Dr. Kermani received her D.V.M degree from University of Tehran Veterinary School and completed a four-year residency in Medical Microbiology, Virology, and Immunology from the University of Tehran Medical School. She received both her M.P.H. in Molecular and Hospital Epidemiology and a Ph.D. in Epidemiology Science (Virology) from the University of Michigan. Following graduation, she completed her postdoctoral training in Pathology followed by fellowship training in Molecular Medicine and Genetic and Hematology and Oncology in the Department of Internal Medicine at the University of Michigan. Then, she accepted dual positions of Adjunct Assistant Professor and Research Investigator at the University of Michigan Medical School. In addition, from 2013-2018, she worked as Assistant Professor at the Cancer Therapy Center at University of Massachusetts Boston. Since 2018, she worked as a Research Assistant Scientist in the Departments of Internal Medicine and Dermatology at University of Michigan.

She served on numerous local and national committees and is a member of many societies including American College of Rheumatology, American Society of Investigative Dermatology, American Society for Virology, American Society for Investigative Pathology, American Urology Association, a Society for Basic Urologic Research and the Skin Biology Disease Research.

Dr. Kermani has published over eighty articles in prestigious scientific journals, given over one hundred invited and other presentations at local, national, and international conferences, has over hundred published abstracts, and received sixteen awards.

Dr. Kermani's research area interests include fibrosis, autoimmunity, and cancer. She is investigating pulmonary and other types of fibrosis such as skin, kidney, liver as well as psoriasis, systemic lupus erythematosus (SLE), scleroderma, and other autoimmune diseases.
Her recent research focuses on the pathogenic mechanisms that drive skin and systemic inflammation in SLE patients, as well as the molecular mechanisms of psoriasis, dermatomyositis, tissue injury, inflammation, fibrosis in cutaneous lupus, and other autoimmune diseases.

As a team Scientist, she is working in several projects as following:
1. Her current research aims to define how the female-biased factor VGLL3 drives fibrosis in the skin and systemic fibrosis such as kidney, liver, and lung and cancer including: a) activation and repression of signaling mechanisms that engage in epithelial, fibroblast proliferation, epithelial, mesenchymal transformation, and myofibroblast differentiation, b) gene transcription by secreted inflammatory cytokines and chemokines in chronic inflammation; cancer, fibrotic diseases of the skin, kidney, liver, and lung, c) gene expression profiles in fibroblasts/myofibroblast and other immune cells populations using single-cell RNA sequencing from skin samples from DLE patients and healthy controls, as well as vgll3 overexpressed mouse skin compared with wild type, d) role of Hippo and TGFB pathways in fibrosis.

2. Ongoing project title: Human skin explant is powerful method for skin photosensitivity study in health and disease: Focus on SLE. SLE patients report photosensitivity leads to lower health-related quality of life and to increased morbidity and mortality. There is a need to understand the mechanism of photosensitivity in SLE patients. She described a human skin explant model that is modifiable with cytokine and inhibitor treatment as a valuable tool to explore photosensitive responses without direct UV exposure in human subjects.

3. Other ongoing project title: Role of hippo signaling in regulation of STING activation in SLE and upregulation IFN production in SLE monocytes. Myeloid cells produce type I IFN production in response to STING activators and are known to be dysfunctional in SLE. Inflammatory gene expression in macrophages have been linked to Hippo signaling. We hypothesized that Hippo dysregulation within myeloid cells contributes to increased IFN production. The preliminary data showed higher YAP phosphorylation in the SLE human monocytes compared to healthy control. Additionally, LATS1/2 inhibition modulates monocyte cGAS/STING-mediated inflammatory phenotypes, which may provide a useful therapeutic agent for SLE patients.

4. Her collaboratives projects: Elucidation of the molecular mechanisms of fibrosis, psoriasis, dermatomyositis, tissue injury, inflammation in cutaneous lupus, organ damage in SLE, scleroderma, atopic dermatitis, and other autoimmune diseases as well as role of ultraviolet light in lupus, SLE, scleroderma, dermatomyositis, and psoriasis, using single cell sequencing, ATAC, Multiomic and spatial sequencing, as well as immunohistochemistry and immunofluorescent assays.

5. Other interesting projects: Role of UV and microbiome in autoimmune diseases such as SLE, psoriasis, scleroderma, and atopic dermatitis.

In addition, she is working on a collaborative project with several industry including:
A) Bristol Myers Squibb Company to dissect the role Tyk2 inhibitor on SLE endothelial dysfunction. Endothelial cells are known to be dysfunctional in SLE. Our data showed that TYK2 inhibitor exerts the protective effects on SLE/CLE endothelial progenitor cells using ex vivo isolation and growth of endothelial stem cells. Our data revealed that Tyk2 inhibitor treatment on SLE endothelial progenitor cells modulates these cells and dysfunction cells become to functional endothelial cells.

B) Ventus Therapeutics Company to validate the UVB induced activation of the cGAS-STING pathway in SLE, and DM patients. Our data indicated that UVB induced activation of the cGAS-STING pathway in SLE, and this effect is through upregulation of STING, by phosphorylation of STING. Thus, inhibition of cGAS-STING signaling pathway induced by UVB treatment may provide a useful therapeutic modality for SLE photosensitive patients.
C) ROME Therapeutics Company to investigate the role of LINE elements in SLE skin. Long Interspersed Element-1 (LINE-1) are retrotransposable DNA elements that make up ~17% of the human genome, and their role in health and disease is still not being evaluated. Published studies have suggested that LINE-1 may contribute to the development and progression of autoimmune diseases such as lupus by triggering the type I IFN production. We examined LINE-1 RNA and protein expression in lupus patient skin biopsies, and the impact on inflammatory signals upon a LINE-1 reverse transcriptase (RT) inhibitor in vitro and in vivo. Our data showed that LINE-1 RNA and protein are increased in SLE skin and is induced by UV exposure. Inhibition of LINE-1 RT activity results in decreased ISG expression and improved disease activity. Inhibition of LINE-1 RT holds promise as a novel therapy for diseases in which type I IFNs drive disease.

Previous interesting project: Include:
I. Elucidation of the molecular and cellular mechanisms involved in aging and inflammation-associated pulmonary, urinary tract and skin fibrosis, particularly the role of TGFB and cc-type chemokines in lung, prostate, bladder kidney fibrosis. My research has identified potential new mechanisms through which TGFB, and cc-type chemokines mediate prostate fibrosis consequent to aging by promoting myofibroblast differentiation and consequent extracellular matrix remodeling, resulting in increased prostate tissue stiffness and urethral dysfunction.

II. Epigenetic regulation of myofibroblast differentiation by DNA methylation; and the role of myofibroblasts in human and in animal models of fibrosis. Evaluation of anti-fibrotic therapeutic agents to treat fibrosis such as, skin, kidney and discoid lupus erythematosus patients who did not respond to commonly prescribed pharmacotherapies.