Available to mentor
Dr. Allison C. Billi is an assistant professor in the University of Michigan Department of Dermatology. Her research aims to define how the skin contributes to systemic autoimmune disease through identifying female-biased pathways and factors in skin that are critical to autoimmunity. In addition, she provides medical dermatology care to patients of all ages within our outpatient clinic at the A. Alfred Taubman Health Care Center.
Dr. Billi is a graduate of the University of Michigan Medical School where she received her medical degree and her PhD in Human Genetics. Following graduation, she completed her transitional year at Beaumont Hospital in Dearborn, Michigan, and a dermatology residency and research fellowship at the University of Michigan Department of Dermatology.
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Center MemberTaubman Institute
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Center MemberSamuel and Jean Frankel Cardiovascular Center
Autoimmune disease shows a striking sex bias, affecting roughly eight times as many women as men, and represents the leading cause of morbidity among women in the United States. Development of new therapies that are safer and more effective than currently available options has been hampered by poor understanding of the mechanisms that cause autoimmune disease, including why women are so disproportionately affected. Furthermore, skin is one of the organs most commonly involved in autoimmune diseases, but the role of skin inflammation in driving these diseases remains largely unknown. The Billi Lab is working to define how the skin contributes to systemic autoimmune disease through identifying female-biased pathways and factors in skin that are critical to autoimmunity.
Current research includes investigating the biological mechanisms that lead to female sex bias in lupus. Using mouse modeling of complex human disease, systems biology applications, and approaches for study of cutaneous and systemic immunology, we are examining how the female-biased factor VGLL3 drives autoimmune disease in the skin of women and exploring whether this pathway could underlie the balance of female-biased autoimmunity and male-biased susceptibility to infection and neoplasm.
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Ma F, Tsou P-S, Gharaee-Kermani M, Plazyo O, Xing X, Kirma J, Wasikowski R, Hile GA, Harms PW, Jiang Y, Xing E, Nakamura M, Ochocki D, Brodie WD, Pillai S, Maverakis E, Pellegrini M, Modlin RL, Varga J, Tsoi LC, Lafyatis R, Kahlenberg JM, Billi AC, Khanna D, Gudjonsson JE. Nat Commun, 2024 Jan 3; 15 (1): 210Journal ArticleSystems-based identification of the Hippo pathway for promoting fibrotic mesenchymal differentiation in systemic sclerosis.
DOI:10.1038/s41467-023-44645-6 PMID: 38172207 -
Bogle R, Patrick MT, Sreeskandarajan S, Gharaee-Kermani M, Zhang H, Li Q, Zhou R, Ma F, Kahlenberg JM, Plazyo O, Elder JT, Billi AC, Gudjonsson JE, Tsoi LC. J Invest Dermatol, 2024 Sep 27;Journal ArticleProfiling lncRNA in psoriatic skin using scRNA-seq.
DOI:10.1016/j.jid.2024.09.010 PMID: 39342985 -
van Drongelen V, Young K, Gharaee-Kermani M, Plazyo O, Griffin E, Syu L, Xing E, Ward NL, Tsoi LC, Kahlenberg M, Dlugosz A, Gudjonsson JE, Billi A. Journal of Investigative Dermatology, 2024 May; 144 (8): s3 - s3.Proceeding / Abstract / Poster016 Investigating therapeutic targeting of the female-biased factor VGLL3 in lupus
DOI:10.1016/j.jid.2024.06.032 -
Jiang R, Kirma J, Xing X, Wasikowski R, Fox J, Billi A, Do TH, Kahlenberg M, Shao S, Tsoi LC, Gudjonsson JE. Journal of Investigative Dermatology, 2022 May; 144 (8): s4 - s4.Proceeding / Abstract / Poster019 Dynamic keratinocyte-neutrophil-fibroblast communication network characterizes inflammatory responses in generalized pustular psoriasis
DOI:10.1016/j.jid.2024.06.035 -
Hile G, Ma F, Tsou P, Gharaee-Kermani M, Zhang L, Victory A, Hurst A, Xu B, Pedersen E, Wasikowski R, Berthier C, Ognenovski V, Nakamura M, Billi A, Gudjonsson JE, Kahlenberg M. Journal of Investigative Dermatology, 2024 Aug; 144 (8): s150Proceeding / Abstract / PosterLB860 Cross-disease comparison of dermatomyositis and SLE identifies non-classical monocytes and JAK-1 signaling as drivers of endothelial cell death in DM skin
DOI:10.1016/j.jid.2024.06.1240 -
Cavagnero KJ, Albright J, Li F, Dokoshi T, Bogle R, Kirma J, Kahlenberg JM, Billi AC, Fox J, Coon A, Dobry CJ, Hinds B, Tsoi LC, Harms PW, Gudjonsson JE, Gallo RL. 2024 Jun 28;PreprintPositionally distinct interferon stimulated dermal immune acting fibroblasts promote neutrophil recruitment in Sweet's syndrome.
DOI:10.1101/2024.06.24.600500 PMID: 38979312 -
Schuler CF, Tsoi LC, Billi AC, Harms PW, Weidinger S, Gudjonsson JE. J Invest Dermatol, 2024 May; 144 (5): 954 - 968.Journal ArticleGenetic and Immunological Pathogenesis of Atopic Dermatitis.
DOI:10.1016/j.jid.2023.10.019 PMID: 38085213 -
Shao S, Sun Z, Chu M, Chen J, Cao T, Swindell WR, Bai Y, Li Q, Ma J, Zhu Z, Schuler A, Helfrich Y, Billi AC, Li Z, Hao J, Xiao C, Dang E, Gudjonsson JE, Wang G. Br J Dermatol, 2024 Mar 15; 190 (4): 536 - 548.Journal ArticleFormylpeptide receptor 1 contributes to epidermal barrier dysfunction-induced skin inflammation through NOD-like receptor C4-dependent keratinocyte activation.
DOI:10.1093/bjd/ljad455 PMID: 37979162