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Published on: September 26, 2013
Th17/Treg immunoregulation and implications in treatment of sulfur mustard gas-induced lung diseases
Maryam Iman1, Ramazan Rezaei2, Sadegh Azimzadeh Jamalkandi1
1a Chemical Injuries Research Center , Baqiyatallah University of Medical Sciences , Tehran , Iran.
Introduction:
Sulfur mustard (SM) is an extremely toxic gas used in chemical warfare to cause massive lung injury and death. Victims exposed to SM gas acutely present with inhalational lung injury, but among those who survive, some develop obstructive airway diseases referred to as SM-lung syndrome. Pathophysiologically, SM-lung shares many characteristics with smoking-induced chronic obstructive pulmonary disease (COPD), including airway remodeling, goblet cell metaplasia, and obstructive ventilation defect. Some of the hallmarks of COPD pathogenesis, which include dysregulated lung inflammation, neutrophilia, recruitment of interleukin 17A (IL -17A) expressing CD4+T cells (Th17), and the paucity of lung regulatory T cells (Tregs), have also been described in SM-lung. Areas covered: A literature search was performed using the MEDLINE, EMBASE, and Web of Science databases inclusive of all literature prior to and including May 2017. Expert commentary: Here we review some of the recent findings that suggest a role for Th17 cell-mediated inflammatory changes associated with pulmonary complications in SM-lung and suggest new therapeutic approaches that could potentially alter disease progression with immune modulating biologics that can restore the lung Th17/Treg balance.
Insights
Sulfur mustard (SM) lung injury shares similarities with COPD. Immune responses involving Th17 cells and regulatory T cells (Tregs) may drive SM-lung, suggesting new immune-modulating therapies.
Area of Science:
- Toxicology
- Immunology
- Pulmonology
Background:
- Sulfur mustard (SM) causes acute lung injury and can lead to SM-lung syndrome, an obstructive airway disease.
- SM-lung shares pathological features with chronic obstructive pulmonary disease (COPD), including airway remodeling and inflammation.
- Key COPD pathogenesis factors like dysregulated inflammation, neutrophilia, and altered T cell populations (Th17/Treg imbalance) are observed in SM-lung.
Purpose of the Study:
- To review recent findings on the role of Th17 cell-mediated inflammation in SM-lung.
- To explore potential therapeutic strategies for SM-lung.
- To investigate immune-modulating biologics for restoring Th17/Treg balance in SM-lung.
Main Methods:
- Literature search of MEDLINE, EMBASE, and Web of Science databases.
- Review of studies published up to May 2017.
- Expert commentary on current research and therapeutic avenues.
Main Results:
- Evidence suggests Th17 cell-mediated inflammation plays a role in SM-lung complications.
- A Th17/Treg imbalance is implicated in the pathogenesis of SM-lung.
- Immune-modulating biologics are proposed as potential therapies.
Conclusions:
- Th17 cell-driven inflammation is a significant factor in SM-lung disease.
- Restoring the lung Th17/Treg balance may offer a therapeutic target.
- Immune-modulating biologics could be a promising approach for treating SM-lung.
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