Differential expression of interleukin 1α by Thy‐1+ and Thy‐1 lung fibroblast subpopulations: Enhancement of interleukin 1α production by tumor necrosis factor‐α

RP Phipps, C Baecher, JG Frelinger… - European journal of …, 1990 - Wiley Online Library
RP Phipps, C Baecher, JG Frelinger, DP Penney, P Keng, D Brown
European journal of immunology, 1990Wiley Online Library
The purpose of this investigation was to determine whether subpopulations of murine lung
fibroblasts produced interleukin 1 (IL 1). We previously identified two major populations of
pulmonary fibroblasts based on the presence or absence of Thy‐1. Thy‐1+ and Thy‐1−
subsets synsthesize fibronectin and type I and III collagen, but only the Thy‐1− population
displays class II major histocompatibility complex antigens after stimulation with interferon‐γ
and presents antigen to T helper clones. Interestingly, in the current study we determined …
Abstract
The purpose of this investigation was to determine whether subpopulations of murine lung fibroblasts produced interleukin 1 (IL 1). We previously identified two major populations of pulmonary fibroblasts based on the presence or absence of Thy‐1. Thy‐1+ and Thy‐1 subsets synsthesize fibronectin and type I and III collagen, but only the Thy‐1 population displays class II major histocompatibility complex antigens after stimulation with interferon‐γ and presents antigen to T helper clones. Interestingly, in the current study we determined that only Thy‐1 fibroblast lines and clones synthesized IL 1. Although constitutive production was low, tumor necrosis factor ‐α (TNF‐α) stimulated 5‐20‐fold increases in IL 1 production in Thy‐1 fibroblasts. The Thy‐1+ fibroblasts did not produce IL 1 even after TNF‐α treatment. Northern blot analysis of TNF‐α treated cells revealed that in the Thy‐1 subset increased mRNA levels for IL 1α were detected, while IL 1β mRNA was not detected. Furthermore, IL 1 activity from TNF‐α‐treated Thy‐1 fibroblast membranes and supernatants was completely neutralized by IL 1α‐specific antibodies. These observations support the hypothesis that the antigen‐presenting Thy‐1 subset is important for promoting the inflammation associated with pulmonary fibrosis. In addition, the existence of functional subsets of lung fibroblasts is further substantiated by differential expression of IL 1.
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