Content area
Full text
1. Introduction
Sulfur mustard (bis-(2-chloroethyl) sulfide; SM) is an alkylating chemical warfare agent which possesses potent mutagenic, carcinogenic, cytotoxic, and blistering properties [1]. Due to its powerful alkylating nature [2, 3], SM is capable of reacting with multiple vital biomolecules such as lipids, proteins, and DNA, thereby leading to the impairment of several body organs immediately after exposure [4, 5]. Skin is among the primary targets of SM which, due to its high penetrability and high surface area, undergoes the most severe damage [6].
Cutaneous complications of SM are not limited to the acute phase but late complications may be present even 15–20 years post exposure. These chronic complications have been repeatedly reported in Iranian patients and shown to significantly affect the quality of life [7–9]. The severity of cutaneous complications is a function of dose and duration of SM exposure [10].
During Iraq-Iran war (1983–88), SM was used against Iranian veterans and civilians for several times rendering about 100.000 Iranians chemically injured of whom a considerable number are still suffering from chronic complications [7, 8, 11]. Chronic skin complications of SM include pruritus (being the most frequent with an incidence of 70–90%), burning sensation, pain erythema, xerosis, hyper- and hypopigmentation, and scarring, atrophy [8, 12–14]. These chronic complications have been repeatedly reported in Iranian patients even 15–20 years post exposure and shown to significantly affect the quality of life [8, 9, 12–14].
In most occasions, SM-induced chronic skin complications are in the form of atopic dermatitis (AD). AD is a common and chronic inflammatory skin disorder which is characterized by eczematous lesions, erythema, xerosis, and severe pruritus. So far, multiple factors have been identified as etiologies of AD such as allergy, climatic conditions, microbial infections, and epidermal dysfunction. However, immune imbalance is regarded as the major pathomechanism of AD [15]. Impaired cellular immunity, reduced IFN-γ and elevated IgE, interleukin-4 (IL-4), and IL-13 are among the frequent immunological features observed in AD. The constellation of these imbalances increases the susceptibility of patient to viral and fungal infections [16].
IFN-γ, also known as type II interferon, is a cytokine which is critically involved in the innate as well as adaptive immunity. IFN-γ is produced by Th1 cells, cytotoxic T cells,...