Serum alpha1-antitrypsin and haptoglobin phenotypes in vitiligo

Ali, Muazzam; Banu, M Almas; Waheed, Mohammed Abdul; Quadri, Giovanni; Habibullah, C. M.

doi:10.1007/bf00372625

Cited by 3 publications

(2 citation statements)

References 8 publications

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“…The earliest attempts to identify genetic markers associated with vitiligo began in the mid-1960s, assaying polymorphic blood proteins such as the ABO and other blood group antigens [24–30], secretor status [26,27,31], and later serum alpha 1-antitrypsin and haptoglobin phenotypes [32], with no positive results. A decade later, numerous investigators reported association studies of vitiligo with HLA types, which have also been associated with many other autoimmune diseases.…”

Section: Early Genetic Marker Studiesmentioning

confidence: 99%

Genetics of Vitiligo

Spritz¹,

Andersen²

2017

Dermatologic Clinics

159

126

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Synopsis Vitiligo is “complex disorder” (also termed polygenic and multifactorial), reflecting simultaneous contributions of multiple genetic risk factors and environmental triggers. Large-scale genome-wide association studies, principally in European-derived whites and in Chinese, have discovered approximately 50 different genetic loci that contribute to vitiligo risk, some of which also contribute to other autoimmune diseases that are epidemiologically associated with vitiligo. At many of these vitiligo susceptibility loci the corresponding relevant genes have now been identified, and for some of these genes the specific DNA sequence variants that contribute to vitiligo risk are also now known. A large fraction of these genes encode proteins involved in immune regulation, a number of others play roles in cellular apoptosis, and still others are involved in regulating functions of melanocytes. For this last group, there appears to be an opposite relationship between susceptibility to vitiligo and susceptibility to melanoma, suggesting that vitiligo may engage a normal mechanism of immune surveillance for melanoma. While many of the specific biologic mechanisms through which these genetic factors operate to cause vitiligo remain to be elucidated, it is now clear that vitiligo is an autoimmune disease involving a complex relationship between programming and function of the immune system, aspects of the melanocyte autoimmune target, and dysregulation of the immune response.

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Section: Early Genetic Marker Studiesmentioning

confidence: 99%

Genetics of Vitiligo

Spritz¹,

Andersen²

2017

Dermatologic Clinics

159

126

View full text Add to dashboard Cite

show abstract

“…The earliest attempts to identify specific genes that may contribute to vitiligo were genetic association studies of vitiligo using a variety of protein polymorphic markers, including ABO and other blood groups, blood group secretor status, and a number of other serum proteins . Essentially, all of these studies proved negative.…”

Section: Pre‐molecular Genetic Studiesmentioning

confidence: 99%

Modern vitiligo genetics sheds new light on an ancient disease

Spritz

2013

The Journal of Dermatology

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Vitiligo is a complex disorder in which autoimmune destruction of melanocytes results in white patches of skin and overlying hair. Over the past several years, extensive genetic studies have outlined a biological framework of vitiligo pathobiology that underscores its relationship to other autoimmune diseases. This biological framework offers insight into both vitiligo pathogenesis and perhaps avenues towards more effective approaches to treatment and even disease prevention.

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