Th2-like immune response in radiation-induced lung fibrosis

Hân, Gia; Zhang, Hui; Xie, Conghua; Zhou, Yun

doi:10.3892/or.2011.1300

Cited by 21 publications

(19 citation statements)

References 26 publications

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“…In line with this study, Han et al also identified increased expression of the type 2 key transcription factor GATA3 in C57BL/6 mice that had received 12 Gy thorax irradiation (176). …”

Section: Role Of Lymphocytes In the Irradiated Lungsupporting

confidence: 80%

“…It is thought that in this context the shift from a T H 1 cytokine profile toward a T H 2 cytokine profile could be a key event. The signature of T H 2 cytokines IL-4, IL-5, IL-10, and IL-13 is known to convey strong anti-inflammatory and pro-fibrotic effects, to mediate fibroblast activation, and activate “alternatively activated” macrophages (M2) with high arginase-1 expression (43, 166, 176, 177). Of further interest is a recent study from 2016 showing that radiation-induced lung fibrosis in a tumor-bearing mouse model was associated with enhanced type 2 immunity (178).…”

Section: Role Of Lymphocytes In the Irradiated Lungmentioning

confidence: 99%

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The Role of Lymphocytes in Radiotherapy-Induced Adverse Late Effects in the Lung

Wirsdörfer¹,

Jendrossek²

2016

Front. Immunol.

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Radiation-induced pneumonitis and fibrosis are dose-limiting side effects of thoracic irradiation. Thoracic irradiation triggers acute and chronic environmental lung changes that are shaped by the damage response of resident cells, by the resulting reaction of the immune system, and by repair processes. Although considerable progress has been made during the last decade in defining involved effector cells and soluble mediators, the network of pathophysiological events and the cellular cross talk linking acute tissue damage to chronic inflammation and fibrosis still require further definition. Infiltration of cells from the innate and adaptive immune systems is a common response of normal tissues to ionizing radiation. Herein, lymphocytes represent a versatile and wide-ranged group of cells of the immune system that can react under specific conditions in various ways and participate in modulating the lung environment by adopting pro-inflammatory, anti-inflammatory, or even pro- or anti-fibrotic phenotypes. The present review provides an overview on published data about the role of lymphocytes in radiation-induced lung disease and related damage-associated pulmonary diseases with a focus on T lymphocytes and B lymphocytes. We also discuss the suspected dual role of specific lymphocyte subsets during the pneumonitic phase and fibrotic phase that is shaped by the environmental conditions as well as the interaction and the intercellular cross talk between cells from the innate and adaptive immune systems and (damaged) resident epithelial cells and stromal cells (e.g., endothelial cells, mesenchymal stem cells, and fibroblasts). Finally, we highlight potential therapeutic targets suited to counteract pathological lymphocyte responses to prevent or treat radiation-induced lung disease.

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“…In line with this study, Han et al also identified increased expression of the type 2 key transcription factor GATA3 in C57BL/6 mice that had received 12 Gy thorax irradiation (176). …”

Section: Role Of Lymphocytes In the Irradiated Lungsupporting

confidence: 80%

Section: Role Of Lymphocytes In the Irradiated Lungmentioning

confidence: 99%

The Role of Lymphocytes in Radiotherapy-Induced Adverse Late Effects in the Lung

Wirsdörfer¹,

Jendrossek²

2016

Front. Immunol.

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“…Th2 cytokines have been implicated in asthma, and evidence is accumulating that type 2 immune responses promote the development of pulmonary fibrosis. In mice, Th2 immune response-associated factors (GATA-3, IL-13 and Arg-1) increased after lung irradiation-induced Th2 polarization [95]. Although the exact molecular mechanism leading to fibrosis is unknown, evidence from preclinical models strongly suggests a critical role for Th2-specific signaling in this disease [19, 96].…”

Section: Cytokines and Related Factors In The Development Of Rilfmentioning

confidence: 99%

Molecular Mechanisms and Treatment of Radiation-Induced Lung Fibrosis

Ding¹,

Li²,

Sun

2013

CDT

193

198

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Radiation-induced lung fibrosis (RILF) is a severe side effect of radiotherapy in lung cancer patients that presents as a progressive pulmonary injury combined with chronic inflammation and exaggerated organ repair. RILF is a major barrier to improving the cure rate and well-being of lung cancer patients because it limits the radiation dose that is required to effectively kill tumor cells and diminishes normal lung function. Although the exact mechanism is unclear, accumulating evidence suggests that various cells, cytokines and regulatory molecules are involved in the tissue reorganization and immune response modulation that occur in RILF. In this review, we will summarize the general symptoms, diagnostics, and current understanding of the cells and molecular factors that are linked to the signaling networks implicated in RILF. Potential approaches for the treatment of RILF will also be discussed. Elucidating the key molecular mediators that initiate and control the extent of RILF in response to therapeutic radiation may reveal additional targets for RILF treatment to significantly improve the efficacy of radiotherapy for lung cancer patients.

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“…These data indicate that thoracic irradiation first induces Th1 polarization during pneumonitis, followed by transition to Th2 polarization at later time points that correspond to fibrosis. While the immediate response to irradiation involves classically activated macrophages, alternatively activated macrophages are predominant during fibrosis and likely have an important role in its development and progression[32]. …”

Section: Macrophages Promote Lung Fibrosismentioning

confidence: 99%

Mechanisms of the alternative activation of macrophages and non-coding RNAs in the development of radiation-induced lung fibrosis

Duru

Wolfson

Zhou

2016

WJBC

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Radiation-induced lung fibrosis (RILF) is a common side effect of thoracic irradiation therapy and leads to high mortality rates after cancer treatment. Radiation injury induces inflammatory M1 macrophage polarization leading to radiation pneumonitis, the first stage of RILF progression. Fibrosis occurs due to the transition of M1 macrophages to the anti-inflammatory pro-fibrotic M2 phenotype, and the resulting imbalance of macrophage regulated inflammatory signaling. Non-coding RNA signaling has been shown to play a large role in the regulation of the M2 mediated signaling pathways that are associated with the development and progression of fibrosis. While many studies show the link between M2 macrophages and fibrosis, there are only a few that explore their distinct role and the regulation of their signaling by non-coding RNA in RILF. In this review we summarize the current body of knowledge describing the roles of M2 macrophages in RILF, with an emphasis on the expression and functions of non-coding RNAs.

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Th2-like immune response in radiation-induced lung fibrosis

Cited by 21 publications

References 26 publications

The Role of Lymphocytes in Radiotherapy-Induced Adverse Late Effects in the Lung

The Role of Lymphocytes in Radiotherapy-Induced Adverse Late Effects in the Lung

Molecular Mechanisms and Treatment of Radiation-Induced Lung Fibrosis

Mechanisms of the alternative activation of macrophages and non-coding RNAs in the development of radiation-induced lung fibrosis

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