About

Maigan A Brusko is a faculty member in the Department of Pathology, Immunology and Laboratory Medicine at the University of Florida College of Medicine. Her research interests include autoimmune disease, immune tolerance, immune-mediated disease, immunology of Type 1 diabetes, and related areas. She teaches courses such as Special Topics in Biomedical Sciences, Current Topics in Immunotherapy, Autoimmunity, Principles of Immunology, and Immunology/Microbiology Journal Colloquy. Her professional contact details include a business phone number (352) 273-9299 and an email address maigan@ufl.edu. Her research profile is associated with an ORCID ID 0000-0002-4331-2202, and her physical address is 1275 Center Drive, Gainesville, FL 32610. She is actively involved in research and education within the field of immunology and autoimmune diseases at the University of Florida.

Research topics

• Biology
• Immunology
• Genetics
• Medicine
• Computer Science
• Artificial Intelligence
• Anatomy
• Computational biology
• Pathology
• Virology
• Cell biology
• Internal medicine

Selected publications

• Spatial transcriptomics from pancreas and local draining lymph node tissue reveals a lymphotoxin-β signature in human type 1 diabetes

  Cell Reports · 2026-03-23

  articleOpen access

  This study explores the inflammatory response observed in the pancreas and pancreatic lymph nodes (pLNs) during the natural history of type 1 diabetes (T1D). Using multicell-resolution spatial transcriptomics (ST), we profile individuals without diabetes (ND), at-risk autoantibody-positive (AAb+) individuals, and T1D donors. In the T1D pancreas, we observed global upregulation of inflammation-associated transcripts, including REG family genes, C3, SOD2, and OLFM4. In the T1D pLN, LTB was significantly upregulated within the lymphoid follicles. Using an orthogonal subcellular-resolution ST platform on an independent donor set, we identified follicular B cells as the primary source of LTB in the pLN and observed increased LTB expression in lymphocytes in insulitic lesions proximal to CCL19/CCL21-expressing endothelium. Collectively, these findings highlight lymphotoxin-β and downstream chemokine signatures in the pancreatic lymphatics as well as within the insulitic lesion, which can inform future therapeutic interventions.

  PublisherDOI

• Divergent chromatin remodeling trajectories in CD66b ⁺ MDSCs distinguishes recovery from chronic critical illness after sepsis

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-23

  articleOpen access

  ABSTRACT Sepsis remains a leading cause of morbidity and mortality worldwide, with survivors often following divergent trajectories: rapid recovery (RAP) or progression to chronic critical illness (CCI). CCI is characterized by persistent organ dysfunction, recurrent infections, and immune dysregulation. Myeloid-derived suppressor cells (MDSCs), which expand in number after sepsis, are implicated in this maladaptive state, yet their epigenetic regulation remains poorly understood. Here, we applied an Omni-ATAC protocol optimized to profile chromatin accessibility in CD66b + MDSCs from healthy participants (HPs) and sepsis patients across time points (day 4, day 14–21, and 6 months) and clinical outcomes (RAP, CCI, and Deceased). Dimensionality reduction analyses of genome-wide chromatin accessibility showed clear separation of sepsis and HP samples. Furthermore, these analyses revealed distinct trajectories post-sepsis diagnosis: RAP samples progressively regained HP-like chromatin states, whereas CCI samples remained epigenetically “locked” in aberrant states. Differential accessibility analysis identified thousands of promoter regions with altered accessibility, including immune checkpoint and inflammatory genes (e.g., ARG1, CD274, S100A8 / 9 ). Pathway analyses predicted global suppression of immune, metabolic, and chromatin remodeling programs in CCI, contrasting with restoration in RAP. These findings from patient-derived CD66b + MDSCs suggest that epigenetic chromatin remodeling underlies divergent recovery trajectories and highlight chromatin-modifying pathways as potential therapeutic targets to restore immune competence in sepsis patients with CCI.

  PublisherOA PDFDOI

• Characterizing cell-type spatial relationships across length scales in spatially resolved omics data

  Nature Communications · 2025-01-03 · 8 citations

  articleOpen access

  Spatially resolved omics (SRO) technologies enable the identification of cell types while preserving their organization within tissues. Application of such technologies offers the opportunity to delineate cell-type spatial relationships, particularly across different length scales, and enhance our understanding of tissue organization and function. To quantify such multi-scale cell-type spatial relationships, we present CRAWDAD, Cell-type Relationship Analysis Workflow Done Across Distances, as an open-source R package. To demonstrate the utility of such multi-scale characterization, recapitulate expected cell-type spatial relationships, and evaluate against other cell-type spatial analyses, we apply CRAWDAD to various simulated and real SRO datasets of diverse tissues assayed by diverse SRO technologies. We further demonstrate how such multi-scale characterization enabled by CRAWDAD can be used to compare cell-type spatial relationships across multiple samples. Finally, we apply CRAWDAD to SRO datasets of the human spleen to identify consistent as well as patient and sample-specific cell-type spatial relationships. In general, we anticipate such multi-scale analysis of SRO data enabled by CRAWDAD will provide useful quantitative metrics to facilitate the identification, characterization, and comparison of cell-type spatial relationships across axes of interest.

  PublisherOA PDFDOI

• 3D imaging of human pancreas suggests islet size and endocrine composition influence their loss in type 1 diabetes

  Research Square · 2025-06-04 · 5 citations

  preprintOpen access
  PublisherOA PDFDOI

• Asynchronous aging and turnover of human circulating and tissue-resident memory T cells across sites

  Immunity · 2025-07-29 · 10 citations

  articleOpen access
  PublisherOA PDFDOI

• 3D imaging of human pancreas suggests islet size and endocrine composition influence their loss in type 1 diabetes

  Nature Communications · 2025-12-11 · 3 citations

  articleOpen access

  A high-definition description of pancreatic islets would prove beneficial for understanding the pathophysiology of type 1 diabetes (T1D), yet significant knowledge gaps exist in terms of their size, endocrine cell composition, and number in both health and disease. Here, 3-dimensional (3D) analyses of pancreata from control persons without diabetes (ND) demonstrate approximately 50% of islets are insulin-positive (INS + ) glucagon-negative (GCG-). Non-diabetic individuals positive for a single Glutamic acid decarboxylase autoantibody (GADA + ) yet at increased risk for disease consistently demonstrate endocrine features, including islet volume and cell composition, closely resembling the age-matched ND controls. In contrast, pancreata from individuals with short-duration T1D demonstrate significantly reduced islet density and a dramatic loss of INS + GCG- islets with preservation of large INS + GCG+ islets. The size and cellular composition of pancreatic islets may, therefore, represent influential factors that impact β-cell loss during T1D disease progression. LSFM imaging revealed 3D islet maps: GADA+ cases mirrored controls, while short-duration T1D showed loss of small INS + GCG– islets but preserved larger mixed INS + GCG+ ones, highlighting islet size- and composition-dependent vulnerability

  PublisherDOI

• Imaging mass cytometry reveals early β-cell dysfunction and changes in immune signatures during type 1 diabetes progression in human pancreata

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-11 · 5 citations

  preprintOpen access

  Summary The natural history and pathogenesis of type 1 diabetes, particularly during the autoantibody- positive stages preceding clinical onset, are not well understood, in part, due to limited availability of human pancreatic samples. Here, we studied 88 organ donors, including 28 single autoantibody-positive and 10 multiple autoantibody-positive donors, by imaging mass cytometry. Approximately 10,000 islets and 16 million single-cells were spatially analyzed using 79 antibodies revealing both β-cell states and the islet-immune interface. We identified IAPP loss from β-cells as an indicator of pre-clinical disease. Alterations in Interferon signatures and downregulation across lineage and functional markers, including markers of endoplasmic reticulum stress, were characteristic of recent-onset disease. Further, in single autoantibody- positive donors, we identified pro-inflammatory myeloid cells and PD1 + memory CD4 + T cells, and in multiple autoantibody-positive samples, found islet-specific and exhausted-like ebector CD8 + T cells. Multiple immune cell subtypes were associated with young age, disease severity and insulitis. This dataset is a major step toward creation of a multi-modal type 1 diabetes disease atlas that will be useful for identifying potential drug targets and association of disease features with clinical co-variates and trial outcomes.

  PublisherOA PDFDOI

• Aberrant immune regulation and enrichment of stem-like CD8 ⁺ T cells in the pancreatic lymph node during type 1 diabetes development

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-27

  preprintOpen access

  Summary Effector CD8 + T cells are key cellular drivers of type 1 diabetes (T1D) pathogenesis, yet questions remain regarding the molecular defects leading to altered cytotoxicity, their signature in peripheral tissues, and their receptor specificity. Thus, we analyzed human pancreatic lymph nodes (pLN) using mass cytometry and single cell RNA sequencing (scRNAseq) with combined proteomic and T cell receptor (TCR) profiling. Cytometric analysis revealed an enriched population of T stem-cell memory (TSCM)-like cells (CD8 + CD45RA + CD27 + CD28 + CCR7 + CXCR3 + T cells) in T1D pLNs. scRNAseq profiling indicated an elevated inflammatory cytokine gene signature ( IFITM3 , LTB ) along with regulators of terminal differentiation ( BCL6 , BCL3 ), coupled with reduced expression of exhaustion-associated genes ( DUSP2 , NR4A2 , TSC22D3 ) in CD8 + T cells in T1D pLN. Additionally, effector CD8 + T cells expressed features of progenitor exhausted cells ( BCL2 ) in T1D pLN. Immune Response Enrichment Analysis (IREA) indicated IL-15 signaling as a significant driver of these phenotypes. Integrated TCR and transcriptomic analysis revealed a cluster of diverse naïve-like CD8 + T cell clones in T1D pLN. When comparing pLN and pancreatic slice cellular isolates, we observed sharing of effector CD8 + T cells, with upregulation of terminal effector signatures detected within the pancreas relative to paired pLN samples. Multiplex imaging revealed differential localization of TCF1 and TOX expressing T cells in the pancreas, with TCF1 + TOX + cells located in closer proximity to the islets and displaying a mixture of activation and exhaustion-associated phenotypes. Thus, we provide multimodal cellular profiles enriched in T1D tissues for consideration in therapeutic targeting.

  PublisherOA PDFDOI

• Age- and Sex- Driven Transcriptional and Metabolic Diversity in Myeloid-Derived Suppressor Cells After Mouse Sepsis

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-07

  preprintOpen access

  Sepsis induces profound immune dysregulation, often resulting in chronic critical illness characterized by persistent immunosuppression and poor outcomes. Myeloid-derived suppressor cells (MDSCs) are central mediators of this immunosuppressive phenotype, yet the influence of age and sex on their transcriptional and metabolic states remain poorly understood. Here, we employed single-cell RNA sequencing of splenic leukocytes from young (3-4 months) and older (18-24 months) adult male and female mice subjected to a clinically relevant murine sepsis model to define age- and sex-specific MDSC phenotypes. We identified significant differences regarding age and sex in MDSC expansion, transcriptome, canonical pathway activation, RNA velocity, mitochondrial metabolism, and predicted cell-cell communication after sepsis. Using drug2cell analysis of total leukocytes we also identified cohort-specific drug target profiles. These findings underscore the importance of age and sex in shaping sepsis-induced MDSC biology and suggest that personalized immunomodulatory strategies targeting MDSCs could improve sepsis outcomes.

  PublisherOA PDFDOI

• 3D imaging of human pancreas suggests islet size and endocrine composition influence their loss in type 1 diabetes

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-18 · 3 citations

  preprintOpen access

  Summary A high-definition description of pancreatic islets would prove beneficial for understanding the pathophysiology of type 1 diabetes (T1D), yet significant knowledge voids exist in terms of their size, endocrine cell composition, and number in both health and disease. Here, 3-dimensional (3D) analyses of pancreata from control persons without diabetes (ND) revealed heretofore underappreciated frequencies (approximately 50%) of insulin-positive (INS+) glucagon-negative (GCG-) islets. Non-diabetic individuals positive for a single Glutamic acid decarboxylase autoantibody (GADA+) yet at increased risk for disease consistently demonstrated endocrine features, including islet volume and cell composition, closely resembling the age-matched ND controls. In contrast, pancreata from individuals with short-duration T1D demonstrated significantly reduced islet density and a dramatic loss of INS+GCG- islets with preservation of large INS+GCG+ islets. The size and cellular composition of pancreatic islets may, therefore, represent influential factors that impact β-cell loss during T1D disease progression. Graphical Abstract Highlights 3D imaging of non-diabetic (ND) pancreas suggests up to 50% of INS+ islets lack GCG INS+GCG- islets are typically small-sized in ND and preferentially lost in T1D In T1D pancreas, INS+ beta cells are preserved in large INS+GCG+ islets Islets from GADA+ individuals appear similar to ND for size and β-to-α cell ratios

  PublisherOA PDFDOI

Frequent coauthors

• Todd M. Brusko

  63 shared

• Philip A. Efron

  University of Florida

  32 shared

• Rhonda Bacher

  University of Florida

  31 shared

• Jaimar C. Rincon

  University of Florida

  30 shared

• Dijoia B. Darden

  Florida College

  30 shared

• Alicia M. Mohr

  University of Florida

  30 shared

• Clive Wasserfall

  University of Florida

  28 shared

• Mark A. Atkinson

  University of Florida

  27 shared

Education

• M.D.

  University of Florida