Inclusion standard
A publication is included only when ProWrite's internal records confirm research or scientific communication assistance and a public journal, DOI, or PubMed source record is available.
ProWrite-assisted publication portfolio
Published research strengthened with ProWrite assistance.
Every record in this portfolio represents a publication that received ProWrite research or scientific communication assistance. The type and scope of support varied by project.
326ProWrite-assisted records
27journals
32specialties
Portfolio attributionAssistance is documented. Authorship remains source-defined.
All publications shown here received ProWrite assistance. Assistance does not by itself establish authorship, commissioning, institutional affiliation, or endorsement. The linked journal, DOI, or PubMed record remains definitive for the published author list and bibliographic details.
Portfolio methodology
What inclusion in this portfolio means.
The record documents ProWrite assistance while preserving researcher ownership, client confidentiality, and the source publication's definitive authorship record.
Scope of assistance
Support may have included research planning, methods, biostatistics, data interpretation, scientific editing, manuscript development, journal preparation, or response-to-review support.
Verification and record identity
Titles, authors, journal, year, classification, and source links are checked against public records. Distinct source records are retained when different DOI or journal URLs share a title.
Disclosure boundary
Project-level contribution details are published only when authorized. Where confidentiality limits detail, the portfolio claims assistance without assigning undisclosed work to a named author or institution.
Accountable portfolio leadDr. Andrie Udal
Review scheduleQuarterly and after correction requests
Last reviewed25 July 2026
Genome-wide CRISPR screen in human T cells reveals regulators of FOXP3
Genome-wide CRISPR screen discovered regulators controlling human FOXP3 induction in T cells.
CCR8-targeted specific depletion of clonally expanded Treg cells in tumor tissues evokes potent tumor immunity with long-lasting memory
Depleted CCR8-expressing tumor-infiltrating Tregs, provoking durable antitumor immunity with minimal autoimmunity.
Distinct Foxp3 enhancer elements coordinate development, maintenance, and function of regulatory T cells
Mapped Foxp3 enhancers coordinating Treg development, maintenance, and functional stability.
Regulatory T Cells and Human Disease
Summarized regulatory T cell dysfunction across autoimmune, cancer, and infectious diseases in humans.
Foxp3: a genetic foundation for regulatory T cell differentiation and function
Perspective on Foxp3 genetics underpinning regulatory T cell differentiation and functions.
Measurement of Organ-Specific and Acute-Phase Blood Protein Levels in Early Lyme Disease
Quantified serum proteins in early Lyme disease, developing a diagnostic panel for improved detection.
FOXP3 and scurfy: how it all began
Historical timeline of the scurfy mutation and FOXP3 discovery in immunology.
Regulatory T cells and immune tolerance
Integrated mechanisms of Treg development and function across immune contexts.
Naturally arising CD4+ regulatory T cells for immunologic self-tolerance and negative control of immune responses
Comprehensively reviewed thymic regulatory T cells controlling immunity and tolerance.
Control of regulatory T cell development by the transcription factor Foxp3
Established Foxp3 as the master transcription factor programming regulatory T cell development and suppressive function.
An essential role for Scurfin in CD4+CD25+ T regulatory cells
Demonstrated Foxp3 (Scurfin) expression in CD4+CD25+ Tregs is required for their suppressive activity.
Foxp3 and natural regulatory T cells: key to a cell lineage?
Discussed Foxp3 significance in defining natural regulatory T cell lineage identity.
Disruption of a new forkhead/winged-helix protein, scurfin, results in the fatal lymphoproliferative disorder of the scurfy mouse
Cloned the Foxp3 (scurfin) mutation causing the fatal lymphoproliferative disorder in the scurfy mouse.
The immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) is caused by mutations of FOXP3
Linked human FOXP3 mutations to IPEX syndrome immune dysregulation pathology.
X-linked neonatal diabetes mellitus, enteropathy and endocrinopathy syndrome is the human equivalent of mouse scurfy
Established the human scurfy equivalent: neonatal diabetes, enteropathy, and endocrinopathy syndrome.
A rare polyadenylation signal mutation of the FOXP3 gene in a patient with IPEX syndrome
Reported a FOXP3 polyadenylation mutation explaining IPEX without coding exonic changes.
Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein
Identified SOST gene loss causing sclerosteosis, a novel cystine knot-containing protein.
Immunologic tolerance maintained by CD25+ CD4+ regulatory T cells: their common role in controlling autoimmunity, tumor immunity, and transplantation tolerance
Reviewed CD25+CD4+ Treg roles in autoimmunity, cancer immunity, and transplantation tolerance.