Expression of HLA-DR in hair follicles in alopecia areata.
Explore the source record for details and available documents.
Alopecia Areata↗
Biomedical subjects
A G Messenger
Publications and source records attributed to A G Messenger.
The culture of dermal papilla cells from human hair follicles.
Dermal papillae were isolated from human hair follicles and primary cell cultures were established from the papilla explants. The cultured papilla cells spread slowly, initially as a monolayer, and eventually formed multi-layered parallel arrays of fibroblast-like cells. At the edges of expanding colonies the cells were large and flattened and showed a tendency to form clumps. The behaviour of human dermal papilla cells in culture is very similar to that reported in cultures of papilla cells from rat vibrissa follicles.
Cell Division↗
Alopecia areata: light and electron microscopic pathology of the regrowing white hair.
Light and electron microscopic studies have been carried out on fifteen regrowing white anagen hair follicles from seven patients with alopecia areata. Seven bulbs showed evidence of cell injury that was concentrated in cortical keratocytes. Lower bulb matrix cells appeared undamaged though in six bulbs apoptotic degeneration was seen in the lower bulb keratocytes, perhaps indicating early catagen transformation. Melanocytes were identified in all the bulbs except those from one patient. The number of melanocytes and their melanization were much less than in the normal pigmented follicle, and pigment transfer was rarely seen. It is proposed that alopecia areata is a disease of differentiating cortical keratocytes. The failure of pigmentation in the regrowing white hair may be post-inflammatory, but the various other pigmentary features of alopecia areata, especially the sparing of senile white hairs, suggest that pigmentary mechanisms in the hair bulb are of primary importance in the pathogenesis of this disorder.
Adult↗
Case clustering in pityriasis rosea: support for role of an infective agent.
One hundred and twenty-six cases of pityriasis rosea seen over two years in north Staffordshire were analysed for clustering in time and space. A statistically significant degree of clustering was found; this was evident among female patients considered separately but not among male patients. The incidence of the condition was higher in patients working in, or attending, educational establishments. These findings support the hypothesis that pityriasis rosea is caused by an infective agent. A search for an infective organism and a transmission mechanism now seems justifiable.
Adolescent↗
Lymphadenopathy mimicking lymphoma associated with cryoglobulinaemia and arteritis.
Two patients are described with polyclonal IgG cryoglobulinaemia and necrotizing arteritis who developed severe lymphadenopathy which clinically mimicked malignant lymphoma. Histological studies demonstrated that the lymphadenopathy resulted from a pseudolymphomatous reaction associated with vascular damage.
Adult↗
A case of lymphomatoid papulosis and systemic lymphoma.
A young man with a 4-year history of lymphomatoid papulosis subsequently developed a systemic lymphoma. Further doubt is therefore cast on the benign nature of this disorder.
Adult↗
Occupational dermatitis due to 1,2-benzisothiazolin-3-one in the pottery industry.
Three men working as mouldmakers in the pottery industry acquired a contact allergic dermatitis to a releasing oil. All three were shown to be sensitized to the biocide (1,2-benzisothiazolin-3-one) in the oil.
Adult↗
Contact dermatitis from zinc pyrithione, an antidandruff agent.
Explore the source record for details and available documents.
Allergens↗
Genetic factors predispose to balding and non-balding in men.
Male pattern balding is a common androgen-dependent trait. The frequency of balding in the population increases with age but not all men develop balding even in old age. It is well-known that balding tends to run in families but the nature of the underlying genetic predisposition and the mode of inheritance are unknown. In this study we examined scalp hair status across a wide age range in 572 men and took family histories of balding in first degree male relatives. The results confirmed that there is an increased frequency of balding in the fathers of young bald men and a high relative risk of balding in young subjects with a balding father but these effects declined with increasing subject age. In contrast, there was a pronounced increase in the frequency of non-balding in the fathers of non-bald elderly subjects and an increased relative risk of non-balding in elderly subjects with a non-bald father, which were not evident in younger subjects. Analysis of the frequencies of balding and non-balding in the brothers of balding and non-balding elderly men, categorised by paternal hair status, failed to show that either balding or non-balding is due to the action of a single gene. Nevertheless, our results indicate that there is a genetic influence on balding in young men and on non-balding in elderly men. It is possible that the same genes are responsible for determining predisposition to balding and to non-balding but, at this stage, we cannot assume that this is necessarily the case. Genetic analysis of balding in young men is complicated by the fact that the destiny of hair status in non-bald siblings is unknown. This difficulty is partly overcome by studying non-balding in elderly men where balding and non-balding in similarly aged siblings are more fully expressed, which may make this age group a better target for future studies in this field.
Adolescent↗
Do androgens influence hair growth by altering the paracrine factors secreted by dermal papilla cells?
Androgens regulate many aspects of human hair growth in both sexes. After puberty they transform tiny vellus follicles in many areas, e.g. the face, to terminal ones producing long, thick, pigmented hairs. In genetically predisposed individuals, androgens also cause the reverse transformation of terminal scalp follicles into vellus ones, causing balding. In the current hypothesis for androgen action, androgens control most follicular cells indirectly acting via the mesenchyme-derived dermal papilla which regulates many aspects of follicular activity. In this model androgens binding to androgen receptors in dermal papilla cells alter their production of regulatory molecules which influence other follicular components; these molecules may be soluble paracrine factors and/or extracellular matrix proteins. This hypothesis is supported by immunohistochemical localisation of androgen receptors in dermal papilla cell nuclei and the demonstrations that androgen receptor content and testosterone metabolism patterns of cultured dermal papilla cells from various body sites reflect hair growth in androgen-insensitivity syndromes. The next question is whether androgens alter the paracrine factors secreted by dermal papilla cells. Cultured dermal papilla cells do release soluble, proteinaceous factors into their media which stimulate the growth of keratinocytes and other dermal papilla cells. This mitogenic potential can cross species from humans to rodents. Importantly, testosterone in vitro stimulates the mitogenic potential of beard cells, but in contrast inhibits production by balding scalp cells reflecting their in vivo androgenic responses. Since androgens in vitro do alter the secretion of paracrine factors the current focus lies in identifying specific factors produced, e.g. IGF-I and stem cell factor (SCF), using ELISA and RT-PCR, and comparing their expression in cells from follicles with varying responses to androgens in vivo or under androgen stimulation in vitro. This should lead to greater understanding of androgen action and enable the development of better treatment for androgen-potentiated disorders.
Androgens↗