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              <text>384–396</text>
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                <text>The contribution of interleukin-2 to effective wound healing.</text>
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                <text>Experimental biology and medicine (Maywood, N.J.)</text>
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                <text>*cutaneous diseases; *cytokines; *immunotherapy; *Interleukin-2; *therapeutic targets; *wound healing; Animals; Cell Differentiation/physiology; Cell Proliferation/physiology; Diabetes Mellitus/metabolism/pathology; Humans; Interleukin-2/*metabolism; Interleukin-2/*metabolism/*therapeutic use; Lupus Erythematosus; Mice; Myocardial Infarction/metabolism/pathology; Receptors; Sarcoidosis/metabolism/pathology; Signal Transduction/physiology; Skin/*injuries; Systemic/metabolism/pathology; T-Lymphocytes/cytology/immunology; Wound Healing/*physiology</text>
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                <text>Doersch Karen M; DelloStritto Daniel J; Newell-Rogers M Karen</text>
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                <text>Ineffective skin wound healing is a significant source of morbidity and mortality. Roughly 6.5 million Americans experience chronically open wounds and the cost of treating these wounds numbers in the billions of dollars annually. In contrast, robust wound healing can lead to the development of either hypertrophic scarring or keloidosis, both of which can cause discomfort and can be cosmetically undesirable. Appropriate wound healing requires the interplay of a variety of factors, including the skin, the local microenvironment, the immune system, and the external environment. When these interactions are perturbed, wounds can be a nidus for infection, which can cause them to remain open an extended period of time, or can scar excessively. Interleukin-2, a cytokine that directs T-cell expansion and phenotypic development, appears to play an important role in wound healing. The best-studied role for Interleukin-2 is in influencing</text>
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                <text>&lt;a href="http://doi.org/10.1177/1535370216675773" target="_blank" rel="noreferrer noopener"&gt;10.1177/1535370216675773&lt;/a&gt;</text>
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