About

Jessica Horvath Williams is an Assistant Professor in the Department of English at the University of Minnesota. Her role involves teaching and research within the field of literature and related areas. Specific details about her research focus, background, or key contributions are not provided in the page text.

Research topics

• Biology
• Medicine
• Immunology
• Cell biology
• Internal medicine
• Cardiology
• Genetics
• Pathology
• Endocrinology

Selected publications

• When Smell Drives Swell: Olfr2 Fuels Inflammation in AAA

  Circulation Research · 2026-01-29

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Complement 3a Receptor mediates high fat diet induced hypothalamic accumulation of lipid associated microglia to regulate neuroinflammation and obesity

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-22

  articleOpen access

  Microglia, the resident macrophages of the central nervous system, are recognized for their heterogeneity and integral role in brain function and diseases. In the context of high fat diet (HFD) feeding and obesity, microglia become overactive, acquiring a prevailing lipid associated microglial phenotype (also known as LAM). Yet, how microgliosis is induced and regulated remains unclear. Here we report a key role for the Complement 3a Receptor (C3aR), on HFD-induced hypothalamic gliosis and weight gain in mice. HFD consumption leads to elevated microglial expression of C3aR, which parallels widespread accumulation of reactive microglia, selectively in the hypothalamus. Conditional microglial C3aR deletion protects mice from HFD-induced hypothalamic reactive microgliosis. C3aR deletion or pharmacological antagonism opposes HFD-induced weight gain in male but not female mice. Mechanistically, we demonstrated that C3aR is essential for lipid-induced lipid droplet formation, and acquisition of a LAM molecular signature. In summary, we uncovered a previously unknown role for C3aR in the acquisition of a LAM signature driving diet-induced gliosis, identifying this receptor as a new viable therapeutic candidate for conditions associated with hypothalamic neuroinflammation.

  PublisherDOI

• Adrenal Gland Macrophage-derived TGF-β Governs Vascular Permeability to Drive Monocyte Recruitment during Stress

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-21

  articleSenior author

  The adrenal glands are central regulators of systemic stress responses through tightly controlled glucocorticoid production. Yet, the contribution of local immune-vascular interactions to adrenal stress adaptation remains poorly understood. Here, we investigated the role of adrenal gland macrophages in coordinating stress-induced immune remodeling and vascular function. By integrating single-cell RNA sequencing datasets across four distinct stress models, including acute cold exposure, chronic social defeat, chronic inflammation, and systemic Candida albicans infection, we identified a conserved increase in monocyte recruitment to the adrenal gland, accompanied by dynamic macrophage transitions. Comparative transcriptomic and ligand-receptor analyses identified transforming growth factor-β (TGFβ) as a dominant macrophage-derived signal targeting adrenal endothelial cells across all stress conditions. Pharmacological blockade of TGFβ receptor signaling reduced endothelial activation, vascular permeability, and monocyte infiltration into the adrenal gland following stress, without directly altering resident macrophage numbers. Using genetic fate-mapping and conditional knockout models, we demonstrate that macrophage-derived, but not endothelial-derived, TGFβ is required to promote enhanced endothelial adhesion molecule expression, vascular fenestration, permeability, and efficient monocyte recruitment. Loss of macrophage TGFβ production also led to exacerbated systemic stress hormone levels. Together, these findings uncover a previously unrecognized macrophage-endothelial axis in the adrenal gland, whereby macrophage-derived TGFβ regulates vascular properties to support immune cell recruitment and stress adaptation. This immune-vascular crosstalk provides new mechanistic insights into adrenal homeostasis and suggests potential therapeutic avenues for disorders associated with dysregulated chronic stress.

  PublisherDOI

• From lipoprotein metabolism to blood clotting: Highlights of the 2025 Fredrickson lipid research conference

  Journal of Lipid Research · 2026-04-16

  articleOpen access

  The biannual Fredrickson Lipid Research conference took place in person in Milwaukee, Wisconsin, from September 3-5, 2025. Each conference highlights the most advanced basic and translational research in lipids and lipoprotein metabolism. As with each Fredrickson Lipid Research conference, the overall theme is focused on "Lipid Metabolism, Lipoproteins, and Atherosclerosis," and this year included a special scientific session exploring the connections between Blood Clotting and Lipid Metabolism. This session underscored ongoing research aimed at explaining the mechanisms by which dyslipidemia alters the coagulation system and drives thrombotic cardiovascular disease. Other scientific session themes at the conference included Biomarkers in Cardiovascular Diseases, Efferocytosis and Inflammation, Regulation of Lipoproteins, Adipocyte Plasticity in Cardiometabolic Diseases, and Novel Therapeutic Strategies for Atherosclerosis. From the six moderated scientific sessions, invited speakers provided summaries of their work to showcase their contributions to the lipid and lipoprotein metabolism fields. This review article aims to serve as a resource for readers to learn more about ongoing research in lipid and lipoprotein metabolism and to encourage future studies and collaborations that advance the field.

  PublisherDOI

• Programming peripheral artery disease in diabetes

  Science Translational Medicine · 2026-04-22

  articleSenior authorCorresponding

  Reprogrammed TREM2 + macrophages drive nonresolving inflammation in peripheral artery disease associated with type 2 diabetes (Malhi et al. , this issue).

  PublisherDOI

• CD44 in myEloid cells is a major driver of liver inflammation and injury in alcohol-related liver disease

  Hepatology · 2025-01-14 · 1 citations

  articleOpen access

  BACKGROUND AND AIMS: Alcohol-associated liver disease (ALD) is one of the leading causes of severe liver disease with limited pharmacological treatments for alcohol-associated steatohepatitis. CD44, a glycoprotein mainly expressed in immune cells, has been implicated in multiple inflammatory diseases but has never been studied in the ALD context. We therefore studied its contribution to alcohol-associated steatohepatitis development in mice and its expression in patients with ALD. APPROACH AND RESULTS: Here, we report that liver CD44 expression is associated with liver injury and inflammation and its deficiency ( Cd44-/- ) partially protected mice on chronic plus binge ethanol feeding. CD44 deletion in myeloid cells ( Cd44myel-KO ) recapitulated the same protective effects associated with reduced inflammatory monocyte infiltration and neutrophil activation in the liver and diminished blood neutrophil-lymphocyte ratio. CD44-deficient neutrophils displayed reduced phorbol 12-myristate 13-acetate-induced inflammatory mediator expression and increased phagocytosis of live bacteria. Cd44myel-KO mice were also protected against hepatic steatosis mediated by chronic plus binge ethanol feeding or chronic ethanol feeding due in part to increased SIRT1-mediated fatty acid beta-oxidation. CD44 neutralization with antibodies strongly decreased liver injury and inflammation (hepatic neutrophil frequency) and blood neutrophil-lymphocyte ratio on chronic plus binge ethanol feeding. In samples from patients with ALD, hepatic CD44 expression increased with ALD severity, correlated with hepatic TNFα and CD11b expression, and CD44-expressing neutrophils were enriched in alcohol-associated hepatitis. CONCLUSIONS: Human and experimental evidence supports CD44 as a marker of hepatic inflammation in ALD. In addition, CD44 modulates neutrophil mobilization and functions, and its targeting partially prevents liver inflammation and injury in the context of acute-on-chronic alcohol drinking.

  PublisherDOI

• MACanalyzeR scRNAseq analysis tool reveals PPARγHIGH/GDF15HIGH lipid-associated macrophages facilitate thermogenic expansion in BAT

  Nature Communications · 2025-05-31 · 8 citations

  articleOpen access

  LAMs as critical mediators of BAT homeostasis.

  PublisherDOI

• CSF1R regulates monocyte subset differentiation and intracellular metabolism

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-21 · 2 citations

  preprintOpen access

  Abstract Monocytes are key circulating effectors of vascular homeostasis, innate immunity and inflammation. Following their generation in mouse bone marrow, classical (Ly6C high ) monocytes are mobilized into the blood circulation where they mature into non-classical (Ly6C low ) patrolling monocytes or are recruited into peripheral tissues where they differentiate into tissue resident or inflammatory macrophages. Monocytes and macrophages express CSF1R (CD115), the receptor for lineage-specific growth factors CSF1 and IL34. Here, we report that acute CSF1R blockade or genetic deletion negatively interferes with monocyte intracellular metabolism and reduces blood Ly6C low monocytes in part by blunting differentiation of Ly6C high monocytes. Based upon lineage-specific deletion of GFPT1 (Glutamine-Fructose-6-Phosphate Transaminase 1), the hexosamine biosynthetic pathway (HBP) is identified as a novel regulator of CSF1R expression and monocyte subset diversity. Our findings provide new insights into the link between CSF1R signaling, metabolic regulation, and monocyte survival and differentiation.

  PublisherOA PDFDOI

• Mechanisms of Innate Immune Modulation by High-Fat Diet: Implications for Obesity and Asthma

  Current Allergy and Asthma Reports · 2025-11-10

  reviewSenior author
  PublisherDOI

• More Than a Cleanup Crew: The Expanding Biology of Efferocytosis

  Arteriosclerosis Thrombosis and Vascular Biology · 2025-12-18 · 1 citations

  reviewOpen access

  Efferocytosis, the process by which phagocytes clear apoptotic cells, is essential for tissue homeostasis, inflammation resolution, and repair. Once considered a passive waste-disposal process, efferocytosis is now recognized as a dynamic, immunometabolic program that integrates apoptotic cell clearance with metabolic reprogramming and inflammation resolution. In cardiovascular contexts, efficient efferocytosis limits necrosis, enhances the deposition of wound healing matrix proteins, and promotes tissue healing, whereas impaired clearance drives chronic inflammation and maladaptive tissue remodeling. We review the molecular mechanisms governing efferocytosis, including the interplay of find-me, eat-me, and don't-eat-me signals with receptor-mediated cytoskeletal remodeling and lysosomal degradation. We highlight how efferocytosis drives lipid efflux, fatty acid oxidation, amino acid catabolism, and nucleotide recycling, processes that sustain continual efferocytosis and resolution programming. Defects in these pathways, amplified by proteolytic cleavage of apoptotic cell receptors, dysregulated metabolism, and inflammatory mediators, underlie impaired efferocytosis in atherosclerosis, myocardial infarction, vascular aging, and metabolic diseases. Finally, we discuss emerging concepts, including nonprofessional phagocyte contributions, crosstalk with adaptive immunity, and therapeutic strategies to enhance efferocytosis or preserve receptor integrity. Collectively, these insights redefine efferocytosis as more than a cleanup mechanism, positioning it as a central contributor to attenuating cardiometabolic diseases.

  PublisherOA PDFDOI

Recent grants

• Regulation of Foamy Macrophage Differentiation and Survival in Atherosclerosis

  NIH · $1.6M · 2024–2027

• NIH Grant R01CA021375

  NIH · $986k · 1994

• Sex and stress hormones control adrenal gland macrophage development and function"

  NIH · $2.2M · 2022–2027

• NIH Grant K99HL138163

  NIH · $125k · 2019

• ATHEROSCLEROTIC LESION INITIATION BY RESIDENT AORTIC MACROPHAGE PROLIFERATION

  NIH · $747k · 2019–2022

Frequent coauthors

• J Shen

  63 shared

• Anita S. Chong

  University of Chicago

  61 shared

• Yingzheng Xu

  University of Minnesota

  41 shared

• Gwendalyn J. Randolph

  40 shared

• L Blinder

  University of Massachusetts Chan Medical School

  36 shared

• Stoyan Ivanov

  Centre Méditerranéen de Médecine Moléculaire

  36 shared

• Howard Sankary

  Loyola University Medical Center

  33 shared

• Patricia L. Foster

  29 shared

Education

• PhD, Pathology

  University of Chicago

  2013

• B.A., Biology

  DePauw University

  2007

Awards & honors

• Emmy Award for her work on the documentary Art + Medicine: D…