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University of Oxford. รายงานการศึกษาระดับปริญญาเอก ณ University of Oxford ประเทศสหราชอาณาจักร ชื่อ/นามสกุล นางสาวหทัยรัตน์ ธนัญชัย ตำแหน่ง อาจารย์ ภาควิชา จุลชีววิทยา

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University of oxford

University of Oxford


University of oxford

University of Oxford

/


University of oxford

( 4)

Immunology

D.Phil

Weatherall Institute of Molecular Medicine

Nuffield Department of Clinical Medicine

University of Oxford

Cellular Immune Responses in HIV-1 Infection: the Role of NK Cells and Their Receptors

Supervisor: Professor Sarah Rowland-Jones


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Killer Immunoglobulin- like receptors ( KIRs )

  • Ig superfamily

  • Two families have been classified

    • KIR2D interact with HLA-C

    • KIR3D interact with HLA-B molecules that display the Bw4 epitope (KIR3DL1) or HLA-A alleles (KIR3DL2).

  • KIRs with short cytoplasmic tail (S) mediate a stimulatory signal

  • KIRs with long cytoplasmic tail (L) mediate an inhibitory signal

Ligands :

Borrego et al. 2001


Kirs and hiv 1 infection

KIRs and HIV-1 Infection

  • HLA class I alleles, haplotype and supertype associate with HIV-1 infection and disease progression.

  • HLA class I molecule also target ligands of KIRs. Thus, these molecules are essential recognition elements of both the acquired and innate immune responses to viruses.

  • KIR3DS1 in combination with HLA class I alleles carrying a Bw4 epitope is associated with delayed progression to AIDS (Martin MP et al. 2002).

  • The presence of the inhibitory KIR3DL1 in combination with the HLA-B*57s alleles that containing the Bw4 epitope, has a highly protective effect against progression to AIDS in Zambian patients ( Lopez-Vazquez et al. 2005).


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KIR3DL1 + Bw4 continuum of protection. Genotypes are ordered bydegree of protection in terms of (a) disease progression and (b) control of viral load.(Martin et al 2007)


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Altfeld and Goulder 2007)

Altfeld and Goulder 2007)

Altfeld and Goulder 2007)

Model of KIR3DL1 and KIR3DS1 interactions with HLA-B Bw4-80I expressed on HIV-uninfected and HIV-infected cells

Alfeld and Goulder 2007


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ligands NK receptor KIR KIR HIV-1

KIR HLA class I HIV-1 HIV-1 Shuang Miao village, Henan province 10


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1. KIR3DL1 HLA-A24 HIV-1 epitope

2. KIR3DL1HLA class I

alleleKIR3DL1HLA class I

3. KIR3DS1 HLA-A24 variant Nef

peptide

4. KIR3DL1*01502 79 HIV-1

China cohort

5. HIV-1

CTL NK cell


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  • Thananchai H, Makadzanga T, Maenaka K, Kuroki K, Peng Y, Conlon C, Rowland-Jones S, Dong T. Reciprocal recognition of HLA-Cw4 restricted HIV-1 gp120 epitope by CD8+T cell and NK cell. AIDS 2009; 23: 189-193. (Impact factor = 5.842)

  • Thananchai H, Gilleapie G, Martin MP, Bashirova A, Yawata N, Yawata M, Easterbrook P, McVicar DW, Maenaka K, Parham P, Carrington M, Dong T, Rowland-Jones S. Cutting Edge: Alleles specific interaction between KIR3DL1 and HLA class I A and B molecules. J Immunol2007; 178 (1): 33-37. (Impact factor = 6.068)

  • Hansasuta P, Dong T, Thananchai H, Weekes M, Willberg C, Aldemir H, Rowland-Jones S, Braud VM. Recognition of HLA-A3 and HLA-A11 by KIR3DL2 is peptide-specific. Eur J Immunol2004; 34(6): 1673-1679. (Impact factor = 4.772)


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Poster presentation

Differences in the recognition of HLA-A and HLA-B molecules expressing the Bw4 epitope by different KIR3DL1 alleles. Keystone Symposia Conference for Molecular and Cellular Determinants of HIV Pathogenesis. 9th-15th April 2005. Banff, Alberta, Canada.

Escape from both CTL and NK cell recognition by HLA-Cw4 restricted HIV-1 gp120 epitope. Keystone Symposia Conference for Molecular and Cellular Determinants of HIV Pathogenesis. 24th-30th March 2007. Whilstler, British Columbia, Canada.


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Oral presentation

  • Differences in the recognition of HLA-A and HLA-B molecules expressing the Bw4 epitope by different KIR3DL1 alleles. KIR polymorphism workshop. 15th 17th September 2005. University of Cambridge, Cambridge, UK.

  • Escape from both CTL and NK cell recognition by HLA-Cw4 restricted HIV-1 gp120 epitope. KIR polymorphism workshop. 8th 10th October 2006. University of Dusseldorf, Dusseldorf, Germany.


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Acknowledgements

SRJ/TD Lab HIU, WIMM

Sarah Rowland-Jones

Tao Dong

Geraldine Gillespie

Yan-Chun Peng

Paul Bowness

Simon Kollnberger

Kyushu University, Japan

Katsumi Maenaka

NCI, Frederick , USA

Mary Carrington

Daniel McVicar

Maureen Pat Martin

Arman Bashirova

Stanford University, USA

Peter Parham

Nobuyo Yawata

Makoto Yawata


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Thank you for your attention


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