Immunologic associations of keloids.
ABSTRACT The mechanisms underlying the pathogenesis of keloids have not been fully characterized despite extensive past and present research. Results of past and present studies have shown that the immune system is actively involved in the development of these lesions. Future investigations into the biochemistry and immunologic factors of keloids are anticipated and expected to produce additional insight. The inability to identify cellular (fibroblast) abnormalities has led most investigators to focus on the humoral regulators of wound healing, that is, biochemical substances, immunologic mediators and growth factors. Future studies are needed to confirm or refute the presence of AFA. AFA, if they exist, may prove to be useful as immunologic markers of keloids and may help distinguish keloids from hypertrophic scar in the early stages of wound healing. The influence of immunologic mediators may be more impressive early in the development of scars. "Young" or "early" is defined as less than two years of age, whereas "old" or "late" keloids are more than two years of age. We suggest that future studies stratify keloids into early versus late and also measure the rates of collagen synthesis of fibroblasts derived from the normal and abnormal specimens from the same patient. Analysis of the leukocyte factors will clarify the role the immune system has in the regulation of collagen synthesis. Preliminary investigations have shown that immunotherapy may be of value in the treatment of keloids. The role of fibroblast heterogeneity needs to be investigated. It is not known which aspects of fibroblast heterogeneity are responsible for the localized and accelerated rates of collagen synthesis of keloid fibroblasts.
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ABSTRACT: The healing of a skin wound is a complex process involving many cell lineages. In adult tissues, repair is always accompanied by a robust inflammatory response, which is necessary to counter the potential for infection at any site where the skin barrier is breached. Unlike embryonic tissues that can repair perfectly without a remnant scar at the wound site, adult tissue repair always leads to formation of a fibrotic scar where the wound has healed. In recent years, it has become clear that the wound inflammatory response may be, at least in part, responsible for fibrosis at sites of tissue repair. In this review, we consider the beneficial vs the detrimental functions of inflammatory cells during the repair response and compare data from other tissues, the lung, and liver, where fibrosis and its resolution may be related to a damage-triggered inflammatory response. We also consider how it may be possible to molecularly disentangle the potentially good from the bad influences of inflammatory cells during tissue repair and how fundamental studies in inflammatory cell biology may prove the way forward for development of drug targets in this respect.Journal of Investigative Dermatology 06/2007; 127(5):1009-17. DOI:10.1038/sj.jid.5700811 · 6.37 Impact Factor
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ABSTRACT: This paper deals with the modeling of a wound healing disease, the keloid, which may provoke onset of malignant cells with higher progression feature, thus generating cells with heterogeneous phenotype. According to medical hypothesis, it is assumed that viruses and the genetic susceptibility of patients are the main causes that trigger the formation. The mathematical model is developed by means of the tools of the kinetic theory for active particles. The competition of the immune system cells with viruses, keloid fibroblast cells, and malignant cells is taken into account. Numerical simulations, obtained by considering the sensitivity analysis of the parameters in the model, show the emerging phenomena that are typical of this disease.Mathematical Models and Methods in Applied Sciences 10/2011; 21(02). DOI:10.1142/S021820251100509X · 2.35 Impact Factor
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ABSTRACT: Keloid and hypertrophic scarring is a dermal fibroproliferative disorder characterized by increased fibroblast proliferation and excessive production of collagen. Excess scar formation occurs after dermal injury as a result of abnormal wound healing. Keloid formation has been ascribed to altered growth factor regulation, aberrant collagen turnover, genetics, immune dysfunction, sebum reaction, and altered mechanics. No single hypothesis adequately explains keloid formation. The thermal denaturations of pathologic human skin scar tissues were monitored by a SETARAM Micro DSC-II calorimeter. All the experiments were performed between 0 and 100 °C. The heating rate was 0.3 K min−1. DSC scans clearly demonstrated significant differences between the different types and conditions of samples (intact skin: T m = 54.8 °C and ΔH cal = 4.5 J g−1; normal scar: T m = 53.8 °C and ΔH cal = 4.2 J g−1; hypertrophic scar: T m = 54.2 °C and ΔH cal = 2.4 J g−1; keloid: T m = 52.9 °C and ΔH cal = 8.3 J g−1). The heat capacity change between native and denatured states of samples increased with the degree of structural alterations indicating significant water loosing. These observations could be explained with the structural alterations caused by the biochemical processes. With our investigations, we could demonstrate that DSC is a useful and well-applicable method for the investigation of collagen tissue of the human keloid and hypertrophic scar tissues. Our results may be of clinical relevance in the future, i.e., in the diagnosis of the two different pathologic scar formations, or in the choice of the optimal therapy of the disease.Journal of Thermal Analysis and Calorimetry 03/2013; 111(3). DOI:10.1007/s10973-012-2839-8 · 2.21 Impact Factor