, Bruce D. Walker, and Darrell J. Irvine. High Avidity CD8+ T Cells Efficiently Eliminate Motile HIV-Infected Targets and Execute a Locally Focused Program of Anti-Viral Function. PLoS One, 9(2):e87873, 2014. PubMed ID: 24551068. Show all entries for this paper.

Displaying record number 59224

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HXB2 Location	Gag(263-272) p24(131-140) DNA(1576..1605)	Gag Epitope Map
Author Location	Gag( NL4-3)
Epitope	KRWIILGLNK	Epitope Alignment
Epitope Name	KK10
Subtype	B
Species (MHC/HLA)	human(B*27:05)
Immunogen	in vitro stimulation or selection
Patient MHC/HLA	285873: A*02:01, A*03:01, B*51:01, C*14:02, C*15:02; 828656: A*03:01, A*26:01, B*15:01, B*27:05, C*02:02, C*03:03
Experimental methods	Other
Keywords	kinetics

Notes

• Flourescence videomircoscopy was developed to image CTL migration and immune response for extended-duration (>10h) imaging within a 3D type I collagen matrix. CTL were matured in co-culture with activated HIV-1-infected or cognate peptide (SL9/KK10)-pulsed CD4+ T-cells. Two stages of CTL dynamics were distinguished: An early 'commitment' phase of engagement and killing of the motile infected-CD4+ target of ˜ 15 min, followed by a prolonged 'secretory' phase when the CTL accumulate TCR signals from their killed target, remaining arrested for 3-10 h more, and they secrete cytokines and chemokines. High functional avidity CTL entered both commintment and secretory phases while low avidity CTL permitted target CD4+ cell escape and migration, failing to mount a robust secretory phase.
• ˜50% of B*27-KK10 CD4+ cells were killed by clone E501 CTL, as the other target cells escaped multiple CTL repeatedly. In KK10-peptide-pulsed CD4+ targets, targets that were killed had tethered for 15-20 min., while escapee targets had a failed tether of ˜ 12 min or brushes of <5 min. Prolonged arrest of B*27-KK10 was not due only to TCR engagement but a function of CTL cell-intrinsic response to the engagement in the secretory phase.

References

Foley2014 Maria Hottelet Foley, Talitha Forcier, Elizabeth McAndrew, Michael Gonzalez, Huabiao Chen, Boris Juelg, Bruce D. Walker, and Darrell J. Irvine. High Avidity CD8+ T Cells Efficiently Eliminate Motile HIV-Infected Targets and Execute a Locally Focused Program of Anti-Viral Function. PLoS One, 9(2):e87873, 2014. PubMed ID: 24551068. Show all entries for this paper.