1. What data in particular will be shared?
   Response - Individual participant data that underlie the results reported in this article, after de-identification (text, tables, figures, and appendices).
   


2. What additional supporting information will be shared?
   Response - Clinical Study Report
   Response -  Analytic Code
   
   
3. Who will be able to view these files?
   Response - Researchers whose proposed use of the data has been approved by an independent review committee identified for this purpose.
   


4. For what types of analyses will this data be available?
   Response - For individual participant data meta-analysis.
   


5. By what mechanism will data be made available?
   Response - Proposals should be directed to [darshanbkd@gmail.com].
   


6. For how long will this data be available start date provided 31-12-2027 and end date provided 31-12-2032?
   Response - Beginning 3 months and ending 5 years following article publication.
   


7. Any URL or additional information regarding plan/policy for sharing IPD? 
   Additional Information - NIL

Despite advances in critical care, early diagnosis and prognosis remain challenging due to non-specific clinical and biochemical markers. In the context of infection, the IL-1 system plays a key role in the activation of inflammation and, in turn, of anti-microbial responses. The IL-1 system consists of eight agonist ligands, three receptor antagonists, and a large receptor family (ILRs) including the negative regulators IL-1R2 and IL-1R8. IL-1R2 lacks a signalling domain and acts as a decoy receptor for IL-1, both as a cell-associated receptor and as a soluble form (sIL-1R2), by interacting with the ligand and with IL-1R3, the accessory protein of the signalling IL-1R1. sIL-1R2 has been recently shown to correlate with the SOFA score and mortality, and the transcript for IL-1R2 has been associated with sepsis-associated signatures in both monocytes and neutrophils. Interleukin-1 receptor 2 (IL1R2) is characterized as a decoy receptor of the interleukin-1 (IL1) receptor family responsible for capturing IL1 and reducing IL1 bioavailability. Proinflammatory and chemotactic molecules inhibit IL1R2 expression or cause its rapid shedding from the membrane. In contrast, upregulation of IL1R2 expression and soluble IL1R2 concentrations in biological fluids have been considered to reflect the activation of endogenous negative regulation of inflammation, or the response to immunosuppressive and anti-inflammatory agents. IL1R2 is expressed natively by a limited set of cell types, including monocytes, macrophages (in particular M2 or M2-like macrophages), microglial cells, neutrophils, B cells, and regulatory T cells. Subsequent to the serum analysis, future expansions or nested sub-studies may involve flow cytometric evaluation of membrane-bound IL-1R2 on CD14+ monocytes to correlate the soluble fraction with the cellular immunosuppressive phenotype.

The expression of IL1R2 may be influenced by comorbid conditions or Immunomodulatory therapies. The biological role of IL1R2 in either protecting against or contributing to adverse outcomes remains underexplored mechanistically.