Ultrastructural Observations on the Hair Bulb Melanocytes and Melanosomes in Acute Alopecia Areata

Tobin, Desmond J.; Fenton, David A.; Kendall, Marion D.

doi:10.1111/1523-1747.ep12874660

Cited by 93 publications

(78 citation statements)

References 11 publications

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“…Active disease often preferentially results in loss of pigmented hair in patients who partially gray, and white hairs are frequently seen with initial regrowth. This observation is supported by ultrastructural evidence that hair bulb melanocytes are specifically damaged in acute AA, even before any damage is morphologically detectable in hair bulb keratinocytes (68). However, since autoantibodies to autologous melanocyte autoantigens were not detected in AA patients (69), a T cell-dependent mechanism was thought to be responsible.…”

Section: Role Of T Cell-dependent Melanocyte Autoantigens In Aamentioning

confidence: 89%

Lymphocytes, neuropeptides, and genes involved in alopecia areata

Gilhar¹,

Paus²,

Kalish³

2007

J. Clin. Invest.

272

278

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Many lessons in autoimmunity -particularly relating to the role of immune privilege and the interplay between genetics and neuroimmunology -can be learned from the study of alopecia areata, the most common cause of inflammation-induced hair loss. Alopecia areata is now understood to represent an organ-restricted, T cell-mediated autoimmune disease of hair follicles. Disease induction is associated with collapse of hair follicle immune privilege in both humans and in animal models. Here, the role of HLA associations, other immunogenetic factors, and neuroendocrine parameters in alopecia areata pathogenesis are reviewed. This instructive and clinically significant model disease deserves more widespread interest in the immunology community.Nonstandard abbreviations used: AA, alopecia areata; AIRE, autoimmune regulator; APECED, autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy; IP-10, IFN-g-inducible protein 10; MIC, MHC class I chain-related; MIF, macrophage migration inhibitory factor; α-MSH, α-melanocyte-stimulating hormone; NALP1, NACHT leucine-rich-repeat protein 1; NGF, nerve growth factor.

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Section: Role Of T Cell-dependent Melanocyte Autoantigens In Aamentioning

confidence: 89%

Lymphocytes, neuropeptides, and genes involved in alopecia areata

Gilhar¹,

Paus²,

Kalish³

2007

J. Clin. Invest.

272

278

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“…Several autoimmune disorders such as thyroid disease, diabetes mellitus, bullous pemphigoid, pemphigus vulgaris, lichen planus or pernicious anaemia, have been reported to occur more frequently in patients with both disorders [1][2][3][4][5][6][7][8][9]. The immune-pathologic basis in these conditions relies on singular and interactive functions of antibodies, T cells, self antigens and organ specificity [10].…”

Section: Text Organizationmentioning

confidence: 99%

Anatomical Colocalization of Vitiligo and Alopecia Areata~!2010-01-18~!2010-05-21~!2010-07-14~!

Rodríguez-Martín¹

2010

TOAUTOJ

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Alopecia areata (AA) and vitiligo are two common disorders in general population and coincidence of these two diseases is thus to be expected. However, anatomical coexistence of both conditions had rarely been reported. Many different etiological hypotheses have been suggested for both diseases. While alopecia areata is considered a T-cell mediated autoimmune disease, in the pathogenesis of vitiligo, both T cells and autoantibodies may play a role. Here we report a case which supports the hypothesis that vitiligo-induced autoimmunity could trigger AA and bulb melanocytes could act as a possible target in AA.We report the case of a 53-year-old woman which was referred to Dermatology Department for treatment of AA. Twenty years previously, she had developed areas of vitiligo on the face and arms which remained stable for years. She presented with a 1-year history of alopecia on the scalp, with a loss of skin and hair color in the same location during this period. In our case, the chronological appearance, association and co-localization of vitiligo and AA could emphasize the hypothesis that melanocytes-derived antigens released during vitiligo pathogenesis could act as auto-antigens, inducing hair loss.

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“…Embryos were then post-fixed in 2% osmium tetroxide, uranyl acetate and embedded in araldite resin as previously described (Tobin et al, 1990;Tobin et al, 1991). Semi-thin HRLM sections were stained with metachromic stain, toluidine blue/borax, examined under light microscope (oil-immersion) and photographed (Leitz, Germany).…”

Section: High Resolution Light Microscopy (Hrlm) and Transmission Elementioning

confidence: 99%

NF-κB transmits Eda A1/EdaR signalling to activate Shh and cyclin D1 expression, and controls post-initiation hair placode down growth

et al. 2006

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A novel function of NF-B in the development of most ectodermal appendages, including two types of murine pelage hair follicles, was detected in a mouse model with suppressed NF-B activity (c IB␣⌬N ). However, the developmental processes regulated by NF-B in hair follicles has remained unknown. Furthermore, the similarity between the phenotypes of c IBA⌬N mice and mice deficient in Eda A1 (tabby) or its receptor EdaR (downless) raised the issue of whether in vivo NF-B regulates or is regulated by these novel TNF family members. We now demonstrate that epidermal NF-B activity is first observed in placodes of primary guard hair follicles at day E14.5, and that in vivo NF-B signalling is activated downstream of Eda A1 and EdaR. Importantly, ectopic signals which activate NF-B can also stimulate guard hair placode formation, suggesting a crucial role for NF-B in placode development. In downless and c IB␣⌬N mice, placodes start to develop, but rapidly abort in the absence of EdaR/NF-B signalling. We show that NF-B activation is essential for induction of Shh and cyclin D1 expression and subsequent placode down growth. However, cyclin D1 induction appears to be indirectly regulated by NF-B, probably via Shh and Wnt. The strongly decreased number of hair follicles observed in c IB␣⌬N mice compared with tabby mice, indicates that additional signals, such as TROY, must regulate NF-B activity in specific hair follicle subtypes.

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Ultrastructural Observations on the Hair Bulb Melanocytes and Melanosomes in Acute Alopecia Areata

Cited by 93 publications

References 11 publications

Lymphocytes, neuropeptides, and genes involved in alopecia areata

Lymphocytes, neuropeptides, and genes involved in alopecia areata

Anatomical Colocalization of Vitiligo and Alopecia Areata~!2010-01-18~!2010-05-21~!2010-07-14~!

NF-κB transmits Eda A1/EdaR signalling to activate Shh and cyclin D1 expression, and controls post-initiation hair placode down growth

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