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Displaying record number 54307

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HXB2 Location	Pol(283-290) RT(128-135) DNA(2931..2954)	Pol Epitope Map
Author Location	Pol(283-288 NL-432)
Epitope	TAFTIPSI	Epitope Alignment
Species (MHC/HLA)	human(B*51:01)
Immunogen	HIV-1 infection
Experimental methods	CTL suppression of replication, Chromium-release assay, Flow cytometric T-cell cytokine assay, Intracellular cytokine staining
Keywords	binding affinity, class I down-regulation by Nef, rate of progression

Notes

• HLA-B*5101 associated with slow progression to the disease state was studied as related to Nef-mediated HLA class I downregulation. It was shown that different CTLs have different ranges of ability to kill HIV-1 infected CD4+ T cells and suppress HIV-1 replication. This was found to be a function of the specific HIV-1 epitope presented by the corresponding HLA allele to the CTL.
• Certain epitope recognising CTL clones or lines were therefore, capable of killing HIV-1 infected cells even in the presence of Nef-mediated MHC 1 downregulation, while other CTL clones recognising different epitopes were not so capable.
• There was no significant difference in cytokine production or cytokine producing cells between CTLs that were capable of killing CD4+ T-cells infected with HIV-1 and those CTLs that could not kill such HIV-1 infected cells.
• On the basis of studies involving binding abilities and cytolytic activities for four different epitopes that correlate with HLA-B*5101-restricted CTLs, it is suggested that the ability of CTLs to kill infected CD4+ T cells is due to the number of epitopes presented by the HLA on the surface of the CD4+ T cells rather than the ability of TCR to recognise the epitope.

References

Tomiyama2005 Hiroko Tomiyama, Mamoru Fujiwara, Shinichi Oka, and Masafumi Takiguchi. Cutting Edge: Epitope-Dependent Effect of Nef-Mediated HLA Class I Down-Regulation on Ability of HIV-1-Specific CTLs to Suppress HIV-1 Replication. J. Immunol., 174(1):36-40, 1 Jan 2005. PubMed ID: 15611225. Show all entries for this paper.

Displaying record number 54306

Download this epitope record as JSON.

HXB2 Location	Pol(743-751) Integrase(28-36) DNA(4311..4337)	Pol Epitope Map
Author Location	Pol(743-749 NL-432)
Epitope	LPPVVAKEI	Epitope Alignment
Species (MHC/HLA)	(B*51:01)
Immunogen	HIV-1 infection
Experimental methods	CTL suppression of replication, Chromium-release assay, Flow cytometric T-cell cytokine assay, Intracellular cytokine staining
Keywords	binding affinity, class I down-regulation by Nef, rate of progression

Notes

• HLA-B*5101 associated with slow progression to the disease state was studied as related to Nef-mediated HLA class I downregulation. It was shown that different CTLs have different ranges of ability to kill HIV-1 infected CD4+ T cells and suppress HIV-1 replication. This was found to be a function of the specific HIV-1 epitope presented by the corresponding HLA allele to the CTL.
• Certain epitope-recognising CTL clones or lines were therefore capable of killing HIV-1 infected cells even in the presence of Nef-mediated MHC 1 downregulation, while other CTL clones recognising different epitopes were not so capable.
• There was no significant difference in cytokine production or cytokine producing cells between CTLs that were capable of killing CD4+ T-cells infected with HIV-1 and those CTLs that could not kill such HIV-1 infected cells.
• On the basis of studies involving binding abilities and cytolytic activities for four different epitopes that correlate with HLA-B*5101-restricted CTLs, it is suggested that the ability of CTLs to kill infected CD4+ T cells is due to the number of epitopes presented by the HLA on the surface of the CD4+ T cells rather than the ability of TCR to recognise the epitope.

References

Tomiyama2005 Hiroko Tomiyama, Mamoru Fujiwara, Shinichi Oka, and Masafumi Takiguchi. Cutting Edge: Epitope-Dependent Effect of Nef-Mediated HLA Class I Down-Regulation on Ability of HIV-1-Specific CTLs to Suppress HIV-1 Replication. J. Immunol., 174(1):36-40, 1 Jan 2005. PubMed ID: 15611225. Show all entries for this paper.