CXCL10 produced from hair follicles induces Th1 and Tc1 cell infiltration in the acute phase of alopecia areata followed by sustained Tc1 accumulation in the chronic phase.

Background: Alopecia areata (AA) is an organ-specific and cell-mediated autoimmune disease. T lymphocytes densely surround lesional hair bulbs, which is histologically referred to as "swarm of bees". However, pathomechanisms of "swarm of bees" are still uncertain.

Corticotropin-releasing hormone stimulates the in situ generation of mast cells from precursors in the human hair follicle mesenchyme.

Hair follicles (HFs) maintain a peripheral, functional equivalent of the hypothalamic-pituitary-adrenal (HPA) axis, whose most proximal element is corticotropin-releasing hormone (CRH). The mast cell (MC)-rich connective-tissue sheath (CTS) of mouse vibrissa HFs harbors MC precursors. Differentiation of these MC precursors into mature MCs can be induced by stem cell factor (SCF).

Combination therapy with oral PUVA and corticosteroid for recalcitrant alopecia areata.

Alopecia areata (AA) is regarded as a tissue-specific autoimmune disease for which several therapies have been suggested to modify the immune reaction against HFs, such as contact immunotherapy, psoralen plus ultraviolet A (PUVA), corticosteroids, cyclosporine, minoxidil, and dithranol. However, severe type AA, such as alopecia totalis (AT) and alopecia universalis (AU), often show resistance against these therapies. We applied a combination therapy with oral corticosteroid and oral PUVA for intractable cases of AT and AU.

Roxithromycin inhibits chemokine-induced chemotaxis of Th1 and Th2 cells but regulatory T cells.

Background: Roxithromycin (RXM), a 14-member macrolide antibiotic, has a variety of bioregulatory functions such as anti-inflammatory effects, anti-oxidant effects, and modulation of immune responses.

Objectives: In this study, we analyzed the effect of RXM on chemokine-induced chemotaxis of Th1, Th2, and regulatory T (Treg) cells established from three normal human peripheral blood lymphocytes by the reported methods.

Methods And Results: Incubation with 10 microM RXM for 18 h did not alter the expression profile of CXCR3 on Th1 cells and CCR4 on Th2 and Treg cells.

Roxithromycin antagonizes catagen induction in murine and human hair follicles: implication of topical roxithromycin as hair restoration reagent.

Roxithromycin (RXM) is a 14-member macrolide antibiotics, with a variety of bioregulatory functions including anti-apoptotic activity to keratinocytes. Therefore, RXM has been used for many kinds of skin diseases. In this study, human and murine hair follicles were treated with RXM in order to find the possibility to cure hair loss disease such as androgenetic alopecia (AGA).

Immune privilege and the skin.

This chapter summarizes the evidence that defined compartments of the hair follicle (HF) and nail epithelium maintain an area of relative immune privilege (IP). HF and nail IP is chiefly characterized by absent or very low level of expression of major histocompatibility complex class Ia antigens, complemented by a number of factors, such as the local production of potent immunosuppressive agents, dysfunction of professional antigen-presenting cells and inhibition of natural killer cell activities. In the hair bulb, IP is seen only in the anagen stage of HF cycling, while the nail apparatus continuously maintains an IP site in its proximal nail matrix, since the nail apparatus does not cycle.

Maintenance of hair follicle immune privilege is linked to prevention of NK cell attack.

Hair follicles (HFs) enjoy a relative immune privilege (IP) that is characterized by downregulation of major histocompatibility complex (MHC) class I and local expression of potent immunosuppressants. Normally, natural killer (NK) cells attack cells with absent/low MHC class I expression. However, because few perifollicular NK cells are found around healthy human anagen HFs, we asked how HFs escape from NK cell attack.

Immunology of the human nail apparatus: the nail matrix is a site of relative immune privilege.

The nail apparatus is constantly exposed to environmental damage. It requires effective immune responses to combat infection, while avoiding the loss of nail production and regeneration by autoaggressive immunity. By immunohistology, we define here previously unknown characteristics of the normal human nail immune system (NIS).

Human hair follicles display a functional equivalent of the hypothalamic-pituitary-adrenal axis and synthesize cortisol.

The skin and its major appendages are prominent target organs and potent sources of key players along the classical hypothalamic-pituitary axis, such as corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and alpha melanocyte stimulating hormone (alpha-MSH), and even express key steroidogenic enzymes. Therefore, it may have established local stress response systems that resemble the hypothalamic-pituitary-adrenal (HPA) axis. However, functional evidence that this is indeed the case in normal human skin in situ has still been missing.

Collapse and restoration of MHC class-I-dependent immune privilege: exploiting the human hair follicle as a model.

The collapse of major histocompatibility complex (MHC) class-I-dependent immune privilege can lead to autoimmune disease or fetal rejection. Pragmatic and instructive models are needed to clarify the as yet obscure controls of MHC class I down-regulation in situ, to dissect the principles of immune privilege generation, maintenance, and collapse as well as to develop more effective strategies for immune privilege restoration. Here, we propose that human scalp hair follicles, which are abundantly available and easily studied, are ideally suited for this purpose: interferon-gamma induces ectopic MHC class I expression in the constitutively MHC class-I-negative hair matrix epithelium of organ-cultured anagen hair bulbs, likely via interferon regulatory factor-1, along with up-regulation of the MHC class I pathway molecules beta(2)microglobulin and transporter associated with antigen processing (TAP-2).

Febrile ulceronecrotic Mucha-Habermann's disease managed with methylprednisolone semipulse and subsequent methotrexate therapies.

Febrile ulceronecrotic Mucha-Habermann's disease is an unusual severe form of pityriasis lichenoides et varioliformis acuta characterized by abrupt onset of ulceronecrotic eruption associated with a high fever and systemic symptoms. To our knowledge, 19 cases of this disease have been reported in the literature, and 4 of them were fatal. We report the case of a 12-year-old boy with this disorder who had abdominal pain, hypoproteinemia, and anemia.

The hair follicle and immune privilege.

This essay reviews the available evidence that the proximal hair follicle epithelium generates and maintains an area of relative immune privilege during a defined segment of the hair cycle (i.e., during anagen).