Search

everythingexperts & clinicslearnfaqsresearchcommunity

for

Search:↓

Developing human skin has immune cells with memory-like features.

In this study, researchers identified unique prenatal lymphocyte features in human fetal skin, including proliferative naive T cells and memory-like T cells, which may influence antigen and allergen responses in utero and infancy.

Certain CD8+ T cells attack hair follicles in alopecia areata, suggesting they could be targeted for treatment.

CD8+ T cells re-expressing CD45RA may predict treatment resistance in severe alopecia areata.

In this study, blocking the CXCR3 receptor in mice prevented the development of alopecia areata by inhibiting the accumulation of specific T cells in the skin, suggesting a potential therapeutic approach for humans.

This study suggests that SOCS3 treatment may effectively inhibit alopecia areata by suppressing CD8+ T cell activity and IFN-γ production.

Specific immune cells and pathways contribute to hair follicle inflammation and hair loss, suggesting potential treatments for lichen planopilaris.

This study found that Ifidancitinib, a JAK1/3 inhibitor, significantly promoted hair regrowth and reduced inflammation in a mouse model of alopecia areata by decreasing pathogenic T cell activity and inducing T cell exhaustion.

Lung immune cells can be trained to better fight infections after a virus.

This review explores the immunological aspects of epidermal differentiation in loricrin knockout mice, offering insights into keratinization and potential intrinsic factors affecting immune function, but provides no new clinical findings.

In this study, iNKT10 cells were found to play a significant role in preventing and treating alopecia areata in a humanized mouse model, suggesting these cells could have potential in managing related autoimmune disorders.

This study highlights the crucial, multifaceted roles of fibroblasts in wound healing and various diseases, including their dysregulation in diabetic foot ulcers, underscoring the need for targeted therapies to address complications and morbidity from such chronic conditions.

This review discusses the dual role of tissue-resident memory T cells in providing immune protection against infections and cancer and contributing to autoimmune skin disease pathology, without presenting new experimental results.

This study found that mouse skin CD4(+) memory T cells are in equilibrium with the circulation under steady state but increase in specific clusters in response to infection or inflammation.

This study found that IL-7 is crucial for the survival of memory regulatory T cells in the skin of mice, whereas IL-2 is essential for their initial generation but not for their maintenance.

In this study, researchers found that CD4 T cells from the skin draining lymph nodes of mice with alopecia areata can transfer the disease to recipient mice, highlighting the key role of these cells and their interaction with CD8 T cells in the disease's development.

In this study, researchers observed that dormant TRP-2+ melanoma cells in bone marrow can interact with CD8+ T cells in tumor-bearing ret transgenic mice, potentially influencing immune responses.

This review discusses the protective roles of skin-resident immune cells in maintaining tissue homeostasis and facilitating wound healing, but reports no new experimental findings.

This study highlights the role of platelets in immune interactions and severe adenovirus infection, noting that activated platelets have a shorter lifespan. Results suggest potential for developing therapies targeting platelet senescence and immunologic mechanisms.

This abstract highlights that alopecia treatment requires moving beyond outdated methods to a sophisticated approach that considers the complex interplay between genetic susceptibility and immune response in different types of hair loss. Results are not reported.

The research found that hair follicle–derived cytokines, particularly IL-15 and IL-7, regulate skin-resident memory T cells and their role in both immune homeostasis and lymphoma in the skin.

In this study, conditional deletion of BRD4 in OX40-expressing cells of mice led to alopecia, dermatitis, and loss of hair follicle stem cell function, revealing BRD4's role in skin inflammation and stem cell regulation.

In this study, researchers demonstrated that CD4 T cells from skin-draining lymph nodes in mice with alopecia areata can transfer the disease to recipient mice, revealing a critical role for CD4 T cells in disease development and suggesting potential therapeutic targets.

This review discusses how tissue resident memory T cells contribute to autoimmune skin diseases like vitiligo and psoriasis, highlighting their role in continuous immune activation, and reports no new clinical results.

The study suggests that refractory chronic alopecia areata cases have more infiltrating skin resident memory T cells, and using a JAK inhibitor may be an effective treatment option.

This study demonstrates that T-cell responses in extensive alopecia areata scalp may be aberrantly regulated, with reduced cytokine production but activated phenotype, providing insight into the disease's immune mechanisms.

This study examines the role of immune phenotypes and cytokines in the development of pathological scars, providing insights that may aid in early identification and treatment strategies for these scars.

This study explored peripheral blood immune dysregulation in alopecia areata through single-cell analyses, identifying systemic changes linked to disease severity and key signaling roles for monocytes, NK cells, and memory T cells, suggesting potential therapeutic targets.

This study identified a novel G207E STING mutation associated with severe inflammatory symptoms and suggested that common polymorphisms in TMEM173 and IFIH1 may modify the phenotype in affected individuals.

In this study, a novel homozygous mutation in the STAT5B gene was identified in a 17-year-old boy with growth hormone-refractory growth failure, severe eczema, and autoimmune disease, suggesting a similarity to known STAT5B deficiency phenotypes.