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2018 ; 9
(ä): 576
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TNFSF14 (LIGHT) Exhibits Inflammatory Activities in Lung Fibroblasts
Complementary to IL-13 and TGF-?
#MMPMID29616048
da Silva Antunes R
; Mehta AK
; Madge L
; Tocker J
; Croft M
Front Immunol
2018[]; 9
(ä): 576
PMID29616048
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The cytokine TNFSF14 [homologous to Lymphotoxin, exhibits Inducible expression
and competes with HSV Glycoprotein D for binding to HVEM, a receptor expressed on
T lymphocytes (LIGHT)] has been shown in mouse models to be important for
development of lung tissue remodeling that is characteristic of asthma,
idiopathic pulmonary fibrosis (IPF), and systemic sclerosis (SSc). However, its
cellular targets are not fully delineated. In the present report, we show that
LT?R and HVEM, the receptors for LIGHT, are constitutively expressed in primary
human lung fibroblasts (HLFs). We asked whether LIGHT could promote inflammatory
and remodeling-relevant activity in HLFs and how this was similar to, or distinct
from, IL-13 or TGF-?, two cytokines strongly implicated in the pathogenesis of
asthma, IPF, and SSc. Accumulation of myofibroblasts expressing alpha smooth
muscle actin is a feature of lung inflammatory diseases. LIGHT promoted cell
cycle progression and proliferation of HLFs, but not alpha smooth muscle actin
expression. In contrast, TGF-? upregulated alpha smooth muscle actin but did not
drive their proliferation. LIGHT also increased the gene or protein expression of
a number of proinflammatory mediators, including ICAM-1 and VCAM-1, IL-6 and
GM-CSF, the chemokines CCL5 and 20, and CXCL5, 11, and 12, and lung
remodeling-associated proteinases MMP-9 and ADAM8. These were dependent on LT?R
but not HVEM. LIGHT displayed overlapping and synergistic activities with IL-13
for a number of the activities, but LIGHT additionally enhanced the gene
expression of several molecules, including the innate cytokines IL-33 and TSLP,
which were not upregulated by IL-13. Our results highlight the varied and
pleiotropic effects of LIGHT in HLFs. LIGHT might then be a therapeutic target
for modulation of inflammation and remodeling associated with asthma and other
similar diseases of the lung that involve fibroblasts.
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