About

Anita S. Chong is a Professor at the University of Chicago in the Department of Surgery-Transplant. Her research focuses on understanding the basis of immunological tolerance and humoral immunity following allogeneic transplantation. She has developed approaches to track endogenous allospecific T and B cell populations, studying their behavior under rejection, memory, sensitization, and tolerance conditions, with the aim of identifying new biomarkers for these states. Her work also investigates the behavior of memory alloreactive B cells in transplantation, seeking strategies to control this subset of cells. Additionally, her research extends into the prevention of infections through vaccination, collaborating with other scientists to identify vaccine candidates and develop nanoparticulate adjuvant-free vaccines that elicit protective immune responses with minimal inflammation, which is particularly relevant for tolerant patients. Her extensive research activities are supported by multiple NIH grants, and she has contributed significantly to the field of transplant immunology through her investigations into immune tolerance, B cell roles in rejection, and vaccine development for transplant stability.

Research topics

• Immunology
• Medicine
• Biology
• Cell biology
• Internal medicine
• Genetics
• Virology
• Materials science
• Microbiology
• Biochemistry
• Pathology
• Nanotechnology
• Chemistry

Selected publications

• High-dimensional spatial proteomics and novel machine learning pipeline identifies disease specific renal damage states

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-15

  articleOpen access

  Lupus nephritis (LuN) and renal allograft rejection (RAR) manifest inflammation and fibrosis that ultimately lead to kidney failure. To quantitatively assess spatial injury patterns, we collected high dimensional spatial proteomics data from 23 LuN, 33 RAR, and 8 kidney control (KC) biopsies. We developed a computational pipeline to segment and classify tubules, capillaries, and glomeruli in whole-slide images using three trained neural networks (Renal Damage diagnosis, RDDx). RDDx achieved high accuracy and generalizability, reliably identifying small capillaries and differentiating tubular and vascular inflammation in kidney tissues. Both LuN and RAR showed reduced tubular and capillary areas with expanded interstitial space. LuN displayed patchy clusters of stressed and inflamed tubules, whereas RAR exhibited diffuse injury. Within RAR, T cell-mediated rejection (TCMR) showed intense tubulitis while antibody-mediated rejection (ABMR) featured proliferating and inflamed capillaries near atrophic tubules. RDDx quantitative metric outputs correlated with histopathological scores, highlighting their reproducibility and clinical relevance. Stressed tubules in mildly inflamed LuN biopsies suggested they were a sensitive injury marker, while proliferating capillaries revealed microvascular remodeling in ABMR. These findings indicated RDDx can identify and quantify damage mechanisms specific to each renal disease thus facilitating future mechanistic studies and therapeutic target discovery.

  PublisherOA PDFDOI

• Dual induction of tissue-resident T and B cell immunity for broad influenza protection with a nanofiber-VLP vaccine

  Journal of Nanobiotechnology · 2026-03-30

  articleOpen access

  Respiratory pathogens pose significant global health challenges, with current vaccines often failing to prevent viral replication at mucosal entry points. To address this, we developed an adjuvant-free intranasal nanovaccine (NP@HA-VLP-Q11) by integrating SpyTag/SpyCatcher-mediated antigen multimerization on virus-like particles (VLPs) with self-assembling Q11 nanofibers. This vaccine leverages the ability of Q11 to induce both humoral and cellular immunity without requiring supplemental adjuvants or eliciting local inflammation to co-deliver a conserved nucleoprotein (NP) CD8+ T cell epitope and influenza hemagglutinin stem domain (miniHA) VLPs. In mouse models, we show that NP@HA-VLP-Q11 elicits systemic neutralizing antibodies and lung-resident memory T cells (TRMs) and B cells (BRMs) that are maintained for at least 12 weeks after immunization and expand rapidly upon heterologous H9N2 challenge. Importantly, intranasal immunization with NP@HA-VLP-Q11 conferred immunity and cross-protection against heterologous influenza strains that were preserved for at least 12 weeks. The dual induction of TRMs and BRMs offers immediate humoral protection and sustained cellular immunity at the infection site, mimicking natural viral exposure while avoiding replication risks. These findings demonstrate the potential of self-assembling nanomaterials combined with stabilized multimerized antigens in VLPs to create next-generation vaccines for broad, broad and effective protection against respiratory pathogens.

  PublisherDOI

• Cell-intrinsic CD4 T cell tolerance: a new frontier in therapy?

  Trends in Immunology · 2025-07-23 · 1 citations

  reviewOpen access
  PublisherOA PDFDOI

• CAR Treg synergy with anti-CD154 promotes infectious tolerance and dictates allogeneic heart transplant acceptance

  JCI Insight · 2025-04-07 · 8 citations

  articleOpen accessSenior author

  Successful allograft-specific tolerance induction would eliminate the need for daily immunosuppression and improve posttransplant quality of life. Adoptive cell therapy with regulatory T cells expressing donor-specific chimeric antigen receptors (CAR Tregs) is a promising strategy but, as monotherapy, cannot prolong survival with allografts with multiple MHC mismatches. Using an HLA-A2-transgenic haplo-mismatched heart transplantation model in immunocompetent C57BL/6 recipients, we showed that HLA-A2-specific CAR (A2.CAR) Tregs were able to synergize with a low dose of anti-CD154 to enhance graft survival. Using haplo-mismatched grafts expressing the 2W-OVA transgene and tetramer-based tracking of 2W- and OVA-specific T cells, we showed that in mice with accepted grafts, A2.CAR Tregs inhibited donor-specific T cell, B cell, and antibody responses and promoted a substantial increase in endogenous FOXP3+ Tregs with indirect donor specificity. By contrast, in mice where A2.CAR Tregs failed to prolong graft survival, FOXP3- A2.CAR T cells preferentially accumulated in rejecting allografts, and endogenous donor-specific responses were not controlled. This study therefore provides evidence for synergy between A2.CAR Tregs and CD154 blockade to promote infectious tolerance in immunocompetent recipients of haplo-mismatched heart grafts and defines features of A2.CAR Tregs when they fail to reshape host immunity toward allograft tolerance.

  PublisherDOI

• Multi-omics analysis of a pig-to-human decedent kidney xenotransplant

  Nature · 2025-11-13 · 13 citations

  articleOpen access
  PublisherOA PDFDOI

• Autoreactive B Cells in the Kidney Chronic Graft Rejection

  American Journal of Transplantation · 2025-08-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Immune cell quantification of in situ inflammation partitions human lupus nephritis into mechanistic subtypes

  Journal of Clinical Investigation · 2025-09-04 · 5 citations

  articleOpen access

  BACKGROUNDIn human lupus nephritis (LuN), tubulointerstitial inflammation (TII) is prognostically more important than glomerular inflammation. However, a comprehensive understanding of both TII complexity and heterogeneity is lacking.METHODSHerein, we used high-dimensional confocal microscopy, spatial transcriptomics, and specialized computer vision techniques to quantify immune cell populations and localize these within normal and diseased renal cortex structures. With these tools, we compared LuN to renal allograft rejection (RAR) and normal kidney tissues on 54 deidentified biopsies.RESULTSIn both LuN and RAR, the 33 characterized immune cell populations formed discrete subgroups whose constituents covaried in prevalence across biopsies. In both diseases, these covariant immune cell subgroups organized into the same unique niches. Therefore, inflammation could be resolved into trajectories representing the relative prevalence and density of cardinal immune cell members of each covariant subgroup. Indeed, in any one biopsy, the inflammatory state could be characterized by quantifying constituent immune cell trajectories. Remarkably, LuN heterogeneity could be captured by quantifying a few myeloid immune cell trajectories, while RAR was more complex with additional T cell trajectories.CONCLUSIONSOur studies identify rules governing renal inflammation and thus provide an approach for resolving LuN into discrete mechanistic categories.FUNDINGNIH (U19 AI 082724 [MRC], R01 AI148705 [MRC and ASC]), Chan Zuckerberg Biohub (MRC), and Lupus Research Alliance (MRC).

  PublisherOA PDFDOI

• Cutting to the chase: Pruning alloreactive T cells

  Immunity · 2025-02-01

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Role of Tregs in maintaining alloreactive Tconv hypofunction in transplantation tolerance 2291

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Regulatory T cells (Tregs) are necessary for the induction of murine cardiac transplantation tolerance via costimulation blockade. Whether Tregs are necessary to maintain Tconv hypofunction long-term after tolerance has been achieved remains to be established. Our preliminary data indicate that complete, though transient, depletion of Tregs using diphtheria toxin (DT) in Foxp3-DTR mice at the maintenance phase of tolerance precipitated the rejection of previously tolerized cardiac allografts and resulted in the de novo production of graft-specific antibodies – potentially implying the reinvigoration of Tconvs which then provide help to B cells. Indeed, RNA-sequencing of graft-specific Tconvs following Treg depletion in tolerant mice demonstrated their transcriptional distinction from Tconvs in tolerant mice that retained Tregs. Conversely, graft-reactive Tconvs from tolerant mice infected with Listeria monocytogenes or having received a hydrodynamic injection of plasmids encoding the proinflammatory cytokines IFNb and IL-6 to break transplantation tolerance, were both transcriptionally similar to Tconvs from unmanipulated tolerant mice. Furthermore, allospecific Tconvs showed renewed cytokine production and proliferative capacity after Treg depletion. This indicates a unique state of potential reinvigoration and implicates Tregs in actively maintaining dysfunction of graft-specific Tconvs. Funding Sources Supported by the American Heart Association Pre-Doctoral Fellowship (https://doi.org/10.58275/AHA.24PRE1192022.pc.gr.190594) and the T32 Cardiovascular Sciences Training Grant (5-T32-HL-7381) Topic Categories Transplantation Immunology (TRAN)

  PublisherOA PDFDOI

• Resolving ScRNA-Seq Signatures of Antigen-Specific CD4 ⁺ T Cells in Tolerance across Semi-Allogeneic Transplantation and Pregnancy

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

  preprintOpen accessSenior author

  SUMMARY Transplantation of allogeneic organs requires lifelong immunosuppression to prevent rejection. Prior sensitization and resultant memory T cells are barriers to achieving successful transplant tolerance. In reproductive immunology by contrast, pregnancy represents a spontaneous model of tolerance where the semi-allogeneic fetus evades rejection even in multiparous or rejection-sensitized mothers. CD8 + T cell phenotypes of tolerance and rejection have been previously reported in transplant and pregnancy, but the transcriptional states of donor and fetus-specific CD4 + T cells remain poorly defined. Here, we performed Single-cell RNA-sequencing on endogenous, antigen-specific CD4 + T cells across models of allogeneic heart transplants and naïve or paternal skin-sensitized pregnancy. We identified expanded T follicular helper (Tfh) and non-follicular effectors in transplant rejection absent in tolerance. Naïve pregnancy resulted in a modest expansion of effector clusters with transcriptional quiescence that mirrored virgin mice. Successful sensitized pregnancy resulted in expanded Tfh clusters consistent with increased fetal-specific antibodies and limited non-Tfh effector responses. Most striking were the extensive changes imposed on donor-specific Foxp3 pos regulatory T cells (Tregs) resulting in the co-clustering together with Foxp3 neg T conventional cells (Tconvs) in transplant tolerance and the emergence of a Foxp3 neg Type I Regulatory cluster observed in pregnancy of sensitized dams. Finally, we showed that these transcriptomes were relevant and enriched in human datasets of health and disease respectively. Thus, the context-dependent signatures of antigen-specific CD4 + T cells provide new insights into their divergent responses to allogeneic conflict at the intersection of transplant and reproductive immunology. Graphical Abstract

  PublisherOA PDFDOI

Recent grants

• Deconstructing B cell transplantation tolerance

  NIH · $2.2M · 2019–2024

• NIH Grant R21DK073529

  NIH · $415k · 2009

• Project-002

  NIH · $43.6M · 2012–2028

• NIH Grant R29CA053805

  NIH · $339k · 1996

• NIH Grant R01AI034061

  NIH · $659k · 1998

Frequent coauthors

• James W. Williams

  University of Newcastle Australia

  157 shared

• Jikun Shen

  153 shared

• Howard Sankary

  Loyola University Medical Center

  142 shared

• Dengping Yin

  125 shared

• Lori J. West

  University of Alberta

  102 shared

• Bethany J. Foster

  102 shared

• Roslyn B. Mannon

  University of Alabama at Birmingham

  100 shared

• Germaine Wong

  University of Sydney

  97 shared

Labs

• Anita Chong LabPI

Education

• M.D.

  University of Chicago

• B.S.

  University of California, San Diego