At our current level of understanding, scars are an unavoidable result of disruption of the integument following trauma and other sources of injury in the postnatal period. Millions of people worldwide suffer from diminished quality of life due to varying degrees of disfigurement, functional impairment, and psychosocial comorbidity. Scars also represent a significant financial burden to the healthcare system at large. Substantial momentum currently exists in scar research associated with innovative techniques and devices devoted to treating scars. In order to properly ascertain and compare responses to various therapies, accurate and reproducible qualitative and quantitative assessments are vital. At least 10 different scar assessment scales and tools have been created to date in an attempt to quantify scar severity. However, a "gold standard" scar scale still does not yet exist. A major limitation of most scar scales is their focus on a relatively narrow group of individual subjective and objective features, while failing to address the overall cosmetic, functional, and psychological sequelae. Herein, we provide a brief review of current scar assessment scales, discuss some of the major advantages and limitations of each, and introduce several characteristics that might be addressed in a new "gold standard" scar scale. The assessment and treatment of scars, particularly large traumatic scars, is frequently a multidisciplinary effort. The creation of an "ideal" scar scale will undoubtedly require input from therapists, surgeons, dermatologists, and other professionals alike.

Protein kinase Cη (PKCη) is highly abundant in T cells and is recruited to the immunological synapse that is formed between a T cell and a cognate antigen-presenting cell; however, its function in T cells is unknown. Here, we showed that PKCη was required for the activation of mature CD8+ T cells by stimulation through the T cell receptor. PKCη−/− T cells showed poor proliferation in response to stimulation by antigen as compared to wild-type T cells, a trait shared with T cells deficient in PKCθ, the most abundant PKC isoform in T cells, and the only PKC previously thought to have a specific role in T cell activation. In contrast, defective homeostatic proliferation, a function requiring recognition of self antigens, was only observed in PKCη- deficient T cells. PKCη was dispensable for the development of thymocytes; however, thymocytes from mice doubly deficient in PKCη and PKCθ exhibited poor positive selection, indicating some redundancy between the PKC isoforms. PKCη and PKCθ had opposing effects on relative numbers of CD4+ and CD8+ T cells, because PKCη−/− mice had a higher ratio of CD4+ to CD8+ T cells compared to that of wild-type mice, whereas PKCθ−/− mice had a lower ratio. In mice deficient in both PKC isoforms, the ratio of CD4+ to CD8+ T cells returned to normal. Together, these data suggest that whereas PKCη shares redundant roles with PKCθ in T cell biology, it also performs nonredundant functions that are important for homeostasis and activation of T cells.

Hypoxia-inducible factor (HIF)-1α is a master regulator of inflammatory activities of myeloid cells, including neutrophils and macrophages. These studies examine the role of myeloid cell HIF-1α in regulating asthma induction and pathogenesis, and for the first time, evaluate the roles of HIF-1α and HIF-2α in the chemotactic properties of eosinophils, the myeloid cells most associated with asthma. Wild-type (WT) and myeloid cell-specific HIF-1α knockout (KO) C57BL/6 mice were studied in an ovalbumin (OVA) model of asthma. Administration of the pharmacological HIF-1α antagonist YC-1 was used to corroborate findings from the genetic model. WT, HIF-1α, and HIF-2α KO eosinophils underwent in vitro chemotaxis assays. We found that deletion of HIF-1α in myeloid cells and systemic treatment with YC-1 during asthma induction decreased airway hyperresponsiveness (AHR). Deletion of HIF-1α in myeloid cells in OVA-induced asthma also reduced eosinophil infiltration, goblet cell hyperplasia, and levels 34 of cytokines IL-4, IL-5, and IL-13 in the lung. HIF-1α inhibition with YC-1 during asthma induction decreased eosinophilia in bronchoalveolar lavage, lung parenchyma, and blood, as well as decreased total lung inflammation, IL-5, and serum OVA-specific IgE levels. Deletion of HIF-1α in eosinophils decreased their chemotaxis, while deletion of the isoform HIF-2α led to increased chemotaxis. This work demonstrates that HIF-1α in myeloid cells plays a role in asthma pathogenesis, particularly in AHR development. Additionally, treatment with HIF-1α inhibitors during asthma induction decreases AHR and eosinophilia. Finally, we show that HIF- 1α and HIF-2α regulate eosinophil migration in opposing ways.

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