Clinical Research Directory

A Study on the Effect of MRD Detected by FAPI PET / CT on the Recurrence of IgG4-RD

This study intends to use the new technology of fibroblast activation protein PET / CT to study whether the tiny residual lesions detected by 68Ga-FAPI PET / CT are related to the recurrence of IgG4-RD in patients with IgG4-RD who have been clinically evaluated for complete remission after treatment.

A Clinical Study of YTS109 Cell in R/R Autoimmune Diseases

This study evaluates the safety and efficacy of YTS109 cells in adults with relapsed/refractory autoimmune diseases, such as Systemic Lupus Erythematosus (SLE), Systemic Sclerosis (SSc), etc. Aproximately 6-12 patients aged 18-65 will receive a single infusion of YTS109 cells (1.5×10⁶ cells/kg). The main purpose of exploratory clinical research is to explore the efficacy and safety of YTS109 cell and the lymphodepletion regimen. The primary endpoint is observations of types, severity, and frequency of adverse events (AEs) and efficacy assessment. This single-arm, open-label trial will enroll patients across Chinese People's Liberation Army (PLA) General Hospital.

The BCMA/CD19 Dual Targeted CAR-T Cell in Participants With Autoimmune Kidney Diseases

This study is a single-center, open-label, dose-escalation exploratory clinical trial, expected to enroll 6 to 12 participants. It will use a BOIN (Bayesian Optimal Interval) design for dose escalation, with four predetermined dose groups (0.3×10\^6 cells/kg, 1.0×10\^6 cells/kg, 3.0×10\^6 cells/kg, and an alternative dose of 0.1×10\^6 cells/kg). Each dose group plans to enroll 1-2 or 3-6 participants with relapsed or refractory autoimmune-mediated kidney diseases (such as lupus nephritis, ANCA-associated vasculitis, membranous nephropathy, and IgG4-related diseases).

AYLo - AutoimmunitY and Loss of y

The AYLo study (AutoimmunitY and Loss of y - Investigating the Role of Hematopoietic Mutations and Mosaic Mutation in the Y Chromosome in Autoimmune Rheumatologic Diseases) aims to systematically investigate hematopoietic mutations, such as hematopoietic (mosaic) loss of the Y chromosome (mLOY), focusing on their underlying causes, pathophysiological significance, patterns of manifestation, and impact on disease progression in autoimmune, rheumatologic disorders. This research seeks to bridge existing knowledge gaps by exploring how such mutations influence immune homeostasis, cellular function, and susceptibility to inflammation-driven pathologies. Through the integration of advanced immunological profiling, the study aspires to uncover key mechanisms that drive the initiation, progression, and complications of autoimmune rheumatic diseases. These analyses will combine single nucleotide polymorphisms (SNP) arrays, multiplex assays, transcriptomics, and flow cytometry staining of peripheral blood mononuclear cells to delineate the interplay between hematopoietic mutations and immune dysregulation. A further objective is the development of a multimodal framework for disease-specific characterization, enabling precise mapping of mutation-driven phenotypes across diverse autoimmune conditions. This framework will incorporate clinical, molecular, and imaging data. Additionally, the AYLo study aims to explore the potential role of mLOY and other hematopoietic mutations as biomarkers for disease stratification, prognosis, and therapeutic response. The findings may open avenues for personalized treatment approaches, leveraging the molecular insights to inform targeted interventions and improve patient outcomes in autoimmune rheumatic disorders. By integrating translational and basic science approaches, this study has the potential to redefine current paradigms in autoimmune disease research and therapy.

BCMA-CD19 CAR-T Therapy for Refractory Autoimmune Diseases

The objective of this study is to evaluate the efficacy and safety of BCMA/CD19 chimeric antigen receptor (CAR)-modified T cells in the treatment of autoimmune diseases.

Key Mechanisms of Abnormal T Cell Activation and Differentiation in IgG4-Related Ophthalmic Disease

IgG4-related disease (IgG4-RD) is a newly recognized chronic inflammatory condition caused by immune system dysfunction. It is characterized by the infiltration of IgG4+ plasma cells, dense fibrosis, and inflammation involving veins and eosinophils. Common symptoms include elevated serum IgG4 levels and the formation of tumor-like growths that can affect almost any organ, leading to pressure on tissues, irreversible damage, and even organ failure. While estimates suggest a prevalence of 0.28 to 1.08 per 100,000 people, this might be an underestimation due to limited awareness, the new definition of the disease, and its subtle onset. IgG4-related ophthalmic disease (IgG4-ROD) is a subtype of IgG4-RD that affects the eye area, particularly the lacrimal glands, extraocular muscles, and surrounding nerves. It often presents as painless swelling of the lacrimal glands in one or both eyes, sometimes with discomfort or a sensation of a foreign body. It can also cause thickening of eye muscles, leading to symptoms like bulging eyes, blurred vision, or double vision. In some cases, mass lesions in the orbit may press on the optic nerve, potentially leading to permanent vision loss. While there is currently no cure for IgG4-ROD, steroids are used as the main treatment to control inflammation and fibrosis. However, the disease often recurs, with recurrence rates for IgG4-RD reported between 24% and 63% in various studies. Understanding the causes of IgG4-ROD could help develop better treatments and reduce the chances of relapse. Studies suggest that T cells play a key role in the development of IgG4-RD, including IgG4-ROD. CD4+ T cells are the main immune cells found in affected tissues. They can help B cells multiply and produce IgG4 antibodies and contribute to tissue fibrosis by releasing certain signaling molecules. Despite treatment with rituximab, a drug that targets B cells, many IgG4-RD patients experience relapses, indicating that T cells remain important in driving the disease. Among the T cell subtypes, T follicular helper cells (Tfh) and CD4+ cytotoxic T cells (CD4+ CTLs) are particularly relevant. Tfh cells support B cells in producing IgG4 antibodies, while CD4+ CTLs can contribute to tissue fibrosis by releasing factors like TGF-β, IL-1β, and IFN-γ. However, the detailed mechanisms of how T cells become abnormally activated and differentiated in IgG4-ROD remain unclear. This study will use samples from the lacrimal glands, blood, and tears of IgG4-ROD patients to investigate how T cells become abnormally active and differentiate in this condition. The findings could identify new targets for therapy, helping to reduce the recurrence of IgG4-ROD and provide insights into treating other forms of IgG4-RD.