research Macrophages Promote Wound-Induced Hair Follicle Regeneration in a CX3CR1- and TGF-β1–Dependent Manner
Macrophages help hair growth after injury through CX3CR1 and TGF-β1.
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30 / 1000+ results research 699 Pharmacological blockade of the CX3CR1/CX3CL1 fractalkine axis prevents alopecia areata in C3H/HeJ mice
research A meta-analysis of chemokines in alopecia areata: recruiting immune cells toward the hair follicle
Alopecia areata involves complex immune dysregulation, mainly driven by Th1 activity, suggesting broader treatment strategies.
research Nucleic acid-induced chemokine expression in keratinocytes: Implications for skin inflammation
Nucleic acids trigger chemokine production in skin cells, affecting skin inflammation.
research Nucleic acid-induced chemokine expression in keratinocytes: Implications for skin inflammation
Nucleic acids trigger chemokine production in skin cells, affecting skin inflammation.
research The Identification of Bipotent Dermal Stem Cells and The Role of Anti-Inflammatory Macrophages During Hair Follicle Regeneration
Bipotent dermal stem cells and specific macrophages are crucial for hair regrowth and regeneration.
research Table 1_A meta-analysis of chemokines in alopecia areata: recruiting immune cells toward the hair follicle.docx
Alopecia areata involves complex immune activity, mainly Th1, with potential benefits from broader immune treatments.
research Table 2_A meta-analysis of chemokines in alopecia areata: recruiting immune cells toward the hair follicle.docx
Alopecia areata involves complex immune responses, suggesting broader treatments could help.
research Image 1_A meta-analysis of chemokines in alopecia areata: recruiting immune cells toward the hair follicle.png
Alopecia areata involves complex immune responses, suggesting broader treatments could help.
research Keratinocyte integrin α3β1 induces expression of the macrophage stimulating factor, CSF-1, through a YAP/TEAD-dependent mechanism.
research CXCR3 Blockade Inhibits T Cell Migration into the Skin and Prevents Development of Alopecia Areata
Blocking the CXCR3 receptor reduces T cell accumulation in the skin and prevents hair loss in mice.
research Signal integrator function of CXXC5 in Cancer
CXXC5 can both suppress and promote cancer, making it a complex target for treatment.
research THE INSUSCEPTIBILITY OF C57 BLACK MICE TO POST-IRRADIATION LEUKEMIA, SOME UNREPORTED POST-IRRADIATION CHANGES
CXCL7 is essential for muscle repair by aiding early neutrophil infiltration.
research Inducible Cutaneous Inflammation Reveals a Protumorigenic Role for Keratinocyte CXCR2 in Skin Carcinogenesis
CXCR2 in skin cells promotes tumor growth.
research Tissue resident and follicular Treg cell differentiation is regulated by CRAC channels
CRAC channels are crucial for the development and function of specialized immune cells, preventing severe inflammation and autoimmune diseases.
research Resident CD34-positive cells contribute to peri-endothelial cells and vascular morphogenesis in salivary gland after irradiation
CD34-positive cells help repair and form new blood vessels in salivary glands after radiation.
research Transient stimulation of TRPV4‐expressing keratinocytes promotes hair follicle regeneration in mice
Activating TRPV4 in skin cells helps regrow hair in mice, possibly offering a treatment for hair loss.
research Cthrc1 deficiency aggravates wound healing and promotes cardiac rupture after myocardial infarction via non-canonical WNT5A signaling pathway
CTHRC1 is essential for healing and preventing heart rupture after a heart attack.
research Tcf3 promotes cell migration and wound repair through regulation of lipocalin 2
Tcf3 helps cells move and heal wounds by controlling lipocalin 2.
research The L412F variant of Toll-like receptor 3 (TLR3) is associated with cutaneous candidiasis, increased susceptibility to cytomegalovirus, and autoimmunity
The L412F variant of TLR3 is linked to skin infections, more viral infections, and autoimmune issues.
research Transcriptional profiling in alopecia areata defines immune and cell cycle control related genes within disease-specific signatures
The study found that immune responses disrupt hair growth cycles, causing hair loss in alopecia areata.
research Author response: Neutrophils promote CXCR3-dependent itch in the development of atopic dermatitis
Neutrophils are important for causing chronic itch in atopic dermatitis, and blocking the CXCR3 receptor may reduce this itch.
research Decision letter: Neutrophils promote CXCR3-dependent itch in the development of atopic dermatitis
Neutrophils are key in causing chronic itch in atopic dermatitis, and blocking CXCR3 could reduce this itch.
research The Dynamics of the Skin’s Immune System
The skin has a complex immune system that is essential for protection and healing, requiring more research for better wound treatment.
research Interrelation of immunity and tissue repair or regeneration
The immune system plays a key role in tissue repair, affecting both healing quality and regenerative ability.
research Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing
Alopecia areata involves immune activation in the scalp, suggesting treatments targeting TH1, TH2, and IL-23 pathways.
research Macrophages Regulate Schwann Cell Maturation after Nerve Injury
Macrophages help heal nerves by aiding the maturation of Schwann cells and are important for nerve repair.
research Macrophages induce AKT/β-catenin-dependent Lgr5+ stem cell activation and hair follicle regeneration through TNF
Macrophages help regrow hair by activating stem cells using AKT/β-catenin and TNF.
research Dental cell type atlas reveals stem and differentiated cell types in mouse and human teeth
The research identified various cell types in mouse and human teeth, which could help in developing dental regenerative treatments.
research Local heroes or villains: tissue-resident memory T cells in human health and disease
Tissue-resident memory T cells can protect against infections and cancer but may also contribute to autoimmune diseases.