A hallmark of exposure to sulfur mustard (SM) is a significant increase in the expression of the pro-inflammatory cytokines, mainly IL-1β, IL-6, IL-8, and TNF-α (1-4). The increased production of IL-8 protein in cultured normal human epidermal keratinocytes (NHEK) cells, in particular, was found to be due to transcriptional activation resulting in elevated levels of its mRNA (2). IL-8 protein appeared in the media of stimulated cells as early as 6 hours, and persisted up to 24 hours post-exposure (2). Additionally, several studies have specifically indicated that over-expression of IL-1, IL-8, TNF-α, and IL-6 was associated with the loss of dermal interstitial collagen in rabbit and mouse skin models (5, 6). Interleukin 10 (IL-10) is a tightly regulated, immunosuppressive, antiinflammatory cytokine that plays a central role in a number of human diseases such as inflammation, autoimmunity, and transplant rejection. In one study, IL-10 was used to suppress development of collagen-induced arthritis in mice through viral-based transfection (7). IL-10 was also used to prolong vascularized cardiac allografts (8), abolish angiogenecity of Burkitt lymphoma (9) and reduce vascularization in colon cancer (10). Human IL-10, thus, represents a logical, naturally occurring target for cellular manipulation of the inflammatory response to SM exposure. We studied the effects of overexpressing IL-10 on cytokine expression and cell death in SM-treated NHEK cells.