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2. HLA-C expression levels define permissible mismatches in hematopoietic cell transplantation

Author

Petersdorf, Effie W., Gooley, Theodore A., Malkki, Mari, Bacigalupo, Andrea P., Cesbron, Anne, Du Toit, Ernette, Ehninger, Gerhard, Egeland, Torstein, Fischer, Gottfried F., Gervais, Thibaut, Haagenson, Michael D., Horowitz, Mary M., Hsu, Katharine, Jindra, Pavel, Madrigal, Alejandro, Oudshoorn, Machteld, Ringdén, Olle, Schroeder, Marlis L., Spellman, Stephen R., Tiercy, Jean-Marie, Velardi, Andrea, Witt, Campbell S., O’Huigin, Colm, Apps, Richard, and Carrington, Mary

Published
2014
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10. Common variants in the HLA-DRB1–HLA-DQA1 HLA class II region are associated with susceptibility to visceral leishmaniasis

Author

Fakiola, Michaela, Strange, Amy, Cordell, Heather J, Miller, E Nancy, Pirinen, Matti, Su, Zhan, Mishra, Anshuman, Mehrotra, Sanjana, Monteiro, Gloria R, Band, Gavin, Bellenguez, Céline, Dronov, Serge, Edkins, Sarah, Freeman, Colin, Giannoulatou, Eleni, Gray, Emma, Hunt, Sarah E, Lacerda, Henio G, Langford, Cordelia, Pearson, Richard, Pontes, Núbia N, Rai, Madhukar, Singh, Shri P, Smith, Linda, Sousa, Olivia, Vukcevic, Damjan, Bramon, Elvira, Brown, Matthew A, Casas, Juan P, Corvin, Aiden, Duncanson, Audrey, Jankowski, Janusz, Markus, Hugh S, Mathew, Christopher G, Palmer, Colin N A, Plomin, Robert, Rautanen, Anna, Sawcer, Stephen J, Trembath, Richard C, Viswanathan, Ananth C, Wood, Nicholas W, Wilson, Mary E, Deloukas, Panos, Peltonen, Leena, Christiansen, Frank, Witt, Campbell, Jeronimo, Selma M B, Sundar, Shyam, Spencer, Chris C A, Blackwell, Jenefer M, and Donnelly, Peter

Published
2013
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32. Stimulation of HIV-specific T cell clonotypes using allogeneic HLA

Author

Almeida, Coral-Ann, primary, van Miert, Paula, additional, O'Driscoll, Kane, additional, Zoet, Yvonne M., additional, Chopra, Abha, additional, Watson, Mark, additional, de Santis, Dianne, additional, Witt, Campbell, additional, John, Mina, additional, Claas, Frans H.J., additional, and D'Orsogna, Lloyd J., additional

Published
2017
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34. Common variants in the HLA-DRB1-HLA-DQA1 HLA class II region are associated with susceptibility to visceral leishmaniasis

Author

LeishGEN Consortium, Wellcome Trust Case Control Consortium 2, Fakiola, Michaela, Strange, Amy, Cordell, Heather J, Miller, E Nancy, Pirinen, Matti, Su, Zhan, Mishra, Anshuman, Mehrotra, Sanjana, Monteiro, Gloria R, Band, Gavin, Bellenguez, Céline, Dronov, Serge, Edkins, Sarah, Freeman, Colin, Giannoulatou, Eleni, Gray, Emma, Hunt, Sarah E, Lacerda, Henio G, Langford, Cordelia, Pearson, Richard, Pontes, Núbia N, Rai, Madhukar, Singh, Shri P, Smith, Linda, Sousa, Olivia, Vukcevic, Damjan, Bramon, Elvira, Brown, Matthew A, Casas, Juan P, Corvin, Aiden, Duncanson, Audrey, Jankowski, Janusz, Markus, Hugh S, Mathew, Christopher G, Palmer, Colin NA, Plomin, Robert, Rautanen, Anna, Sawcer, Stephen J, Trembath, Richard C, Viswanathan, Ananth C, Wood, Nicholas W, Wilson, Mary E, Deloukas, Panos, Peltonen, Leena, Christiansen, Frank, Witt, Campbell, Jeronimo, Selma MB, Sundar, Shyam, Spencer, Chris CA, Blackwell, Jenefer M, and Donnelly, Peter

Abstract

To identify susceptibility loci for visceral leishmaniasis, we undertook genome-wide association studies in two populations: 989 cases and 1,089 controls from India and 357 cases in 308 Brazilian families (1,970 individuals). The HLA-DRB1-HLA-DQA1 locus was the only region to show strong evidence of association in both populations. Replication at this region was undertaken in a second Indian population comprising 941 cases and 990 controls, and combined analysis across the three cohorts for rs9271858 at this locus showed P(combined) = 2.76 × 10(-17) and odds ratio (OR) = 1.41, 95% confidence interval (CI) = 1.30-1.52. A conditional analysis provided evidence for multiple associations within the HLA-DRB1-HLA-DQA1 region, and a model in which risk differed between three groups of haplotypes better explained the signal and was significant in the Indian discovery and replication cohorts. In conclusion, the HLA-DRB1-HLA-DQA1 HLA class II region contributes to visceral leishmaniasis susceptibility in India and Brazil, suggesting shared genetic risk factors for visceral leishmaniasis that cross the epidemiological divides of geography and parasite species.

Published
2013

35. Drug‐induced alloreactivity: A new paradigm for allorecognition

Author

D'Orsogna, Lloyd J., Almeida, Coral‐Ann M., Miert, Paula, Zoet, Yvonne M., Anholts, Jacqueline D. H., Chopra, Abha, Watson, Mark, Witt, Campbell, John, Mina, and Claas, Frans H. J.

Abstract

Abacavir administration is associated with drug‐induced hypersensitivity reactions in HIV+ individuals expressing the HLA‐B*57:01 allele. However, the immunological effects of abacavir administration in an HLA‐B57 mismatched transplantation setting have not been studied. We hypothesized that abacavir exposure could induce de novo HLA‐B57‐specific allorecognition. HIV‐specific CD8 T cell clones were generated from HIV+ individuals, using single cell sorting based on HIVpeptide/HLAtetramer staining. The T cell clones were assayed for alloreactivity against a panel of single HLA‐expressing cell lines, in the presence or absence of abacavir. Cytokine assay, CD137 upregulation, and cytotoxicity were used as readout. Abacavir exposure can induce de novo HLA‐B57 allorecognition by HIV‐specific T cells. A HIVGag RK9/HLA‐A3‐specific T cell did exhibit interferon‐γ production, CD137 upregulation, and cytolytic effector function against allogeneic HLA‐B57, but only in the presence of abacavir. Allorecognition was specific to the virus specificity, HLArestriction, and T cell receptor TRBVuse of the T cell. We provide proof‐of‐principle evidence that administration of a drug could induce specific allorecognition of mismatched HLAmolecules in the transplant setting. We suggest that HIV‐seropositive recipients of an HLA‐B57 mismatched graft should not receive abacavir until further studies are completed. Using single cell sorted HIV‐specific T cell clones and single HLA transfected cell lines, the authors provide proof‐of‐principle evidence that exposure to a drug could induce pre‐existing virus‐specific memory T cells to crossreact against allogeneic HLA molecules in a transplant setting.

Published
2019
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38. Human papillomavirus, high-grade intraepithelial neoplasia and killer immunoglogulin-like receptors: a Western Australian cohort study

Author

Brestovac, Brian, Wong, Michelle, Tjendera, Raymond, Costantino, Paul, Mamotte, Cyril, Witt, Campbell, Brestovac, Brian, Wong, Michelle, Tjendera, Raymond, Costantino, Paul, Mamotte, Cyril, and Witt, Campbell

Abstract

Background: Human papillomavirus (HPV) is the causative agent in cervical cancer and HPV genotypes 16 and 18 cause the majority of these cancers. Natural killer (NK) cells destroy virally infected and tumour cells via killer immunoglobulin-like receptors (KIR) that recognize decreased MHC class I expression. These NK cells may contribute to clearance of HPV infected and/or dysplastic cells, however since KIR controls NK cell activity, KIR gene variation may determine outcome of infection.Methods: KIR gene frequencies were compared between 147 patients with a history of high-grade cervical intraepithelial neoplasia (CIN) and a control population of 187, to determine if any KIR genes are associated with high-grade CIN. In addition a comparison was also made between cases of high grade CIN derived from 30 patients infected with HPV 16/18 and 29 patients infected with non-16/18 HPV to determine if KIR variation contributes to the disproportional carcinogenesis derived from HPV 16/18 infection.Results: High-grade CIN was weakly associated with the absence of KIR2DL2 and KIR2DS2 (p = 0.046 and 0.049 respectively, OR 0.6; 95% CI 0.4 – 0.9) but this association was lost after correction for multi-gene statistical analysis.No difference in KIR gene frequencies was found between high-grade CIN caused by HPV 16/18 and non-16/18.Conclusion: No strong association between KIR genes, high-grade CIN and HPV genotype was found in the Western Australian population.

Published
2013

43. KIR2DL4 (CD158d) genotype influences expression and function in NK cells

Author

Goodridge, Jodie, Witt, Campbell, Christiansen, Frank, Warren, Hilary, Goodridge, Jodie, Witt, Campbell, Christiansen, Frank, and Warren, Hilary

Abstract

The expression and function of the NK cell receptor KIR2DL4 are controversial. Two common alleles of the transmembrane domain of KIR2DL4 exist. The 10A allele with 10 adenines at the end of the transmembrane exon encodes a full length receptor, whereas the 9A allele has only 9 adenines resulting in a frame shift which in turn generates a stop codon early in the first cytoplasmic exon. The possibility that the 10A and 9A alleles might result in differences in expression and function of KIR2DL4 was explored using mAbs to KIR2DL4. Transfection experiments with cDNA from the 10A and 9A alleles revealed significant membrane expression only with the protein encoded by the 10A allele. Analysis of peripheral blood NK cells demonstrated that only in subjects with at least one 10A allele was cell surface expression of KIR2DL4 detectable, and then only on the minor CD56bright NK cell subset. The major CD56dim NK cell subset did not cell surface express KIR2DL4 but, interestingly, did so after in vitro culture. Functional analysis using cultured NK cells in redirected lysis assays demonstrated that KIR2DL4 is an activating receptor for NK cells with at least one 10A allele. No significant activity was detected for NK cells generated from subjects homozygous for the 9A allele. These data show that genotype influences cell surface expression and function of KIR2DL4 which may account for reported differences in KIR2DL4 expression and function.

Published
2003

47. 38-OR

Author

Langan, Leanne L., primary, Hughes, Tiffany L., additional, Park, Larry P., additional, Luxton, Grant, additional, Witt, Campbell S., additional, Irish, Ashley B., additional, and Christiansen, Frank T., additional

Published
2006
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49. MHC Haplotype Analysis by Artificial Neural Networks

Author

Bellgard, Matthew I, Tay, Guan K, Hiew, H.L, Witt, Campbell S, Ketheesan, Natkunam, Christiansen, Frank T, Dawkins, Roger L, Bellgard, Matthew I, Tay, Guan K, Hiew, H.L, Witt, Campbell S, Ketheesan, Natkunam, Christiansen, Frank T, and Dawkins, Roger L

Published
1998

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