
Jeremy Levine
VerifiedUniversity of Michigan · Public Policy
Active 1959–2026
About
Jeremy Levine is an associate professor of Organizational Studies, with courtesy appointments in Public Policy and Sociology at the University of Michigan. He is a political and urban sociologist whose research primarily focuses on questions related to inequality and public policy, especially urban and criminal justice policy. Levine has collaborated with legislators and advocates in New York on legislative campaigns concerning crime victims and the criminal legal system, and has contributed to the design of the Boston-Area Research Initiative (BARI), a collaboration between social scientists and city government officials. His analyses have supported the passage of the Fair Access to Victim Compensation Act in New York State in late 2023. Levine's first book, 'Constructing Community,' is an ethnography examining urban governance and development in Boston’s poorest neighborhoods. His scholarly work has been published in prominent journals such as the American Journal of Sociology, American Sociological Review, and Social Forces, and has received awards from the Comparative-Historical, Political, and Urban Sociology sections of the American Sociological Association. Currently, he is working on his second book, which explores the historical development and contemporary consequences of crime victim policy in the United States, with a particular focus on the relationship between victim policy, punishment, and racial and gender inequality. His ongoing research and expertise have been recognized in profiles such as the University of Michigan LSA Magazine.
Research topics
- Medicine
- Internal medicine
- Oncology
- Surgery
Selected publications
Differential Effects of GVHD Therapies on Intestinal Epithelium
Transplantation and Cellular Therapy · 2026-02-01
articleTransplantation and Cellular Therapy · 2026-05-01
articleOpen accessAcute graft-versus-host disease (GVHD) is a well-established complication of allogeneic hematopoietic cell transplantation. Although the incidence of severe acute GVHD is decreasing with advances in prophylactic approaches, many clinical questions remain. Herein, acute GVHD diagnosis, grading, and treatment are reviewed and critically evaluated. Specific criteria were used for searching the published literature, grading the quality and strength of evidence, and grading the strength of recommendations. A panel of experts developed consensus recommendations for the clinical management of acute GVHD, providing guidance on behalf of the American Society for Transplantation and Cellular Therapy. Key recommendations include: 1) The MAGIC grading scheme is supported as the consensus grading scheme for acute GVHD; 2) Clinical tools and non-invasive blood-based biomarkers can aid in risk stratification of patients with newly diagnosed acute GVHD; 3) Corticosteroids remain the recommended first-line systemic therapy for acute GVHD, despite innovative approaches to improve front-line treatment; 4) Ruxolitinib is supported as the second-line therapy standard, while acknowledging remestemcel-L-rknd is a recognized alternative standard for pediatric patients. Finally, no consensus treatment exists for third-line therapy. Ongoing and future studies will seek to improve upon the current treatment paradigm through risk-adapted strategies. Innovative investigative approaches will be needed to address the unmet needs in acute GVHD.
Systemic steroid treatment of grade I acute GVHD increases steroid-refractory GVHD and NRM
Blood Immunology & Cellular Therapy · 2026-03-24
articleOpen access= .026). MAGIC biomarkers identified most patients with grade I GVHD as low risk and unlikely to progress to severe GVHD regardless of treatment. Nevertheless, low-risk patients who received up-front steroids experienced a threefold increase in infectious deaths compared with those treated topically. This study supports the consensus recommendation of topical therapy for patients with low-risk grade I GVHD, a strategy that can be supported by biomarkers to avoid unnecessary steroid exposure and increased NRM.
Transplantation and Cellular Therapy · 2026-02-01
articleUNC Libraries · 2026-04-17
articleOpen accessTo the Editor: HLA-matched sibling donor transplantation accounts for the majority of transplants performed for sickle cell disease (SCD). However, only about 18% of patients in the United States with SCD will have unaffected human leukocyte antigen (HLA)-matched siblings or one with sickle trait, limiting applicability. A Blood and Marrow Transplant Clinical Trials Network phase II trial of HLA-matched unrelated donor bone marrow transplantation (URD BMT) for severe SCD was conducted between 2008 and 2014 and enrolled patients aged 3–19 years (BMT CTN 0601, NCT00745420).1 A reduced intensity immunosuppressive conditioning regimen (RIC) of alemtuzumab (45 mg; days −22 to −19), fludarabine (150 mg/m2; day −8 to −4) and melphalan (140 mg/m2; day −3) was employed using alemtuzumab early to provide recipient immune suppression to overcome a higher risk of graft rejection (GR) with URD BMT in SCD patients while also limiting toxicities associated with myeloablative agents.1 The trial met a pre-specified primary endpoint of 75% 1-year event-free survival (EFS). However, as previously reported, the incidence of 1-year acute and extensive chronic graft-versus-host disease (GVHD) were unacceptably high at 17% and 38% respectively. This report details long-term outcomes in this previously reported cohort as an important consideration for therapeutic trials as follow-up is usually limited to early time-points.
Transplantation and Cellular Therapy · 2026-02-01
articleTransplantation and Cellular Therapy · 2025-04-28 · 3 citations
articleGastroenterology · 2025-05-01
articleBlood Advances · 2025-08-15 · 4 citations
articleOpen accessABSTRACT: Changes in the clinical symptoms of acute graft-versus-host disease (GVHD) are currently used to assess treatment responses. The Mount Sinai Acute GVHD International Consortium (MAGIC) consortium has recently revealed that the integration of serum biomarkers with clinical symptoms at the onset of treatment in a MAGIC composite score (MCS) more accurately predicts treatment response and 6-month nonrelapse mortality (NRM) than clinical symptoms alone. In this study, we evaluated whether the integration of serum biomarkers and clinical symptoms on day 28 (D28) would also better predict NRM than clinical response only (CRO). We analyzed data from 1135 patients receiving systemic treatment for acute GVHD and created a fourth MCS category for patients with complete resolution of symptoms and low-risk clinical biomarkers on D28. Using a classification and regression tree model with 6-month NRM as the end point, we identified status of MCS 0 or MCS 1 at D28 as responses, which we termed the MAGIC composite response (MCR). In the validation cohort (n = 309), MCR more accurately predicted 6-month NRM than CRO (area under the curve: 0.77 vs 0.69; P = .014) and demonstrated higher negative and positive predictive values. MCR correctly reclassified both clinical nonresponders and responders: 28 of 213 clinical responders (13%) became nonresponders with fivefold higher NRM (34.3% vs 6.8%, P < .001) and a larger group (29/96, 30%) of clinical nonresponders became responders with sixfold lower NRM (7.6% vs 50.7%, P < .001). These findings support the use of MCR as a superior surrogate end point for long-term GVHD control and survival in future clinical trials.
Blood · 2025-11-03
articleOpen accessAbstract Introduction: Graft Failure (GF) is a rare but devastating outcome of HCT. Primary GF (PGF), defined as a failure of neutrophil recovery by Day+28, is straightforward to diagnose. Diagnosing secondary GF (SGF) is more challenging, with its broad time-range, multiple confounding diagnoses, and lack of predictive biomarkers. In BMT CTN1703/1801, we analyzed patients receiving RIC HCT for heme malignancies with either Tac/MTX (n=159) or PT-Cy (n=165) GVHD prophylaxis. SGF was defined as donor chimerism &lt;5% after initial donor engraftment. With Tac/MTX, there were 3 PGF and 1 SGF diagnoses. With PT-Cy, there were 4 PGF and 6 SGF. Median SGF diagnosis was Day +64 (range: Day+28-215). There were too few Tac/MTX patients to analyze SGF, but sufficient events with PT-Cy. To identify PT-Cy SGF predictors, we leveraged lymphocyte, T, B, and NK cell reconstitution analysis. In SGF we found an early, profound deficit in the reconstitution of all major lymphocyte populations, including total lymphocytes, T, B, and NK cells, as early as Day+28. This enabled the modeling of a SGF risk classifier based on the Absolute Lymphocyte Count (ALC). Methods: Clinical ALC measurements were performed on all SGF patients (n=6) and on non-GF controls with ALCs available (146 of 155 non-GF patients). Flow cytometry was performed on all PT-Cy SGF patients (n = 6) and from a subset of non-GF controls (n = 18: controls were chosen as patients without relapse or severe GVHD, to reduce confounders introduced by immunologic interventions, and for whom all samples, including from the graft infusion, were available). T, B, and NK counts, as well as T cell subsets, were compared (using Welch's T test) on Days 7, 14, 21, 28, 42, 63, 98, 180, 270, 365, 730, with SGF patients censored on the day of GF diagnosis. To interrogate the optimal ALC cutoff, the cumulative incidence of SGF was computed at Days +28 and +42, with death without GF as a competing risk. Results: We have previously demonstrated that, compared to Tac/MTX, PT-Cy patients exhibited an early decrease in reconstitution of all T cell populations (with normal NK and B cell reconstitution). Here we focused specifically on PT-Cy patients with or without SGF. Graft CD34 counts/kg were not different between SGF patients and non-GF patients (mean CD34/kg = 1.38 x10e6 (SGF) vs 0.67 x10e6 (non-GF, p = 0.61) However, even amidst the overarching early suppression in T cell reconstitution with PT-Cy, SGF patients could be easily distinguished from the larger PT-Cy cohort, based on more profound deficits in ALC, T, B and NK cells reconstitution, measured using 2 strategies: (1) SGF patients demonstrated significant early (Day +28) quantitative defects in the reconstitution of the ALC (mean +/- SEM 262+/-32 cells/µL (non-GF) vs 60 +/- 25 (SGF, p&lt;0.0001), CD4 T cells (62 +/- 12 cells/µL vs 19+/-15, p=0.048), CD8 T cells (15 +/-3 cells/µL vs 3.5 +/-1 p=0.0009), all CD8 T cell subpopulations, as well as NK cells (116+/-31 cells/µL vs 2.9+/-1.4 cells/µL, p= 0.002) and B cells (3.5 +/-1.4 cells/µL vs 0.16+/-0.07 p =0.03). (2) In SGF, there was a significant deficit in the rate of rise of all major lymphocyte populations between Days 28-42-60 vs non-GF, including CD4 T cells (p&lt;0.0001), CD8 T cells (p = 0.0002), B cells (p&lt;0.0001), and NK cells (p =0.048). These discoveries suggested that a classifier could be identified to risk-stratify patients for SGF. We explored an ALC cutpoint, amenable to standard clinical lab analysis. A statistically significant threshold was identified at both Days+28 and +42, with Day+42 being most predictive: A threshold of 120 cells/µL was identified as optimal, with landmark analysis documenting a SGF rate of 34.7% below the cutpoint, and SGF of 1% above it (HR = 45.9, 95% CI 5.7 - 366). Conclusions: Despite the small number of events, PT-Cy patients with SGF demonstrated a distinctive reconstitution trajectory that encompassed an early, substantial, and sustained deficit in all lymphocyte counts, as well as a lack of their longitudinal expansion. This enabled the discovery of a candidate ALC biomarker cutpoint at Day+42 that could distinguish patients who were more likely to develop SGF. If confirmed, these data could generate a predictive biomarker for SGF, which would enable the design of trials evaluating early interventions (e.g. CD34+ boosts, DLI, modification of immunosuppression) to improve outcomes for these patients.
Recent grants
NIH · $307k · 1994
Cellular and Molecular Studies of Bone Marrow Transplant
NIH · $83.9M · 1997–2027
NIH · $959k · 2017
NIH · $680k · 2006
BMT CTN Core - Mount Sinai Consortium
NIH · $1.7M · 2017–2031
Frequent coauthors
- 221 shared
James L.M. Ferrara
Icahn School of Medicine at Mount Sinai
- 131 shared
Gregory A. Yanik
- 122 shared
Carrie L. Kitko
Vanderbilt University Medical Center
- 111 shared
Michael A. Pulsipher
- 95 shared
Muna Qayed
Aflac (United States)
- 81 shared
Francis Ayuk
University Medical Center Hamburg-Eppendorf
- 80 shared
Sung Won Choi
University of Michigan–Ann Arbor
- 77 shared
Mary M. Horowitz
Medical College of Wisconsin
Labs
Jeremy Levine LabPI
Awards & honors
- Awards from the Comparative-Historical, Political, and Urban…
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