About

Professor Booki Min is a principal investigator at Northwestern University, with a background that includes a DVM and PhD. Her research focuses on immunology, with particular interest in immune regulation and cellular mechanisms. Her work involves studying immune responses, including the roles of T cells, regulatory T cells, and immune checkpoints such as LAG3, in various contexts including inflammation, asthma, and cancer. She has a strong background in neuroscience and immunology, and her research aims to elucidate immune pathways and develop insights into immune-related diseases.

Research topics

• Immunology
• Cell biology
• Biology
• Medicine
• Biochemistry
• Cancer research
• Chemistry
• Internal medicine
• Endocrinology
• Psychology
• Neuroscience

Selected publications

• Steroid Refractory GI Acute GVHD Is Associated with Distinct Immune Cell Infiltrates and Gene Expression Profiles

  Transplantation and Cellular Therapy · 2026-02-01

  article
  PublisherDOI

• IL-27 limits HSPC differentiation during infection and protects from stem cell exhaustion

  eLife · 2025-09-01 · 1 citations

  articleOpen access

  Abstract Many inflammatory stimuli can induce progenitor cells in the bone marrow to produce increased numbers of myeloid cells as part of the process of emergency myelopoiesis. These events are associated with trained immunity and have long-term impacts on hematopoietic stem and progenitor cell (HSPC) development but can also compromise their function. While many cytokines support emergency myelopoiesis, less is known about the mechanisms that temper these events. When mice that lack the cytokine IL-27 were infected with Toxoplasma gondii, there was enhanced generation of monocyte progenitors and increased numbers of inflammatory monocytes. In the bone marrow of infected mice there was increased production of IL-27 that localized with HSPCs and a survey of cytokine receptor expression highlighted that HSPCs were uniquely poised to respond to IL-27. Furthermore, the use of in vitro differentiation assays and mixed bone marrow chimeras revealed that HSPCs from IL-27 deficient mice are pre-disposed towards the monocyte lineage. Additional studies highlighted that after infection loss of the IL-27R resulted in reduced HSPC fitness that manifested as reduced proliferative responses and a decreased ability to reconstitute the hematopoietic system. Thus, the ability of IL-27 to act on HSPC provides a regulatory brake on differentiation to limit monocyte induction and preserve HSPC stemness.

  PublisherDOI

• Targeting Impaired Type I Interferon–IL-27 Signaling Rescues T Regulatory Cell Suppressive Function in Relapsing-Remitting Multiple Sclerosis

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-28

  preprintOpen access

  Abstract T Regulatory T cells (Tregs) from patients with relapsing-remitting multiple sclerosis (RRMS) exhibit impaired suppressive function, yet the underlying molecular mechanisms remain elusive. Single-cell RNA sequencing (scRNAseq) of ex vivo- sorted Tregs from RRMS patients and matched healthy controls (HCs) revealed down-regulation of type I IFN (IFN) and IL-27 signaling pathways in RRMS Tregs. These Tregs showed reduced expression of IFN-stimulated genes (ISGs) ( ISG15, MX1, IFITM1, IFI44L, OAS1 ), as well as key mediators of Treg suppressive function ( LGALS3, CD81, FCRL3, CD7, CSTB ), all suggesting a key role of decreased IFN signaling in RRMS Treg dysfunction. To therapeutically target IFN signaling pathways and improve Treg suppressive functions, we used cGAMP-loaded microparticles (MPs) to activate the stimulator of IFN genes (STING) in experimental autoimmune encephalomyelitis (EAE). cGAMP-MP treatment ameliorated EAE via induction of Tregs expressing IL-27R, IL-10, TGF-b, and Granzyme B. This effect was abolished in Treg-specific IL-27R (Treg ΔIl27ra ) knockout mice, confirming that IL-27 signaling is essential for Treg suppression. In vitro IL-27 stimulation of RRMS-derived Tregs restored expression of IFN pathway genes ( IRF1, IFNGR, IFI16 ) and Treg suppressive genes ( ICOS, IKZF3, IL7R, TIGIT ). Thus, we propose that IL-27 pre-stimulation may restore their suppressive function and migration (via CCR6, CCR7, S100A11 and S1PR4 ) to the central nervous system (CNS) in future clinical trials. Significance Several studies have reported a role for type I IFN and IL-27 signaling in the induction of suppressive Tregs in autoimmune diseases. We report that RRMS Tregs have decreased expression of type I IFN and IL-27 signalling-related genes in comparison to HCs. The animal model of MS (EAE) was successfully treated with cGAMP-MPs, which, via induction of type I IFN, IL-27 and IL-10, restored Treg suppressive function. A scRNAseq study of Tregs from MS patients revealed that IL-27 in vitro stimulation normalized the expression of type I IFN genes and Treg suppressive genes. We propose that IL-27 pre-treatment may enhance Treg suppressive function and migration to the CNS in future clinical trials.

  PublisherOA PDFDOI

• Author response: IL-27 limits HSPC differentiation during infection and protects from stem cell exhaustion

  2025-12-15

  peer-reviewOpen access

  Functional analyses showcase that in the absence of IL-27, hematopoietic stem and progenitor cells are more likely to become monocytes during toxoplasmosis, making them less responsive after infection.

  PublisherDOI

• IL-27 limits HSPC differentiation during infection and protects from stem cell exhaustion

  eLife · 2025-12-15 · 1 citations

  articleOpen access

  Many inflammatory stimuli can induce progenitor cells in the bone marrow to produce increased numbers of myeloid cells as part of the process of emergency myelopoiesis. These events are associated with trained immunity and have long-term impacts on hematopoietic stem and progenitor cell (HSPC) development but can also compromise their function. While many cytokines support emergency myelopoiesis, less is known about the mechanisms that temper these events. When mice that lack the cytokine IL-27 were infected with Toxoplasma gondii , there was enhanced generation of monocyte progenitors and increased numbers of inflammatory monocytes. In the bone marrow of infected mice, there was increased production of IL-27 that localized with HSPCs, and a survey of cytokine receptor expression highlighted that HSPCs were uniquely poised to respond to IL-27. Furthermore, the use of in vitro differentiation assays and mixed bone marrow chimeras revealed that HSPCs from IL-27-deficient mice are predisposed toward the monocyte lineage. Additional studies highlighted that after infection, loss of the IL-27R resulted in reduced HSPC fitness that manifested as reduced proliferative responses and a decreased ability to reconstitute the hematopoietic system. Thus, the ability of IL-27 to act on HSPC provides a regulatory brake on differentiation to limit monocyte induction and preserve HSPC stemness.

  PublisherDOI

• IL-27 limits HSPC differentiation during infection and protects from stem cell exhaustion

  eLife · 2025-04-23

  preprintOpen access

  Abstract Many inflammatory stimuli can induce progenitor cells in the bone marrow to produce increased numbers of myeloid cells as part of the process of emergency myelopoiesis. These events are associated with innate training and can have long-term impacts on hematopoietic stem and progenitor cell (HSPC) development but can also compromise their function. While many cytokines support emergency myelopoiesis, less is known about the mechanisms that temper these events. When mice that lack the cytokine IL-27 were infected with Toxoplasma gondii, there was enhanced generation of monocyte progenitors and increased numbers of inflammatory monocytes. In the bone marrow of infected mice there was increased production of IL-27 that localized with HSPCs and a survey of cytokine receptor expression highlighted that HSPCs were uniquely poised to respond to IL-27. Furthermore, the use of in vitro differentiation assays and mixed bone marrow chimeras revealed that HSPCs from IL-27 deficient mice are pre-disposed towards the monocyte lineage. Additional studies highlighted that after infection loss of the IL-27R resulted in reduced HSPC fitness that manifested as reduced proliferative responses and a decreased ability to reconstitute the hematopoietic system. Thus, the ability of IL-27 to act on HSPC provides a regulatory brake on differentiation to limit monocyte induction and preserve HSPC stemness.

  PublisherDOI

• IL-27 limits HSPC differentiation during infection and protects from stem cell exhaustion

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-19 · 1 citations

  preprintOpen access

  Abstract Many inflammatory stimuli can induce progenitor cells in the bone marrow to produce increased numbers of myeloid cells as part of the process of emergency myelopoiesis. These events are associated with trained immunity and have long-term impacts on hematopoietic stem and progenitor cell (HSPC) development but can also compromise their function. While many cytokines support emergency myelopoiesis, less is known about the mechanisms that temper these events. When mice that lack the cytokine IL-27 were infected with Toxoplasma gondii , there was enhanced generation of monocyte progenitors and increased numbers of inflammatory monocytes. In the bone marrow of infected mice there was increased production of IL-27 that localized with HSPCs and a survey of cytokine receptor expression highlighted that HSPCs were uniquely poised to respond to IL-27. Furthermore, the use of in vitro differentiation assays and mixed bone marrow chimeras revealed that HSPCs from IL-27 deficient mice are pre-disposed towards the monocyte lineage. Additional studies highlighted that after infection loss of the IL-27R resulted in reduced HSPC fitness that manifested as reduced proliferative responses and a decreased ability to reconstitute the hematopoietic system. Thus, the ability of IL-27 to act on HSPC provides a regulatory brake on differentiation to limit monocyte induction and preserve HSPC stemness.

  PublisherDOI

• IL-27 promotes Treg cell expression of CD122 and fitness at homeostasis

  Proceedings of the National Academy of Sciences · 2025-12-09 · 1 citations

  articleOpen access

  Regulatory T (Treg) cells express high levels of the IL-27R, and in the setting of infection and autoimmunity, the cytokine IL-27 promotes Treg cell activities that mitigate tissue pathology. However, IL-27 appears dispensable for Treg cell development and maintenance as lineage-specific depletion of the IL-27R on Treg cells does not impact these populations at steady state. In contrast, when mice were generated in which the Treg compartment comprised a mix of IL-27R-sufficient and -deficient Treg cells, those that lacked IL-27R were at a competitive disadvantage. Aging experiments illustrate that IL-27R-deficient Treg cells are preferentially eroded, and this defect was associated with reduced expression of CD122, the β chain of the IL-2/15R. Moreover, blockade of CD122 led to a similar loss of Treg cells, and in vitro and in vivo studies highlight that IL-27 promotes Treg cell expression of CD122 and improves responsiveness to IL-2/15. These datasets reveal that homeostatic IL-27 signals provide a competitive advantage that shapes the composition of the Treg cell pool by modulating responsiveness to growth factors.

  PublisherOA PDFDOI

• Ligand-receptor interactions induce and mediate regulatory functions of BATF3 ⁺ B cells

  Science Advances · 2025-10-08 · 1 citations

  articleOpen access

  B cells express many protein ligands, yet their regulatory functions are incompletely understood. We profiled ligand expression across murine B sublineage cells, including those activated by defined receptor signals, and assessed their regulatory capacities and specificities through in silico analysis of ligand-receptor interactions. Consequently, we identified a B cell subset that expressed cytokine interleukin-27 (IL-27) and chemokine CXCL10. Through the IL-27–IL-27 receptor interaction, these IL-27/CXCL10-producing B cells targeted CD40-activated B cells in vitro and, upon induction by immunization and viral infection, optimized antibody responses and antiviral immunity in vivo. Also present in breast cancer tumors and retained there through CXCL10-CXCR3 interaction–mediated self-targeting, these cells promoted B cell PD-L1 expression and immune evasion. Mechanistically, Il27 and Cxcl10 transcription was induced by synergizing Toll-like receptor (TLR) and CD40 signals and driven by coinduced transcription factor BATF3, which directly targeted these genes. By applying a discovery framework focusing on regulatory cells, our findings expand the recognized scope of B cell regulatory functions.

  PublisherDOI

• LAG3 regulates antibody responses in a murine model of kidney transplantation

  Journal of Clinical Investigation · 2025-05-13 · 1 citations

  articleOpen access

  Lymphocyte activation gene 3 (LAG3) is a coinhibitory receptor expressed by various immune cells. Although the immunomodulatory potential of LAG3 is being explored in cancer and autoimmunity, there is no information on its role after organ transplantation. Our study investigated the functions of LAG3 in a mouse model of renal allograft rejection. LAG3-/- recipients rapidly rejected MHC-mismatched renal allografts that were spontaneously accepted by WT recipients, with graft histology characteristic of antibody-mediated rejection. Depletion of recipient B cells but not CD8+ T cells significantly extended kidney allograft survival in LAG3-/- recipients. Treatment of WT recipients with an antagonistic LAG3 antibody enhanced anti-donor immune responses and induced kidney damage associated with chronic rejection. The studies of conditional LAG3-/- recipients and mixed bone marrow chimeras demonstrated that LAG3 expression on either T or B cells is sufficient to regulate anti-donor humoral immunity but not to induce acute allograft rejection. The numbers and proinflammatory functions of graft-infiltrating NK cells were markedly increased in LAG3-/- recipients, suggesting that LAG3 also regulates the effector stage of antibody-mediated rejection. These findings identified LAG3 as a regulator of immune responses to kidney allografts and a potential therapeutic target for antibody-mediated rejection prevention and treatment.

  PublisherOA PDFDOI

Recent grants

• The role of IL-27/Lag3 axis in regulating Foxp3+ regulatory T cell function

  NIH · $3.4M · 2017–2028

• NIH Grant R01AI074932

  NIH · $1.9M · 2013

• Foxp3+ regulatory T cell-dependent treatment of allergic inflammation by glucocorticoids

  NIH · $2.2M · 2020–2025

• NIH Grant R21AI121524

  NIH · $436k · 2019

• NIH Grant P01NS064932

  NIH · $16.2M · 2015

Frequent coauthors

• Anabelle Visperas

  Cleveland Clinic

  58 shared

• William E. Paul

  National Institutes of Health

  48 shared

• Jeong‐su Do

  City of Hope

  47 shared

• Dongkyun Kim

  24 shared

• Graham Le Gros

  Malaghan Institute of Medical Research

  22 shared

• Sohee Kim

  Northwestern University

  19 shared

• William M. Baldwin

  19 shared

• Robert L. Fairchild

  18 shared

Labs

• Min LaboratoryPI