Schuster, Cornelia, Badr Kiaf, Teri Hatzihristidis, Anna Ruckdeschel, Janice Nieves-Bonilla, Yuki Ishikawa, Bin Zhao, Peilin Zheng, Paul Love, and Stephan Kissler. In Press. “CD5 controls gut immunity by shaping the cytokine profile of intestinal T cells”. Frontiers in Immunology, In Press.
Publications
In Press
2022
Kissler, Stephan. 2022. “Toward a precision medicine approach for autoimmunity”. Proc Natl Acad Sci USA 119 (19): e2204841119.
Kissler, Stephan. 2022. “Genetic Modifiers of Thymic Selection and Central Tolerance in Type 1 Diabetes”. Frontiers in Immunology 13: 889856.
2020
Cai, EP, Ishikawa, Zhang, NC Leite, Li, Hou, Kiaf, et al. 2020. “Genome-scale in vivo CRISPR screen identifies RNLS as a target for beta cell protection in type 1 diabetes”. Nature Metabolism 2 (9): 934-45.
A, Haeger, Alexander S, . , Kissler S, and Friedl P. 2020. “Collective Cancer Invasion Forms an Integrin-Dependent Radioresistant Niche”. J Exp Med 217 (1).
2019
E, Dirice, Kahraman S, De Jesus D, . , Kissler S, and Kulkarni RN. 2019. “Increased β-Cell Proliferation Before Immune Cell Invasion Prevents Progression of Type 1 Diabetes”. Nat Metab 1 (5): 509-18.
X, Shi, Shao F, Li Z, Kang L, Liu J, Kissler S, Zhou Z, Jia L, and Zheng P. 2019. “Regulation of B Cell Homeostasis by Ptpn22 Contributes to Type 1 Diabetes in NOD Mice”. Endocrine.
J, Gaglia, and Kissler S. 2019. “Anti-CD3 Antibody for the Prevention of Type 1 Diabetes: A Story of Perseverance”. Biochemistry 58 (40): 4107-11.
Nieves-Bonilla, Janice, Badr Kiaf, Cornelia Schuster, and Stephan Kissler. 2019. “The type 1 diabetes candidate gene Dexi does not affect disease risk in the nonobese diabetic mouse model”. Genes Immun. https://doi.org/10.1038/s41435-019-0083-y.
Genome-wide association studies have implicated more than 50 genomic regions in type 1 diabetes (T1D). A T1D region at chromosome 16p13.13 includes the candidate genes CLEC16A and DEXI. Conclusive evidence as to which gene is causal for the disease association of this region is missing. We previously reported that Clec16a deficiency modified immune reactivity and protected against autoimmunity in the nonobese diabetic (NOD) mouse model for T1D. However, the diabetes-associated SNPs at 16p13.13 were described to also impact on DEXI expression and others have argued that DEXI is the causal gene in this disease locus. To help resolve whether DEXI affects disease, we generated Dexi knockout (KO) NOD mice. We found that Dexi deficiency had no effect on the frequency of diabetes. To test for possible interactions between Dexi and Clec16a, we intercrossed Dexi KO and Clec16a knockdown (KD) NOD mice. Dexi KO did not modify the disease protection afforded by Clec16a KD. We conclude that Dexi plays no role in autoimmune diabetes in the NOD model. Our data provide strongly suggestive evidence that CLEC16A, not DEXI, is causal for the T1D association of variants in the 16p13.13 region.
2018
Duke-Cohan, JS, Ishikawa, Yoshizawa, YI Choi, Lee, Acuto, Kissler*, and EL Reinherz*. 2018. “Regulation of thymocyte trafficking by tagap, a GAP-domain protein linked to human autoimmunity”. Science Signaling 11 (534): eaan8799.