Depletion and Repopulation of Langerhans Cells in Nonsegmental Type Vitiligo

Kao, Chien-Han; Yu, Hsin‐Su

doi:10.1111/j.1346-8138.1990.tb01643.x

Cited by 39 publications

(26 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This cytotoxicity was relatively specific for melanocyte targets [82]. We demonstrated a depletion of epidermal Langerhans cells in patients with active vitiligo, and conversely, a repopulation of these cells in stable vitiligo [55]. These findings support the theory that antibodydependent cellular cytotoxicity is involved in MC destruction in vitiligo.…”

Section: The Immune Hypothesissupporting

confidence: 77%

“…We demonstrated that PUVA depletes vitiligo-associated MC antigens and stimulates tyrosinase activity in vitro [56]. Furthermore, PUVA treatment in vivo depletes epidermal Langerhans cells [55]. These may result in (1) blocking the binding of anti-MC autoantibodies to MCs; (2) blocking the progression of antibody-dependent cytotoxicity to MCs in vitiligo; and (3) stimulating melanogenesis.…”

Section: Effects Of Medical Therapies On Repigmentation In Vitiligomentioning

confidence: 96%

See 1 more Smart Citation

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

2002

J Biomed Sci

Self Cite

View full text Add to dashboard Cite

Melanocytes (MCs) are melanin-producing cells of the skin that are derived from neural crest cells. Vitiligo vulgaris is a common depigmentation disorder resulting from the destruction of functional MCs in the affected skin. The three prevailing pathomechanisms of vitiligo are the immune hypothesis, the neural hypothesis and the autocytotoxic hypothesis. None of these mechanisms has been conclusively proven. Melanoblasts (MBs) in the outer root sheath of the hair follicles are the reservoir cells for repigmentation. Recovery from vitiligo is initiated by activation and proliferation of these MBs, followed by upward migration to the nearby epidermis that forms perifollicular pigmentation islands. Migration, proliferation and differentiation of MCs and MBs are regulated by keratinocyte-derived factors and some coat color genes. Any therapy for vitiligo must explain not only the repopulation of MCs but also their functional development. In patients with vitiligo, MCs are destroyed in the skin, the eyes, and possibly the ears. However, the concept of vitiligo as a systemic disease will be clearly established only when the mechanisms involved in vitiligo are identified. Recent advances in the fields of neural crest cell culture and molecular genetics have opened new perspectives in the understanding of vitiligo. Not only will this result in better treatments for vitiligo patients, but possibly will also provide a key to triggering nerve cell regrowth in other nervous diseases.

show abstract

Section: The Immune Hypothesissupporting

confidence: 77%

Section: Effects Of Medical Therapies On Repigmentation In Vitiligomentioning

confidence: 96%

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

2002

J Biomed Sci

Self Cite

View full text Add to dashboard Cite

show abstract

“…PUVA and topical corticotherapy are known to induce a depletion in the density of epidermal Langerhans cells. As these treatments induce repigmentation of vitiligo, it was suggested that a therapeutically-induced depletion in stable vitiligo may aid in repigmentation (Kao and Yu, 1990). However, this hypothesis is not supported by another study demonstrating an increase in the number of epidermal Langerhans cells in repigmenting vitiligo (Iyenger et al, 1990).…”

Section: Langerhans Cell Involvementmentioning

confidence: 44%

Vitiligo: Where Do We Stand?

Ortonne

Bose

1993

Pigment Cell Research

140

107

View full text Add to dashboard Cite

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.

show abstract

“…We observed a decreased number of lesional Langerhans cells in seven of ten patients. Four of these patients were receiving UVA radiation therapy and it has been reported that UVA therapy leads to a decreased presence of Langerhans cells in L vitiligo skin (Kao and Yu, 1990;Westerhof et al, 1986). Surprisingly, the tendency toward a more basal location of Langerhans cells seen in PL and L skin was independent of UVA radiation exposure; this is in agreement with the results reported in literature (Birbeck et al, 1961;Westerhof et al, 1986).…”

Section: Immune Infiltrates In Progressive Vitiligomentioning

confidence: 99%

Local Immune Response in Skin of Generalized Vitiligo Patients

Wijngaard

Wańkowicz-Kalińska

Poole

et al. 2000

Laboratory Investigation

221

View full text Add to dashboard Cite

SUMMARY:In situ immune infiltrates in lesional, perilesional, and nonlesional skin biopsies from patients with vitiligo were analyzed by immunohistochemistry and compared with immune infiltrates found in the skin of normal healthy donors and relevant disease controls. An increased influx of activated skin-homing T cells and macrophages were seen in the perilesional biopsies. The overall percentages of cutaneous leukocyte-associated antigen-positive (CLA ϩ ) T cells were similar to those found in normal healthy donors. This is compatible with the similar expression of E-selectin. Most strikingly, however, the CLA ϩ T cells in perilesional skin were mainly clustered in the vicinity of disappearing melanocytes, and 60% to 66% of these interacting T cells expressed perforin and granzyme-B. The perforin ϩ /granzyme-B ϩ cells were not seen in locations different from that of disappearing melanocytes. Interestingly, the majority of the infiltrating T cells were HLA-DR/CD8 ϩ . Another hallmark of the present study is the focal expression of intercellular adhesion molecule (ICAM)-1 and HLA-DR in the epidermis at the site of interaction between the immune infiltrates and the disappearing melanocytes. The data presented in this study are consistent with a major role for skin-homing T cells in the death of melanocytes seen in vitiligo. (Lab Invest 2000, 80:1299-1309.

show abstract

Depletion and Repopulation of Langerhans Cells in Nonsegmental Type Vitiligo

Cited by 39 publications

References 22 publications

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

Vitiligo: Where Do We Stand?

Local Immune Response in Skin of Generalized Vitiligo Patients

Contact Info

Product

Resources

About