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01 · ABSTRACT

Abstract

Interaction of programmed cell death 1 (PD-1) receptor and its ligand 1 (PD-L1) is well studied in the field of fibrotic lung diseases, supporting its use as a biomarker of progression of interstitial lung disease. Anti PD-L1 therapy has shown effectiveness in improvement of many malignancies and murine models of autoimmune fibrotic lung diseases. Higher PD-1 expression on T cells and PD-L1 expression on human lung fibroblasts are known to contribute towards severity in sarcoidosis and idiopathic pulmonary fibrosis (IPF), respectively.  The focus of this investigation was to determine if soluble form of PD-L1 (sPD-L1) serves as predictive biomarker of disease severity in interstitial lung disease (ILD), such as scleroderma, sarcoidosis and IPF.  Comparison of local environments, such as bronchoalveolar lavage, revealed significantly higher sPD-L1 levels compared to systemic environments, such as peripheral blood (p=0.001, paired two-tailed Student’s t test).  Investigation of serum samples of healthy control, IPF, scleroderma and sarcoidosis patients reveal significantly higher levels in sarcoidosis and IPF patients, compared to patients with scleroderma (p=0.001; p=0.02, one-way ANOVA with Tukey’s respectively).   Comparison of serum levels between sarcoidosis patients and healthy controls revealed no significant differences (p=0.09, unpaired two-tailed t test).  In addition, comparison of physiologic parameters, such as percent predicated Forced Vital Capacity (FVC) and sPD-L1 levels in sarcoidosis and IPF patients revealed no correlation.   These observations suggest that sPD-L1 will not serve as a biomarker of sarcoidosis disease severity. Additional investigation of sPD-L1 in local environments is warranted.

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02 · PUBLICATION RECORD

Article details

JournalMedical Research Archives
IssueVol 9 No 9 (2021): Vol.9 Issue 9 September 2021
SectionResearch Articles
Published27 September 2021
DOI10.18103/mra.v9i9.2525
ISSN2375-1924
03 · RIGHTS & REUSE

Rights & reuse

This article is published under a Creative Commons Attribution License (CC BY 3.0) and may be shared or distributed by anyone as long as attribution is given to the journal.

Authors & affiliations

BS

Binal Shah-Gandhi

Department of Medicine, Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, TN 37232, USA

OC

Ozioma S. Chioma

Department of Medicine, Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, TN 37232, USA

KA

Kenny A. Abel

Department of Medicine, Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, TN 37232, USA

EW

Erin M. Wilfong

Department of Medicine, Divisions of Rheumatology and Immunology, and Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA

WM

Wendi R. Mason

Department of Medicine, Divisions of Rheumatology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA

WD

Wonder P. Drake

Department of Medicine, Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, TN 37232, USA; Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, 1161 21st Avenue South, A2200 Medical Center North, Nashville, TN 37232, USA

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