PXD076286-1

PXD076286 is an original dataset announced via ProteomeXchange.

Title	A human-specific long noncoding RNA regulator of antigen-presenting cell viability and antimicrobial defense - 14-3-3β CoIP with blood-derived MФ and 14-3-3β CoIP with THP1 cells
Description	Macrophages are essential for pathogen clearance and to preserve tissue homeostasis, yet the molecular regulators of this equilibrium remain incompletely defined. Here, we identify SAILR, a primate-specific long noncoding RNA (lncRNA), as a critical modulator of macrophage viability under infection conditions. SAILR is induced during monocyte-to-macrophage differentiation, but rapidly downregulated upon bacterial challenge in an NFκB-dependent manner. In both naïve and immune-activated macrophages, SAILR dampens the expression of adhesion, phagocytosis and invasion factors, including SIGLEC1 and MMP7. During Salmonella Typhimurium infection, depletion of SAILR sensitizes macrophages to apoptosis, resulting in loss of intracellular replication niches and reduced bacterial recovery. Conversely, enforced SAILR expression promotes macrophage survival and increases intracellular pathogen burden. Mechanistically, SAILR interacts with the anti-apoptotic adaptor protein 14-3-3β to support macrophage survival. Notably, downregulation of SAILR is mirrored in circulating immune cells from patients with severe COVID-19 and sepsis. Together, our findings position SAILR as a central regulator linking macrophage survival to host-pathogen interaction and disease pathophysiology. Long noncoding RNAs (lncRNAs) are a class of regulatory molecules whose roles in the immune system remain poorly understood. In this study, we identify a human-specific lncRNA named SAILR that modulates the viability of macrophages - immune cells essential for pathogen clearance. SAILR interacts with the adaptor protein 14-3-3β and is rapidly downregulated upon bacterial infection, which sensitizes macrophages to cell death. This may limit the formation of intracellular niches that support pathogen propagation. Reduced SAILR levels in patients suffering from severe infections (sepsis and COVID-19) further suggest clinical relevance. Together, our findings reveal an RNA-based mechanism linking macrophage survival control to host defense and suggest SAILR as a potential diagnostic marker or therapeutic target in infectious and inflammatory diseases.
HostingRepository	PRIDE
AnnounceDate	2026-07-02
AnnouncementXML	Submission_2026-07-02_08:00:16.139.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Uwe Linne
SpeciesList	scientific name: Homo sapiens (Human); NCBI TaxID: NEWT:9606;
ModificationList	No PTMs are included in the dataset
Instrument	timsTOF Pro

Revision	Datetime	Status	ChangeLog Entry
0	2026-03-28 07:15:28	ID requested
⏵ 1	2026-07-02 08:00:17	announced

Dataset with its publication pending

submitter keyword: None

Uwe Linne
contact affiliation	Faculty of Chemistry and Center for Synthetic Microbiology (SYNMIKRO) Head of the Core-Facility for Mass Spectrometry Marburg University Hans-Meerwein-Str. 4 35032 Marburg GERMANY
contact email	linneu@staff.uni-marburg.de
lab head
Uwe Linne
contact affiliation	Head of Core Facility Mass Spectrometry, Faculty of Chemistry, Philipps-University Marburg
contact email	linneu@staff.uni-marburg.de
dataset submitter

Dataset FTP location NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/07/PXD076286

PRIDE project URI

• PRIDE
  1. PXD076286
     1. Label: PRIDE project
     2. Name: A human-specific long noncoding RNA regulator of antigen-presenting cell viability and antimicrobial defense - 14-3-3β CoIP with blood-derived MФ and 14-3-3β CoIP with THP1 cells