The detection of melanocyte autoantibodies in the Smyth chicken model for vitiligo

Austin, Lisa M.; Boissy, Raymond E.; Jacobson, Bernard; Smyth, J. Robert

doi:10.1016/0090-1229(92)90188-t

Cited by 43 publications

(26 citation statements)

References 27 publications

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“…Serum from Smyth line (SL) chickens (Smyth, 1989) contains autoantibodies against the melanogenic enzyme tyrosinase-related protein-1 (Austin et al, 1992;Searle et al, 1993;Austin and Boissy, 1995), and we have shown that SL serum is an excellent early marker for embryonic melanoblasts . In this study, we used SL serum to examine the timing of melanoblast specification and the patterns of melanoblast migration at the vagal level and in Silkie chickens.…”

Section: Introductionmentioning

confidence: 97%

Specification and migration of melanoblasts at the vagal level and in hyperpigmented silkie chickens

1998

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Section: Introductionmentioning

confidence: 97%

Specification and migration of melanoblasts at the vagal level and in hyperpigmented silkie chickens

1998

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“…The data summarized in Table 1 (references (5,(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), indicate that both cellular and humoral autoimmune phenomena observed in NSV correlate with disease activity and association with other autoimmune disorders. Disease specificity is not clearly demonstrated since autoantibodies as well as melanocyte antigen-specific T-cell clones have been detected, albeit less frequently, in controls without NSV.…”

Section: Melanocyte Destructionmentioning

confidence: 99%

“…Concerning antibody driven damage to melanocytes (23)(24)(25)(26)(27)(28)(29)(30), these mechanisms could be at work in vivo, because very few inflammatory cells may be required to induce antibody-dependent cell-mediated cytotoxicity (ADCC) which target cell membrane antigens. Furthermore, complement membrane attack complexes do not require cellular support to lyse targeted cells (26).…”

Section: Melanocyte Destructionmentioning

confidence: 99%

A Critical Appraisal of Vitiligo Etiologic Theories. Is Melanocyte Loss a Melanocytorrhagy?

Gauthier

andre

Taı̈eb

2003

Pigment Cell Research

264

211

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Common generalized vitiligo is an acquired depigmenting disorder characterized by a chronic and progressive loss of melanocytes from the epidermis and follicular reservoir. However, the mechanism of melanocyte disappearance has never been clearly understood, and the intervention of cellular and humoral autoimmune phenomena as primary events remains unproven. In this review, is discussed the data supporting the major theories of vitiligo, namely melanocyte destruction (autoimmune, neural and impaired redox status) and melanocyte inhibition or defective adhesion. Based on recent morphologic findings in vivo supporting a chronic detachment and transepidermal loss of melanocytes in common generalized vitiligo, a new theory is suggested proposing melanocytorrhagy as the primary defect underlying melanocyte loss, integrating most of the possible triggering/precipitating/ enhancing effects of other known factors.

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“…However, it remains to be established that melanoma associated leukoderma is identical to vitiligo. "Vitiligo antibodies" may also occur in nnimnle coneidorod as models of human vitilign (Nnuyhltrri et al, 1986a;Austin et al, 1992a).…”

Section: Is Vitiligo An Autoimmune Disease?mentioning

confidence: 99%

Vitiligo: Where Do We Stand?

Ortonne

Bose

1993

Pigment Cell Research

140

107

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Vitiligo is a puzzling disorder characterized by a disappearance of epidermal and/or follicular melanocytes by unknown mechanisms. This very common disorder involving 1-4% of the world population is thus of great importance for the practicing dermatologist. The cellular and molecular mechanisms leading to the destruction of melanocytes in this disorder have not yet been elucidated, making it of major interest for the cell biologist involved in melanocyte research.Recent advances in this field, due largely to the availability of techniques for culturing normal human melanocytes, opened new perspectives in the underitanding of vitiligo. Although vitiligo has long been considered a disorder confined to the skin, there is now good evidence that it also inwlves the extracutaneous compartment of the "melanocyte organ." It is also clear that vitiligo is not only a melanocyte disorder, but that it also involves cells, such as keratinocytes and Langerhans cells, found in the epidermis and follicular epithelium.The three prevailing theories of the pathogenesis of vitiligo are the immune hypothesis, the neural hypothesis, and the self-destruct hypothesis. New hypotheses suggest that vitiligo may be due to (1) a deficiency in an unidentified melanocyte growth factor, (2) an intrinsic defect of the structure and function of the rough endoplasmic reticulum in vitiligo melanocytes, (3) abnormalities in a putative melatonin receptor on melanocytes and (4) a breakdown in free radical defense in the epidermis. None of these hypotheses has been demonstrated, and according to the available data, it is likely that the loss of epidermal and follicular melanocytes in vitiligo may be the result of several different pathogenetic mechanisms.

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The detection of melanocyte autoantibodies in the Smyth chicken model for vitiligo

Cited by 43 publications

References 27 publications

Specification and migration of melanoblasts at the vagal level and in hyperpigmented silkie chickens

Specification and migration of melanoblasts at the vagal level and in hyperpigmented silkie chickens

A Critical Appraisal of Vitiligo Etiologic Theories. Is Melanocyte Loss a Melanocytorrhagy?

Vitiligo: Where Do We Stand?

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