TROVE2 Blocking Peptide
- Known as:
- TROVE2 Blocking Peptide
- Catalog number:
- 33r-7498
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- TROVE2 Blocking Peptide
Related genes to: TROVE2 Blocking Peptide
- Gene:
- RO60 NIH gene
- Name:
- Ro60, Y RNA binding protein
- Previous symbol:
- SSA2, TROVE2
- Synonyms:
- Ro60
- Chromosome:
- 1q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-06-17
- Date modifiied:
- 2018-11-07
Related products to: TROVE2 Blocking Peptide
Related articles to: TROVE2 Blocking Peptide
- Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease driven by uncensored B and T cell autoreactivity. Understanding this pathogenic process has been hampered by lack of studies of secondary lymphoid organs in human SLE. Using minimally invasive lymph node fine needle aspirates (LN-FNAs), we profiled tissue-resident immune cells from 59 SLE patients and 34 healthy controls through high-dimensional 43-color flow cytometry, antigen-specific tetramer probing, and sc-RNA sequencing with paired VH/VL repertoire analysis. Our findings reveal hyperactive lymph node immunity in SLE characterized by spontaneous germinal center (GC) activation, plasma cell accumulation enriched in mature CD19 and CD138 antibody-secreting cells, and increased frequencies of both GC-T and PD-1 CXCR5 T extra-follicular helper cells. SLE lymph nodes harbored large oligoclonal B cell families with altered isotype usage, dominated by IgG1 and IgG4. Critically, self-reactive 9G4 and Ro60 B cells showed defective tolerance checkpoint control, accumulating in activated naïve, GC, and plasma cell compartments with distinctive PD-1 Tox expression absent in viral-specific responses. Single-cell repertoire analysis revealed VH clones in SLE B and B , that in contrast to HD, had not experienced clonal redemption. Instead, SLE VH clones displayed low somatic hypermutation and preserved the AVY hydrophobic patch associated with autoreactivity. Monoclonal antibody testing confirmed that unmutated AVY VH clones retained polyreactivity against naïve B cells, apoptotic cells, and multiple self-antigens. Together, these results define "clonal damnation" as a key mechanism in SLE whereby autoreactive VH clones of pathogenic potential escape tolerance checkpoints, expand in germinal centers, and differentiate into tissue plasma cells while preserving germline-encoded self-reactivity. Combined, our study defines critical mechanisms of tolerance breakdown in lupus pathogenesis. - Source: PubMed
Publication date: 2026/05/18
Faliti Caterina EGhimire MidushiGarcia-Vega MelissaWatermeier Rachel CCallahan AmandaBurke JuliaPosadas OliviaMishra Ashish KKhurana SurenderGreiff VictorScharer Chris DLindner John MKing R GlennNewell MaryKhosroshahi ArezouLee F Eun-HyungSanz Iñaki - B cells collaborate with T helper cells sharing the same antigen specificity to produce pathogenic antibodies to the Ro60 autoantigen in Sjögren's disease. - Source: PubMed
Publication date: 2026/06/03
Farris A DariseJupudi Ananth Aditya - Sjögren's disease (SjD) is an autoimmune disorder characterized by lymphocytic infiltration of exocrine glands. Although B cells producing anti-Ro60 autoantibodies are frequently found in salivary gland lesions, the antigen specificity of CD4 T cells has remained unclear. Given accumulating evidence for T cell involvement in local autoantibody production, we comprehensively investigated Ro60 reactivity among lesion-infiltrating CD4 T cells. Over 200 T cell receptors (TCRs) enriched in salivary glands from Japanese and Caucasian patients with SjD were screened using a TCR reporter system, identifying 13 Ro60-reactive TCRs predominantly expressed in T peripheral helper/T follicular helper subset, along with human leukocyte antigen alleles linked to SjD susceptibility. Ro60 was efficiently phagocytosed by antigen-presenting cells in the presence of autoantibodies and presented to Ro60-specific T cells, triggering their activation. This suggests that Ro60-specific B and CD4 T cells orchestrate a pathological loop in salivary glands. Our study provides the first molecular identification of a major CD4 T cell antigen in systemic autoimmunity and highlights coordinated T-B cell responses against a shared autoantigen. - Source: PubMed
Publication date: 2026/06/03
Takeshita MasaruInamo JunWakui SeikiNagashima RyosukeNishino TakahiroTsunoda KazuyukiUsuda SatoshiInokuchi HajimeIshigaki KazuyoshiSasaki TakashiKagoya YukiSuzuki KatsuyaKaneko Yuko - Sjögren's syndrome (SS) is a systemic autoimmune disease with heterogeneous clinical, laboratory, and histopathological manifestations, which complicate timely diagnosis. Minor salivary gland biopsy (MSGB) is a key component of SS classification, although its relationship with clinical and serological features remains incompletely characterized. This study aimed to evaluate the association between MSGB findings and clinical-laboratory variables in patients with SS and to identify variables associated with a positive biopsy. - Source: PubMed
Publication date: 2026/04/25
Matos Sousa RitaDuarte MartaMartins Ana FilipaCapela Carlos - To understand the dysregulation of autoreactive B cells in SLE, we tracked Ro60-specific cells in seropositive (SP) and seronegative (SN) patients and healthy donors (HD), using flow cytometry and monoclonal antibodies. Consistent with permissive central tolerance, Ro60 naïve B cells were present in all groups with increased anergy in HD. HD and SN SLE also had greatly decreased or absent Ro60 memory and ASC, which were greatly increased in active SP SLE, thereby indicating defective distal tolerance in the latter group. Notably, Ro60 autoreactivity was strictly purged from naïve-derived extra-follicular B cells in HD and SN SLE, but expanded in SP SLE, suggesting the importance of autoreactivity censoring in this pathway. SLE clustering of the distribution of Ro60 B cells identified disease heterogeneity in tolerance enforcement in SLE. Finally, we demonstrate a much higher degree of polyreactivity against other lupus antigens in SLE Ro60 naïve cells, which is greatly attenuated in memory cells. Our work represents the first systematic study of antigen-specific autoreactive B cells and ASC in SLE. It enhances our understanding of human B cell tolerance and defines new approaches to measuring autoimmune activity in the course of SLE, including the assessment of immune resetting after B cell depletion therapies. - Source: PubMed
Publication date: 2026/05/13
Rahaman OindrilaCastrillon CarlosBugrovsky ReginaDas RakshaGhimire MidushiVan Trinh T PLin MartinUsman Sabeena YAmoss R TobyArora Aakriti AlishaKhosroshahi ArezouLee Frances Eun-HyungSanz Ignacio