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Increased regulatory T cell activity may lead to better outcomes in acute diffuse and total alopecia.

Trichodysplasia spinulosa is a rare skin disease in immunocompromised patients caused by a specific virus targeting hair follicle cells.

PD‐L1 and PD‐L2 may not effectively control immune activation in alopecia areata.

Hair follicle cells help protect against immune attacks by regulating T-cell activity.

Certain immune cells may cause hair loss by reacting to stressed hair follicles.

Melanocyte-associated antigens may play a key role in alopecia areata and could be targets for new treatments.

Fetal skin has unique immune cells different from adult skin.

Live vaccines can be safely given to infants with a FOXN1 variant if their immune function improves over time.

Merkel cell increase is specific to certain skin diseases, not general skin growth.

A rare type of skin cancer with mucosal involvement was partially treated but eventually relapsed.

The muscle damage was caused by T-cell large granular lymphocytic leukemia, not dermatomyositis.

Immature hair cells can grow and change into different types of hair cells over time.

Proinflammatory fibroblasts and vascular endothelial cells are key in keloid development.

The study suggested certain immune cells might cause alopecia areata, but it was retracted.

A mutation in the IKZF1 gene causes immune system overactivity, linked to autoimmune diseases like lupus.

An automated system can predict death risk in thin melanoma by analyzing immune cells.

Cytotoxic T cells cause hair loss in chronic alopecia areata.

Scientists found a new type of skin cell that could help with skin repair and these cells work better with a certain protein.

Targeting MIG and MCP-1 may help treat inflammation in alopecia areata.

HPV16-transformed cells can change human skin cell properties, aiding tumor growth.

NK cells play a role in skin diseases like eczema and psoriasis.

Topical immunotherapy for alopecia areata may work by creating immune cell clusters in the skin.

ILC1-like cells can independently cause alopecia areata.

Active and quiescent stem cells work together in mammals to maintain and repair tissues.

Human sweat glands contain stem cells capable of self-renewal and forming different cell types.

Fibroblasts can be mistaken for neural cells, so functional validation is needed.

Arg1+ macrophages may play a role in causing alopecia areata.

CD3+ T-cell presence is a reliable marker to tell apart alopecia areata from pattern hair loss.

The model showed that immune system guardians and the cytokine interferon-γ are key in alopecia areata progression.

Different types of inactive melanocyte stem cells exist with unique characteristics and potential to develop into other cells.