About

Chunlin Li is an Assistant Professor of Statistics at the University of Virginia. His research is centered on causal inference and its intersections with machine learning and public health applications. Before joining UVA, Chunlin Li was an Assistant Professor at Iowa State University. He obtained his PhD in Statistics from the University of Minnesota, Twin Cities in 2022 and his BS in Computational Mathematics from City University of Hong Kong in 2017.

Research topics

• Internal medicine
• Immunology
• Biology
• Medicine
• Virology

Selected publications

• Targeting pyroptosis in metabolic dysfunction-associated steatotic liver disease: from molecular mechanisms to therapeutic innovation

  Molecular Biology Reports · 2026-05-14

  article1st authorCorresponding
  PublisherDOI

• Response to Neoadjuvant Systemic Therapy May Serve as an Indicator for Omitting Post-BCS Radiation Therapy in Women with Early-Stage Breast Cancer

  Cancer Research and Treatment · 2025-09-10

  articleOpen access1st authorCorresponding

  Purpose: To avoid unnecessary toxicities and optimize the allocation of healthcare resources, it is crucial to adequately select patients with extremely low recurrence risk to downgrade or eliminate radiation therapy. Materials and Methods: From the SEER database, clinical data of 7,291 female patients with early-stage breast cancer who underwent neoadjuvant systemic therapy (NST) and breast-conserving surgery (BCS) were collected for this study. The patients were stratified by their response to NST, and the long-term survival, and risk of recurrence were assessed using Cox regression analysis and Fine-gray competing risk models for those with and without post-BCS RT, respectively. Results: Our results showed that female with early-stage breast cancer who achieved complete response (CR) to NST, omitting post-BCS RT achieved the same OS and DFS as those who received the post-BCS RT, and the omission did not increase the risk of recurrence or BCSD. For patients who did not achieve CR to NST, five clinical indicators (including age, N stage, grade, response to NST, and molecular subtype) were employed to construct a nomogram for clinical prediction of the risk of recurrence. The validated results affirmed our model's ability to accurately discriminate high- and low-risk patients and its promising clinical application value. Conclusion: Post-BCS RT can be omitted for women with early-stage breast cancer who achieved CR to NST. For those who failed to achieve CR to NST, a nomogram was constructed for clinicians to decide whether to omit post-BCS RT or not based on the individualized assessment.

  PublisherOA PDFDOI

• Dual-Function Adjuvant Cyclosporin A: Enhancing RSV-Specific Humoral Immunity via Treg-Driven B-Cell Activation

  Vaccines · 2025-09-23

  articleOpen access1st author

  BACKGROUND: Respiratory syncytial virus (RSV) remains a leading cause of respiratory illness globally, with limited vaccine options, particularly for infants and high-risk populations. This study investigates Cyclosporin A (CsA), traditionally an immunosuppressant, as a novel adjuvant to enhance RSV-specific immunity. METHODS: BALB/c mice were subcutaneously immunized with RSV G protein co-administered with varying Cyclosporin A doses, challenged intranasally with RSV, and analyzed for RSV-specific humoral immunity and mechanistic Treg-dependent B-cell responses. RESULTS: We demonstrate that co-administration of CsA with the RSV G protein (G+CsA) dose-dependently boosts RSV-specific IgG and neutralizing antibodies, with selective augmentation of IgG1 and IgG2 subclasses. Mechanistically, G+CsA induces regulatory T cells (Tregs) expressing CD40L and IL-10, which directly promote B-cell activation, proliferation, and plasma cell differentiation. Depletion of Tregs or neutralization of IL-10/CD40L abrogated antibody production, confirming these pathways as critical mediators. Notably, G+CsA-induced Tregs adopt a helper phenotype distinct from conventional Tregs, balancing immune enhancement and homeostasis. CONCLUSIONS: CsA demonstrates dual adjuvant properties by enhancing RSV-specific neutralizing IgG titers through Treg-driven B-cell activation, offering a potential strategy to optimize vaccine-induced humoral immunity.

  PublisherOA PDFDOI

• Macrophage peroxisomes guide alveolar regeneration and limit SARS-CoV-2 tissue sequelae

  Science · 2025-03-06 · 39 citations

  articleOpen access

  Peroxisomes are vital but often overlooked metabolic organelles. We found that excessive interferon signaling remodeled macrophage peroxisomes. This loss of peroxisomes impaired inflammation resolution and lung repair during severe respiratory viral infections. Peroxisomes were found to modulate lipid metabolism and mitochondrial health in a macrophage type-specific manner and enhanced alveolar macrophage-mediated tissue repair and alveolar regeneration after viral infection. Peroxisomes also prevented excessive macrophage inflammasome activation and IL-1β release, limiting accumulation of KRT8 high dysplastic epithelial progenitors following viral injury. Pharmacologically enhancing peroxisome biogenesis mitigated both acute symptoms and post-acute sequelae of COVID-19 (PASC) in animal models. Thus, macrophage peroxisome dysfunction contributes to chronic lung pathology and fibrosis after severe acute respiratory syndrome coronavirus 2 infection.

  PublisherOA PDFDOI

• Glycosylation in T2 high and Th17 Asthma: A Narrative Review

  Journal of Asthma and Allergy · 2025-04-01 · 3 citations

  reviewOpen access

  Glycosylation, a fundamental biochemical process, entails the covalent attachment of sugar molecules to proteins, DNA, or RNA. Beginning with an overview of the pathophysiological features of asthma, this review proceeds to elucidate various facets of glycosylation in asthma pathology, specifically in T2 high asthma and Th17-mediated responses. We examined glycosylation's involvement in regulating airway inflammation, encompassing the modulation of pro-inflammatory cytokine release such as IL-4, IL-5, and IL-13, key components of T2 inflammation, as well as its significance in modulating immune cell functionality, notably T cells and dendritic cells. Moreover, we explored glycosylation's impact on airway remodeling processes, including its regulation of airway smooth muscle cell proliferation and migration. Addressing molecular mechanisms, this review delved into several glycosylation modifications of proteins and genes implicated in asthma pathogenesis, including IgE, IL-4 receptor, TGF-β, and the regulation of select glycosylation enzymes. Additionally, the review highlights the role of Th17 cells in T2 high asthma and their modulation through glycosylation. We underscored future research imperatives, including biomarker discovery, therapeutic realization, and the potential utility of glycosylation modifications in asthma prevention and management. In short, this review provides an in-depth analysis of the critical role of glycosylation in the pathogenesis of T2 high asthma and Th17 responses.

  PublisherOA PDFDOI

• Computed tomography manifestations and clinical features of acquired immune deficiency syndrome patients with cervical lymph node tuberculosis

  International Journal of Radiation Research · 2025-01-01

  articleOpen access

  Background:To analyze the computed tomography (CT) findings and clinical features of acquired immune deficiency syndrome (AIDS) patients with cervical lymph node tuberculosis (CLNT).Materials and Methods: The clinical data of 100 patients diagnosed with CLNT in our hospital from January 2020 to December 2022 were retrospectively analyzed.Based on whether AIDS was combined, 20 cases of CLNT patients with AIDS were included in observation group (OG), and 80 cases of CLNT patients without AIDS were included in control group (CG).CT imaging features and general clinical data were analyzed and compared between groups.Results: Cervical lymph nodes in the OG showed irregular shape, blurred boundary, and short diameter >3 cm, with statistical difference relative to the CG (P<0.05).The complete necrosis type of cervical lymph node necrosis in the OG presented higher relative to the CG (P<0.05).The OG was more likely to involve lymph nodes in region I and II of the neck (P<0.05).Besides, the lymph node lesions involving 3 regions and 4 regions, proportion of males and mean age of patients were elevated in the OG (P<0.05).The mean CD4+T lymphocyte count was lower in the OG (P<0.05).The OG also showed higher incidence of clinical symptoms and the proportion of combined clinical symptoms 3 relative to the CG (P<0.05).Conclusion: The CT manifestations of AIDS patients have certain commonality compared with non-AIDS patients, which might provide clues for clinical diagnosis.

  PublisherOA PDFDOI

• Human pluripotent stem cell-derived skin organoids enabled pathophysiological model of Mycobacterium tuberculosis infection

  Nature Communications · 2025-12-02 · 1 citations

  articleOpen access

  Cutaneous tuberculosis (CTB) is an infectious disease highly associated with extracellular matrix remodeling and granuloma-driven fibrosis. Fibroblasts play crucial roles in this fibrotic process, but their specific roles in Mycobacterium tuberculosis (Mtb) skin infections remain unclear due to the lack of proper in vitro models. Here, we demonstrate that skin organoids (SKOs) derived from human induced pluripotent stem cells can model CTB infected by Mtb. Single-cell RNA analyses reveal an increase in fibroblasts, upregulation of genes involved in collagen synthesis, and enhanced collagen degradation induced by MMP2 and MMP14 in Mtb-infected SKOs. This is accompanied by the destruction of nerve cells and adipocytes. Importantly, the onset of fibrosis in Mtb-infected SKOs is dependent on the activation of the PI3K-AKT signaling pathway and transcription factor AP1 in fibroblasts. Pharmacological inhibition of PI3K-AKT and AP1 alleviates fibrosis and collagen deposition. Our findings have uncovered distinct alterations in cell populations during Mtb-induced skin fibrosis, highlighting the crucial roles of PI3K-AKT and AP1. The study demonstrates the utility of SKOs for investigating CTB pathogenesis and evaluating potential antifibrotic treatments. Cutaneous tuberculosis is an infectious disease associated with extracellular matrix remodeling and granuloma-driven fibrosis. Here, the authors present an in vitro model of this disease using skin organoids infected with Mycobacterium tuberculosis, and describe infection-induced alterations in specific pathways and cell populations.

  PublisherOA PDFDOI

• Unraveling asthma through single-cell RNA sequencing in understanding disease mechanisms

  Journal of Asthma · 2025-02-27 · 1 citations

  review

  OBJECTIVE: To elucidate the fundamental principles of single-cell RNA sequencing (scRNA-seq) and summarize its application in asthma research, aiming to enhance understanding of asthma pathophysiology and guide future research directions. DATASOURCE: Recent advances and emerging research in scRNA-seq and its role in the pathogenesis of asthma. STUDY SELECTIONS: This review incorporates studies that analyzed the heterogeneity of asthma cell types and their functional states using scRNA-seq, with particular emphasis on immune cells and airway remodeling. The selection of specific cell types and markers was based on their relevance to asthma pathogenesis, and we discuss the rationale for favoring certain scRNA-seq technologies in these investigations. RESULTS: ScRNA-seq technology has provided insights into the key mechanisms underlying inflammation and airway remodeling in asthma. It has uncovered the diversity of immune cell subtypes and their specific roles in asthma pathogenesis, revealing critical pathways that contribute to disease progression. These findings offer a theoretical foundation for the development of targeted therapeutic strategies, paving the way for personalized medicine and improved patient outcomes. CONCLUSION: ScRNA-seq reveals the complex heterogeneity and functional roles of immune cells in asthma, offering key insights into disease mechanisms and the potential for targeted therapies. However, challenges remain, such as the need for further refinement of data integration methods and addressing the limited clinical applicability of current findings. Future research should focus on overcoming these limitations, improving cell type annotation, and expanding studies to include longitudinal and clinical data to better understand disease dynamics and therapy responses.

  PublisherDOI

• Mechanisms of superior respiratory IgA responses against SARS-CoV-2 after mucosal vaccination 2158

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Mucosal immunization and respiratory IgA responses offer significant promise in protecting against airborne pathogens, including SARS-CoV-2. However, However, the conditions and mechanisms that lead to the robust induction of respiratory IgA responses following mucosal vaccination remain poorly understood. It is also currently debatable whether mucosal vaccination is still warranted given that most individuals in developed countries have established a hybrid immunity from vaccination and infection. Here, we analyzed respiratory immune responses in humans following SARS-CoV-2 infection, vaccination, or both. We found that hybrid immunity resulted in moderately increased respiratory IgA and neutralizing antibody responses compared to infection or vaccination alone. However, a direct comparison of hybrid immunity and a mucosal adenovirus-based booster vaccination in animal models revealed that respiratory booster immunization elicited markedly stronger and more durable respiratory IgA, T cell response and protective immunity, supporting the promise of respiratory vaccination. Mechanistically, mucosal boosters prompted IgA-secreting cells in the respiratory mucosa with help from local IL-21-producing Blimp1+ Th1 cells. Furthermore, lung macrophages were important for this respiratory IgA response via TGF-β. Our findings highlight a local network for robust respiratory IgA responses, supporting mucosal vaccination strategies against SARS-CoV-2 and other respiratory pathogens. Funding Sources AI147394, AG069264, AI112844, HL170961, and AI154598 to J.S, AI176171 to W.G.T. and J.S.; U54CA260582 to S.L.L; R01AI168684 to G. Z. Topic Categories Vaccines and Immunotherapy (VAC)

  PublisherOA PDFDOI

• Exhausted KLRG1hi CD8+ T and pathogenic GZMA+ Th17 cells are associated with the mild Mycoplasma pneumoniae pneumonia in children

  Journal of Infection · 2025-10-30 · 3 citations

  articleOpen access

  T cells and polarization of IgM secreting cells might help explain the ill-controlled bacterial replication in MMPP. Furthermore, compared to the healthy controls, IL-17A producing Th17 cells were reduced in MMPP, but cytotoxic granzymes increased significantly. Reduced IL-17A would suggest elevated M. pneumoniae colonization and reduced bacterial clearance in the respiratory tract, whereas cytotoxic property of this pathogenic Th17 cells might play a role in the pulmonary hyper inflammation. Therefore, this work managed to characterize the landscape of dysfunctional T and B lymphocytes that associates with the immune evasion and immunopathogenesis of MMPP.

  PublisherDOI

Frequent coauthors

• Jie Sun

  China Tourism Academy

  138 shared

• In Su Cheon

  University of Virginia

  96 shared

• Yue Wu

  Carter Center

  81 shared

• Young Min Son

  Chung-Ang University

  67 shared

• Jinyi Tang

  Carter Center

  52 shared

• Mark H. Kaplan

  Bristol-Myers Squibb (United States)

  41 shared

• Xiaoqin Wei

  University of Virginia

  39 shared

• Zheng Wang

  Jiangsu Province Hospital

  33 shared