PIPages
Labs

Xuefang Cao

University of Maryland, Baltimore, MD·Microbiology & Immunology

After a bone marrow or stem cell transplant from a donor, the donor's immune T cells can attack the patient's body. This dangerous complication is called graft-versus-host disease (GVHD).

Fields

Microbiology & Immunology

Medicine & Clinical Research

Pharmacology

Topics

graft-versus-host disease

allogeneic hematopoietic cell transplantation

allo-HCT

Grants
3 known grants, through Aug 2027

What they work on

  1. Determine whether blood-forming stem and progenitor cells use the receptor CD27 to directly suppress donor T cells, using transplants into Rag1 knockout mice that lack CD27 and NK cells, in vivo and in vitro.
  2. Identify previously unrecognized innate immune cells or non-blood cells that use CD27, which pairs with the molecule CD70, to suppress inflammatory T cell responses and graft-versus-host disease.
  3. Define how β2-adrenergic receptor (β2AR) signaling, triggered by norepinephrine and epinephrine, controls T cell development in the thymus, immune recovery and GVHD, using cell type-specific Cre-LoxP knockout mice.
  4. Determine how β2AR signaling regulates CD115+ myeloid cell development and recovery after transplant, using RNA sequencing, flow cytometry, CyTOF mass cytometry and Seahorse metabolic assays.
  5. Test whether existing drugs that activate or block β2AR can reduce GVHD while preserving the donor cells' attack on tumors after allogeneic transplantation in mice.

More about the research

It limits a procedure that can cure blood cancers and other blood and immune diseases. These grants ask what naturally keeps overactive immune cells in check and how the immune system rebuilds itself after allogeneic hematopoietic cell transplantation (allo-HCT), meaning a transplant of blood-forming cells from a different person. One project asks whether blood-forming stem cells themselves suppress T cells through a receptor called CD27. A second asks how stress-hormone signals from the nervous system shape immune development. Both use mouse transplant models of GVHD. The work is also part of a cancer center program on immune-based cancer treatment.

Why it matters

Patients receiving donor stem cell transplants for blood cancers and other blood or immune diseases risk graft-versus-host disease. Finding a stem cell-based brake on overactive T cells could offer new ways to enhance stem cell therapies for immune disorders. Because drugs that activate or block β2AR are already widely available, findings on this receptor could lead quickly to clinical trials in transplant patients.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Tumor Immunology and Immunotherapy Program

NIH · Aug 2008 – Aug 2027

CD27-mediated immune suppression by HSPCs, innate immune cells or non-hematopoietic cells

NIH · Aug 2025 – Jul 2027

Beta-2 adrenergic signaling in immune homeostasis and reconstitution

NIH · Apr 2022 – Mar 2027

Closest labs

Jaebok Choi

Washington University in St Louis, MO·Microbiology & Immunology

Test whether drug blockade of VLDLR, a receptor on T cells, prevents graft-versus-host disease while preserving the graft-versus-leukemia effect, in two independent mouse models of allogeneic hematopoietic cell transplantation.

John Wagner

University of Minnesota, MN·Medicine & Clinical Research

Establish the safety and maximum tolerated dose of donor CAR19 regulatory T cells, given with and without IL-2, in patients with relapsed or refractory CD19+ acute lymphocytic leukemia, measuring cell persistence and tumor killing.

Benjamin Vincent

University of North Carolina at Chapel Hill, NC·Microbiology & Immunology

Evaluate how large structural DNA variants contribute immunogenic minor histocompatibility antigens that donor T cells target after HLA-matched stem cell transplantation for AML.

The school

University of Maryland, Baltimore: 23 labs on PI Pages, $1.5B a year on research, 79 research doctorates a year.

More about University of Maryland, Baltimore

Reach out

A start for your email. Fill in the brackets.