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This article focuses on the questions of academic freedom, scholar activism, public science, and social engagement. The five authors represent scholars from different disciplines and scientific paradigms as well as diverse gender, sexual orientation, nationality, ethnic, and class backgrounds, yet they share a joint passion for academic 'activism'. The paper, therefore, reflects a multitude of transdisciplinary perspectives and positionalities. This dialogue was born out of the group's desire to investigate the role of scientists in public and political matters, including engagement in social justice. The interdisciplinary nature of the dialogue allows for comparisons between how activism is defined, perceived, practiced, and considered (un)welcome in the disciplines of Sociology, Psychology, Law, Media Studies, and Medical Sciences. [ABSTRACT FROM AUTHOR]

Central memory T cells (TCM) patrol lymph nodes, providing central immunosurveillance against known pathogens, but have not been described as conducting primary tissue immunosurveillance. We analyzed the expression of tissue-homing addressins in human TCM vs effector memory T cells (TEM) from the same donors. In humans, the majority of human TCM were tropic for either skin or gut, and the overall tissue tropism of TCM was comparable to that of TEM TCM were present in healthy, noninflamed human skin, lung, colon, and cervix, suggesting a role for TCM in the primary immunosurveillance of peripheral tissues. TCM also had potent effector functions; 80% of CD8+ TCM produced TC1/TC2/TC17/TC22 cytokines. TCM injected into human skin-grafted mice migrated into skin and induced inflammatory eruptions comparable to TEM-injected mice. In summary, human TCM express peripheral tissue-homing receptors at levels similar to their effector memory counterparts, are found in healthy human tissues, have impressive effector functions, and can act alone to induce skin inflammation in human engrafted mice. Our studies support a novel role for human TCM in primary immunosurveillance of peripheral tissues and highlight the important role of this long-lived cell type in tissue-based immune responses.

Introduction Graft-versus-host disease (GVHD) is a major cause of morbidity and mortality in hematopoietic stem cell transplantation (HSCT) (1-6). Current dogma holds that donor T cells, either transferred with or [...], Graft-versus-host disease (GVHD) is a major cause of morbidity and mortality in hematopoietic stem cell transplantation (HSCT). Donor T cells are key mediators in pathogenesis, but a contribution from host T cells has not been explored, as conditioning regimens are believed to deplete host T cells. To evaluate a potential role for host T cells in GVHD, the origin of skin and blood T cells was assessed prospectively in patients after HSCT in the absence of GVHD. While blood contained primarily donor-derived T cells, most T cells in the skin were host derived. We next examined patient skin, colon, and blood during acute GVHD. Host T cells were present in all skin and colon acute GVHD specimens studied, yet were largely absent in blood. We observed acute skin GVHD in the presence of 100% host T cells. Analysis demonstrated that a subset of host T cells in peripheral tissues were proliferating ([Ki67.sup.+]) and producing the proinflammatory cytokines IFN-[gamma] and IL-17 in situ. Comparatively, the majority of antigen-presenting cells (APCs) in tissue in acute GVHD were donor derived, and donor-derived APCs were observed directly adjacent to host T cells. A humanized mouse model demonstrated that host skin-resident T cells could be activated by donor monocytes to generate a GVHD-like dermatitis. Thus, host tissue-resident T cells may play a previously unappreciated pathogenic role in acute GVHD.

Introduction Psoriasis is a T cell- and IL-17-mediated inflammatory skin disease, characterized by inflamed skin lesions and systemic complications as well as arthritis in some patients (1, 2). Psoriatic skin [...], In psoriasis, an IL-17-mediated inflammatory skin disease, skin lesions resolve with therapy, but often recur in the same locations when therapy is discontinued. We propose that residual T cell populations in resolved psoriatic lesions represent the pathogenic T cells of origin in this disease. Utilizing high-throughput screening (HTS) of the T cell receptor (TCR) and immunostaining, we found that clinically resolved psoriatic lesions contained oligoclonal populations of T cells that produced IL-17A in both resolved and active psoriatic lesions. Putative pathogenic clones preferentially utilized particular V[beta] and V[alpha] subfamilies. We identified 15 TCR[beta] and 4 TCR[alpha] antigen receptor sequences shared between psoriasis patients and not observed in healthy controls or other inflammatory skin conditions. To address the relative roles of [alpha][beta] versus [gamma][delta] T cells in psoriasis, we carried out TCR/8 HTS. These studies demonstrated that the majority of T cells in psoriasis and healthy skin are [alpha][beta] T cells. [gamma][delta] T cells made up 1% of T cells in active psoriasis, less than 1% in resolved psoriatic lesions, and less than 2% in healthy skin. All of the 70 most frequent putative pathogenic T cell clones were [alpha][beta] T cells. In summary, IL-17-producing [alpha][beta] T cell clones with psoriasis-specific antigen receptors exist in clinically resolved psoriatic skin lesions. These cells likely represent the disease-initiating pathogenic T cells in psoriasis, suggesting that lasting control of this disease will require suppression of these resident T cell populations.

This article discusses the challenges of securing funding for research in dermatovenereology and highlights various funding opportunities in the EU framework program for skin disease. The authors emphasize the importance of advocating for better care for skin cancer patients in Europe and present examples of funded projects in the field. They also mention funding opportunities in the Innovative Health Initiative and Horizon Europe, specifically in the areas of personalized prevention in non-communicable diseases and cancer research. The article concludes by emphasizing the significance of EU funding opportunities in fostering innovation, research, and collaboration in dermatovenereology. [Extracted from the article]

The European Academy of Dermatology & Venereology has drafted recommendations to address the health risks associated with indoor tanning. The incidence of skin cancer has been increasing due to ultraviolet (UV) exposure, with one out of three cancers being skin cancer. Studies have shown a correlation between indoor tanning and early-onset skin cancers. The European Commission is expected to release recommendations on reducing cancer associated with sunbed use. Measures such as banning the use of sunbeds by minors, stricter legislation on sunbed use, and dissemination of messages on the risks of sunbed use are suggested. These recommendations aim to decrease the prevalence of skin cancers and improve overall well-being. [Extracted from the article]

Ultraviolet radiation (UVR) can have a beneficial biologic impact on skin, but it is also the most significant environmental risk factor for skin cancer development. Photocarcinogenesis comprises a complex interplay between the carcinogenic UVR, skin, and the immune system. UVB is absorbed by the superficial skin layers and is mainly responsible for direct DNA damage, which, if unrepaired, can lead to mutations in key cancer genes. UVA is less carcinogenic, penetrates deeper in the dermis, and mainly causes indirect oxidative damage to cellular DNA, proteins, and lipids, via photosensitized reactions. UVR not only induces mutagenesis, altering proliferation and differentiation of skin cells, but also has several immunosuppressive effects that compromise tumor immunosurveillance by impairing antigen presentation, inducing suppressive cells, and modulating the cytokine environment. This review focuses upon molecular and cellular effects of UVR, regarding its role in skin cancer development. [ABSTRACT FROM AUTHOR]

The article looks at a study regarding the phenotypically discrete populations of resident and recirculating memory T cells in human-engrafted mice and lymphoma patients using alemtuzumab. Topics discussed include epithelial barrier tissues are infiltrated by a combination of resident and recirculating T cells in mice, patients with cutaneous T cell lymphoma induced distinct inflammatory skin lesions and human skin is protected by four functionally distinct populations of T cells.