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2. Intrinsic Defects in B Cell Development and Differentiation, T Cell Exhaustion and Altered Unconventional T Cell Generation Characterize Human Adenosine Deaminase Type 2 Deficiency

Author

Yap, Jin Yan, Moens, Leen, Lin, Ming-Wei, Kane, Alisa, Kelleher, Anthony, Toong, Catherine, Wu, Kathy H.C., Sewell, William A., Phan, Tri Giang, Hollway, Georgina E., Enthoven, Karen, Gray, Paul E., Casas-Martin, Jose, Wouters, Carine, De Somer, Lien, Hershfield, Michael, Bucciol, Giorgia, Delafontaine, Selket, Ma, Cindy S., Tangye, Stuart G., and Meyts, Isabelle

Published
2021
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3. Everolimus-Induced Remission of Classic Kaposi’s Sarcoma Secondary to Cryptic Splicing Mediated CTLA4 Haploinsufficiency

Author

Yap, Jin Yan, Gloss, Brian, Batten, Marcel, Hsu, Peter, Berglund, Lucinda, Cai, Fenfen, Dai, Pei, Parker, Andrew, Qiu, Min, Miley, Wendell, Roshan, Romin, Marshall, Vickie, Whitby, Denise, Wegman, Eric, Garsia, Roger, Wu, Kathy H.C., Kirk, Edwin, Polizzotto, Mark, Deenick, Elissa K., Tangye, Stuart G., Ma, Cindy S., CIRCA, and Phan, Tri Giang

Published
2020
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5. Denisovan, modern human and mouse TNFAIP3 alleles tune A20 phosphorylation and immunity

Author

Zammit, Nathan W., Siggs, Owen M., Gray, Paul E., Horikawa, Keisuke, Langley, David B., Walters, Stacey N., Daley, Stephen R., Loetsch, Claudia, Warren, Joanna, Yap, Jin Yan, Cultrone, Daniele, Russell, Amanda, Malle, Elisabeth K., Villanueva, Jeanette E., Cowley, Mark J., Gayevskiy, Velimir, Dinger, Marcel E., Brink, Robert, Zahra, David, Chaudhri, Geeta, Karupiah, Gunasegaran, Whittle, Belinda, Roots, Carla, Bertram, Edward, Yamada, Michiko, Jeelall, Yogesh, Enders, Anselm, Clifton, Benjamin E., Mabbitt, Peter D., Jackson, Colin J., Watson, Susan R., Jenne, Craig N., Lanier, Lewis L., Wiltshire, Tim, Spitzer, Matthew H., Nolan, Garry P., Schmitz, Frank, Aderem, Alan, Porebski, Benjamin T., Buckle, Ashley M., Abbott, Derek W., Ziegler, John B., Craig, Maria E., Benitez-Aguirre, Paul, Teo, Juliana, Tangye, Stuart G., King, Cecile, Wong, Melanie, Cox, Murray P., Phung, Wilson, Tang, Jia, Sandoval, Wendy, Wertz, Ingrid E., Christ, Daniel, Goodnow, Christopher C., and Grey, Shane T.

Published
2019
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6. Environmental and genetic disease modifiers of haploinsuffciency of A20

Author

Zammit, Nathan N, primary, Gray, Paul, additional, Siggs, Owen M, additional, Yap, Jin Yan, additional, Russell, Amanda, additional, Cultrone, Daniele, additional, Warren, Joanna, additional, Walters, Stacey N, additional, Brink, Robert T, additional, Zahra, David, additional, Burnett, Deborah L., additional, Gayevskiy, Velimir, additional, Minoche, Andre E, additional, Ziegler, John B., additional, Craig, Maria E., additional, Wong, Melanie, additional, Benitez-Aguirre, Paul, additional, Teo, Juliana, additional, Cowley, Mark J., additional, Dinger, Marcel E., additional, Tangye, Stuart G., additional, Burk, Catherine, additional, Phan, Tri G., additional, Goodnow, Christopher J, additional, and Grey, Shane T, additional

Published
2022
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7. Hyper-IgE Syndrome due to an Elusive Novel Intronic Homozygous Variant in DOCK8

Author

Tangye, Stuart G., primary, Gray, Paul E., additional, Pillay, Bethany A., additional, Yap, Jin Yan, additional, Figgett, William A., additional, Reeves, John, additional, Kummerfeld, Sarah K., additional, Stoddard, Jennifer, additional, Uzel, Gulbu, additional, Jing, Huie, additional, Su, Helen C., additional, Campbell, Dianne E., additional, Sullivan, Anna, additional, Burnett, Leslie, additional, Peake, Jane, additional, and Ma, Cindy S., additional

Published
2021
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8. Nfkb2 variants reveal a p100-degradation threshold that defines autoimmune susceptibility

Author

Wirasinha, Rushika C., primary, Davies, Ainsley R., additional, Srivastava, Monika, additional, Sheridan, Julie M., additional, Sng, Xavier Y.X., additional, Delmonte, Ottavia M., additional, Dobbs, Kerry, additional, Loh, Khai L., additional, Miosge, Lisa A., additional, Lee, Cindy Eunhee, additional, Chand, Rochna, additional, Chan, Anna, additional, Yap, Jin Yan, additional, Keller, Michael D., additional, Chen, Karin, additional, Rossjohn, Jamie, additional, La Gruta, Nicole L., additional, Vinuesa, Carola G., additional, Reid, Hugh H., additional, Lionakis, Michail S., additional, Notarangelo, Luigi D., additional, Gray, Daniel H.D., additional, Goodnow, Christopher C., additional, Cook, Matthew C., additional, and Daley, Stephen R., additional

Published
2020
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10. Phylogenetic Analysis of Different Breeds of Domestic Chickens in Selected Area of Peninsular Malaysia Inferred from Partial CytochromebGene Information and RAPD Markers

Author

Nelly Warau Kamau, Yap Jin Yan, Justina Lee Ning Zhen, Jayaraj Vijaya Kumaran, Fook Choy Yap, and Kiung Teh Loon

Subjects
Genetic Markers, Veterinary medicine, animal structures, Population, Bioengineering, Biology, DNA, Mitochondrial, Polymorphism, Single Nucleotide, Species Specificity, Phylogenetics, Genetic variation, Animals, Cluster Analysis, education, Phylogeny, Genetics, education.field_of_study, Phylogenetic tree, Cytochrome b, Malaysia, Computational Biology, DNA, Sequence Analysis, DNA, Cytochromes b, Random Amplified Polymorphic DNA Technique, RAPD, Maximum parsimony, Genetics, Population, Genetic marker, embryonic structures, Animal Science and Zoology, Chickens, Biotechnology
Abstract

The present investigation was carried out in an attempt to study the phylogenetic analysis of different breeds of domestic chickens in Peninsular Malaysia inferred from partial cytochrome b gene information and random amplified polymorphic DNA (RAPD) markers. Phylogenetic analysis using both neighbor-joining (NJ) and maximum parsimony (MP) methods produced three clusters that encompassed Type-I village chickens, the red jungle fowl subspecies and the Japanese Chunky broilers. The phylogenetic analysis also revealed that majority of the Malaysian commercial chickens were randomly assembled with the Type-II village chickens. In RAPD assay, phylogenetic analysis using neighbor-joining produced six clusters that were completely distinguished based on the locality of chickens. High levels of genetic variations were observed among the village chickens, the commercial broilers, and between the commercial broilers and layer chickens. In this study, it was found that Type-I village chickens could be distinguished from the commercial chickens and Type-II village chickens at the position of the 27th nucleotide of the 351 bp cytochrome b gene. This study also revealed that RAPD markers were unable to differentiate the type of chickens, but it showed the effectiveness of RAPD in evaluating the genetic variation and the genetic relationships between chicken lines and populations.

Published
2010

11. A timeline demarcating two waves of clonal deletion and Foxp3 upregulation during thymocyte development

Author

Hu, Daniel, Yap, Jin Yan, Wirasinha, Rushika, Howard, Debbie, Goodnow, Christopher, Daley, Stephen, Hu, Daniel, Yap, Jin Yan, Wirasinha, Rushika, Howard, Debbie, Goodnow, Christopher, and Daley, Stephen

Abstract

Thymocytes that bind strongly to self-antigens are prevented from becoming naive T cells by several mechanisms. They undergo clonal deletion at two stages of development; wave 1 in immature thymocytes lacking the medulla-homing chemokine receptor, CCR7, or wave 2 in more mature CCR7+ thymocytes. Alternatively, self-reactive thymocytes upregulate Foxp3 to become T-regulatory cells. Here, we describe the differential timing of the two waves of deletion and Foxp3 upregulation relative to the immature proliferating stage. Proliferating thymocytes were pulse-labeled in normal C57BL/6 mice with 5-ethynyl-2'-deoxyuridine (EdU). Thymocytes progressed into wave 1 (CCR7-) and wave 2 (CCR7+) of clonal deletion ~2 and 5 days after proliferation, respectively. Foxp3 upregulation occurred between 4 and 8 days after proliferation, predominantly in thymocytes with a Helios+ CCR7+ phenotype. These findings establish a timeline that suggests that wave 1 of clonal deletion occurs in the thymic cortex, whereas wave 2 and Foxp3 upregulation both occur in the thymic medulla.Immunology and Cell Biology advance online publication, 24 November 2015; doi:10.1038/icb.2015.95.

Published
2015

12. Denisovan, modern human and mouse TNFAIP3alleles tune A20 phosphorylation and immunity

Author

Zammit, Nathan W., Siggs, Owen M., Gray, Paul E., Horikawa, Keisuke, Langley, David B., Walters, Stacey N., Daley, Stephen R., Loetsch, Claudia, Warren, Joanna, Yap, Jin Yan, Cultrone, Daniele, Russell, Amanda, Malle, Elisabeth K., Villanueva, Jeanette E., Cowley, Mark J., Gayevskiy, Velimir, Dinger, Marcel E., Brink, Robert, Zahra, David, Chaudhri, Geeta, Karupiah, Gunasegaran, Whittle, Belinda, Roots, Carla, Bertram, Edward, Yamada, Michiko, Jeelall, Yogesh, Enders, Anselm, Clifton, Benjamin E., Mabbitt, Peter D., Jackson, Colin J., Watson, Susan R., Jenne, Craig N., Lanier, Lewis L., Wiltshire, Tim, Spitzer, Matthew H., Nolan, Garry P., Schmitz, Frank, Aderem, Alan, Porebski, Benjamin T., Buckle, Ashley M., Abbott, Derek W., Ziegler, John B., Craig, Maria E., Benitez-Aguirre, Paul, Teo, Juliana, Tangye, Stuart G., King, Cecile, Wong, Melanie, Cox, Murray P., Phung, Wilson, Tang, Jia, Sandoval, Wendy, Wertz, Ingrid E., Christ, Daniel, Goodnow, Christopher C., and Grey, Shane T.

Abstract

Resisting and tolerating microbes are alternative strategies to survive infection, but little is known about the evolutionary mechanisms controlling this balance. Here genomic analyses of anatomically modern humans, extinct Denisovan hominins and mice revealed a TNFAIP3allelic series with alterations in the encoded immune response inhibitor A20. Each TNFAIP3allele encoded substitutions at non-catalytic residues of the ubiquitin protease OTU domain that diminished IκB kinase-dependent phosphorylation and activation of A20. Two TNFAIP3alleles encoding A20 proteins with partial phosphorylation deficits seemed to be beneficial by increasing immunity without causing spontaneous inflammatory disease: A20 T108A;I207L, originating in Denisovans and introgressed in modern humans throughout Oceania, and A20 I325N, from an N-ethyl-N-nitrosourea (ENU)-mutagenized mouse strain. By contrast, a rare human TNFAIP3allele encoding an A20 protein with 95% loss of phosphorylation, C243Y, caused spontaneous inflammatory disease in humans and mice. Analysis of the partial-phosphorylation A20 I325N allele in mice revealed diminished tolerance of bacterial lipopolysaccharide and poxvirus inoculation as tradeoffs for enhanced immunity.

Published
2019
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13. Nfkb2 variants reveal a p100-degradation threshold that defines autoimmune susceptibility

Author

Wirasinha, Rushika C., Davies, Ainsley R., Srivastava, Monika, Sheridan, Julie M., Sng, Xavier Y.X., Delmonte, Ottavia M., Dobbs, Kerry, Loh, Khai L., Miosge, Lisa A., Lee, Cindy Eunhee, Chand, Rochna, Chan, Anna, Yap, Jin Yan, Keller, Michael D., Chen, Karin, Rossjohn, Jamie, La Gruta, Nicole L., Vinuesa, Carola G., Reid, Hugh H., Lionakis, Michail S., Notarangelo, Luigi D., Gray, Daniel H.D., Goodnow, Christopher C., Cook, Matthew C., and Daley, Stephen R.

Abstract

NF-κB2/p100 (p100) is an inhibitor of κB (IκB) protein that is partially degraded to produce the NF-κB2/p52 (p52) transcription factor. Heterozygous NFKB2 mutations cause a human syndrome of immunodeficiency and autoimmunity, but whether autoimmunity arises from insufficiency of p52 or IκB function of mutated p100 is unclear. Here, we studied mice bearing mutations in the p100 degron, a domain that harbors most of the clinically recognized mutations and is required for signal-dependent p100 degradation. Distinct mutations caused graded increases in p100-degradation resistance. Severe p100-degradation resistance, due to inheritance of one highly degradation-resistant allele or two subclinical alleles, caused thymic medullary hypoplasia and autoimmune disease, whereas the absence of p100 and p52 did not. We inferred a similar mechanism occurs in humans, as the T cell receptor repertoires of affected humans and mice contained a hydrophobic signature of increased self-reactivity. Autoimmunity in autosomal dominant NFKB2 syndrome arises largely from defects in nonhematopoietic cells caused by the IκB function of degradation-resistant p100.

Published
2021
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