Epithelial damage and tissue γδ T cells promote a unique tumor-protective IgE response

IgE is an ancient and conserved immunoglobulin isotype with potent immunological function. Nevertheless, the regulation of IgE responses remains an enigma, and evidence of a role for IgE in host defense is limited. Here we report that topical exposure to a common environmental DNA-damaging xenobiotic initiated stress surveillance by γδTCR+ intraepithelial lymphocytes that resulted in class switching to IgE in B cells and the accumulation of autoreactive IgE. High-throughput antibody sequencing revealed that γδ T cells shaped the IgE repertoire by supporting specific variable-diversity-joining (VDJ) rearrangements with unique characteristics of the complementarity-determining region CDRH3. This endogenous IgE response, via the IgE receptor FcεRI, provided protection against epithelial carcinogenesis, and expression of the gene encoding FcεRI in human squamous-cell carcinoma correlated with good disease prognosis. These data indicate a joint role for immunosurveillance by T cells and by B cells in epithelial tissues and suggest that IgE is part of the host defense against epithelial damage and tumor development

Dressings/Wound Care for Laser Treatment

Ablative and non-ablative lasers have different effects on the skin. Various postoperative treatments have been used, e.g., topical agents and/or dressings (open vs closed techniques).Additional research is needed to determine the optimal postoperative care after laser procedures

Androgen Signaling in the Tumor Microenvironment.

The key function of mesenchymal/stromal androgen receptor (AR) signaling for prostate development has been well documented by tissue recombination experiments. Some studies have addressed the expression and function of AR in stromal cells in prostate cancer, yet our understanding of the role of stromal AR in other tissues beyond prostate is still insufficient.Genomic analysis has revealed that cellular responses to androgens differ between epithelial and stromal cells. AR in stromal cells seems not to act via classical AR transcription factors such as FOXA1 but rather depends on the JUN/AP1 complex. Stromal AR appears to have tumor-promoting and tumor-protective functions depending on tumor stage. Loss of AR signaling in fibroblasts has been detected already in premalignant lesions in the skin and prostate and has been associated with tumor induction in xenografts of skin cancer and aggressive disease features and poor patient prognosis in prostate cancer. Moreover, AR expression is found on virtually all tissue-infiltrating immune cells and plays critical roles in immune cell function. These findings suggest a potential deleterious impact of current androgen deprivation therapies which inhibit both epithelial and stromal AR, highlighting the need to develop tissue-specific AR inhibitors