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Biomedical subjects

O Baadsgaard

Publications and source records attributed to O Baadsgaard.

At least 91 records · Page 5Linked to original sources
PubMed1988

Rapid occurrence of nodular cutaneous T-lymphocyte infiltrates with cyclosporine therapy.

Cyclosporine, a potent immunosuppressive agent, has been successfully used in the treatment of several dermatologic conditions including psoriasis. However, the drug does have an array of toxic side effects that need to be carefully considered when determining the risk-benefit ratio for the treatment of skin disease. We present another potential adverse effect of cyclosporine, namely, a benign lymphocytic infiltrate. This eruption developed in a patient with psoriasis after only ten days of cyclosporine therapy. The exact mechanism by which cyclosporine induced the lymphocytic infiltrate is unknown, but it is postulated that cyclosporine caused an imbalance of T-cell regulatory systems, thus resulting in an expanded T-cell subpopulation and the clinical manifestation of erythematous papules and nodules.

Biopsy↗
PubMed1987

Reduction of the number of immunocompetent cells in the acute stage of herpes zoster.

Circulating and in situ mononuclear cell subsets were phenotypically characterized during both the acute and convalescent phase of herpes zoster infections in 14 patients. In peripheral blood a significant reduction in the absolute number of Leu 4+ T cells, Leu 2a+ suppressor/cytotoxic T cells, Leu 3a+ helper/inducer T cells, Leu 7+ killer cells, and B1+ B cells were found during the acute stage compared to convalescents and normal controls. In contrast no change in the absolute number of MO2+ monocytes was seen in the acute stage of the disease. During convalescence a return to normal values in the lymphocyte subsets and killer cells was seen within 1-2 months after the initial disease presentation. In skin biopsy specimens from 4 of the 14 patients with active herpes zoster lesions the cellular infiltrate consisted of T cells (Leu 4+) the majority being helper/inducer T cells (Leu 3a+). Most of the cells expressed HLA-DR (Ia) antigens and were according to this in an activated state. The observed changes in effector and regulatory cell numbers may have implications for the acquisition of Varicella-zoster virus infections, the immune deficiency state associated with the disease, and/or the immune response to resolve the infection.

Aged↗
PubMed1987

Dose response and time course for induction of T6- DR+ human epidermal antigen-presenting cells by in vivo ultraviolet A, B, and C irradiation.

In vivo ultraviolet (UV) exposure of human skin abrogates the antigen-presenting function of T6+ DR+ Langerhans cells and induces the appearance of antigen-presenting T6- DR+ epidermal melanophages. UV-exposed epidermal cells containing T6- DR+ epidermal antigen-presenting cells, in contrast to unexposed epidermal cells containing T6+ DR+ Langerhans cells, potently activate autoreactive regulatory T cells in the absence of exogenous antigens. Autoreactive T cells may be important for regulation of other immune responses such as those which occur in photosensitive lupus erythematosus and in immune surveillance of UV-induced skin cancers. It is therefore imperative to determine the factors that govern their appearance in the skin. It was found that UVB and UVC, but not UVA, induced a dose-dependent appearance of T6- DR+ epidermal melanophages. The optimal time of appearance was 2 or 3 days after UVB and UVC exposure. In contrast, UVA was a poor inducer of T6- DR+ cells at all doses and all time points tested. Although UVA was a poor inducer of T6- DR+ epidermal cells, UVA radiation resulted in depletion of T6+ DR+ Langerhans cells from the epidermis, as did UVB and UVC radiation. This differential effect of UV wave bands on the immunocompetent cells in human skin may be related to the greater potential of UVB exposure to induce skin cancers and to exacerbate systemic lupus erythematosus.

Adult↗
PubMed1987

UVB and UVC, but not UVA, potently induce the appearance of T6- DR+ antigen-presenting cells in human epidermis.

Non-Langerhans cell, antigen-presenting T6- DR+ epidermal cells (EC) appear 3 days following broad band ultraviolet radiation exposure of human skin and are responsible for the increased antigen presentation capacity of EC seen 3 days after UV exposure. To determine the UV wavelengths that induce T6- DR+ EC, volar forearm skin of 10 human volunteers was irradiated in vivo with 4 minimal erythema doses (MED) each of pure UVA (mean 482 J cm-2), UVB (mean 0.390 J cm-2), and UVC (mean 0.397 J cm-2). The purity of the light sources was as follows: UVB, 98% of the emission was in the UVB range; UVC, 97% of the irradiance was in the UVC range; UVA, 100% of the energy had wavelengths longer than 340 nm. Three days after UV irradiation with 4 MED of each wavelength band, suction blister-derived EC suspensions were prepared from the UV-exposed and unirradiated sites. Percentages of T6+ DR+ Langerhans cells (LC) and T6- DR+ EC were quantitated. Relative to control EC, which contained 2.4 +/- 0.3% T6+ DR+ LC, the mean percentage (+/- SEM) of T6+ DR+ LC contained within UV-exposed EC was significantly decreased as follows: UVB, 0.5 +/- 0.2%; UVC, 0.9 +/- 0.1%; UVA, 0.5 +/- 0.2% (n = 10). T6- DR+ EC, absent in control EC, were induced both by UVB, 5.2 +/- 1.7% and UVC; 1.5 +/- 0.4%. Despite the use of more than 1200 times greater doses in J cm-2 of UVA than UVB and UVC, UVA was a poor inducer of T6- DR+ EC (0.5 +/- 0.2%) and in about half of these individuals, T6- DR+ EC were undetectable. The UV wavelengths for induction of T6- DR+ EC lies predominantly within the UVB band, but also to a lesser extent within the UVC band. These wavelengths appear to be analogous to both the wavelengths for generation of increased host susceptibility to UV-induced murine tumors and to the wavelengths for UV-induced systemic suppression of contact hypersensitivity. However, our data indicate that UV wavelengths for decreasing the number of T6+ DR+ LC in humans differs from the wavelengths for induction of systemic suppression of contact hypersensitivity in mice. Taken together, these data suggest that the appearance of T6- DR+ EC, but not the disappearance of T6+ DR+ LC, following UV exposure may be related to the induction of such antigen-specific suppressor T cells.

Antigen-Presenting Cells↗
PubMed1986

Cyclosporine improves psoriasis in a double-blind study.

In a double-blind trial, 21 patients with severe plaque psoriasis were randomly assigned to receive oral cyclosporine, 14 mg/kg/d, or its vehicle. After four weeks of therapy the 11 cyclosporine recipients had the following response to treatment: two had total clearing and six improved markedly, two moderately, and one minimally; whereas ten vehicle-treated patients showed no change or minimal improvement. Vehicle-treated patients, after a switch to cyclosporine for four weeks, demonstrated impressive improvement similar to that seen in patients who initially received only cyclosporine. Moderate or marked improvement or total clearing was noted in 17 (81%) of 21 and 20 (95%) of 21 after one and four weeks of therapy, respectively. Mitotic figures and leukotriene B4 levels in lesions decreased 86% and 64%, respectively, after seven days of cyclosporine therapy. Mononuclear (including activated T cells) and polymorphonuclear leukocyte infiltrates were markedly reduced in lesions of all patients after seven days of cyclosporine therapy. These results suggest that psoriasis may have an immunologic basis mediated by activated T cells and/or other immune cells; if a long-term regimen with a favorable efficacy-side effect ratio can be determined, cyclosporine would be a significant advance in the treatment of psoriasis.

Adult↗
PubMed1986

Circulating and in situ lymphocyte subsets and Langerhans cells in patients with compositae oleoresin dermatitis and increased ultraviolet A sensitivity during treatment with azathioprine.

Circulating and in situ lymphocyte subsets and Langerhans cells in four patients with compositae oleoresin dermatitis and increased ultraviolet A sensitivity before and during treatment with azathioprine were estimated. It was found that the number of Leu 6+ Langerhans cells decreased during therapy. This decrease was accompanied by a reduction in the number of Leu 2a+, Leu 3a+, Leu 4+, DR+, and Leu M2+ cells in the blood and a reduction in the number of Leu 2a+, Leu 3a+, Leu 4+, and DR+ cells in the skin. Concomitantly with the changes in the number of immunocompetent cells, the eczema cleared.

Adult↗
PubMed1986

Circulating lymphocyte subsets in patients with alopecia areata.

Lymphocyte subsets in peripheral blood of fourteen patients with patchy alopecia areata or alopecia universalis were estimated using monoclonal antibodies and immunofluorescence. The median percentage of circulating Leu 2a, 3a, 4 and 7 positive cells ("T-suppressor/cytotoxic", "T-helper/effector", total T-cells and killer and natural killer cells) were normal.

Adolescent↗
PubMed1985

Lymphocyte subsets in patients with compositae oleoresin dermatitis and increased UVA sensitivity during treatment with azathioprine.

Four patients with severe contact dermatitis resulting from compositae oleoresin were found to have increased sensitivity to ultraviolet light. All showed a clear reduction of Leu-3a-positive lymphocytes (T helper/inducer cells) and cells expressing the Ia phenotype in their blood. The numbers of T suppressor/cytotoxic (Leu 2a) lymphocytes, monocytes and B lymphocytes were within the normal range. Treatment with azathioprine (150 mg daily) improved the eczema. The number of Leu-3a-positive lymphocytes normalized during therapy, but the number of Ia-positive cells did not.

Aged↗
PubMed1985

Delusions of infestation treated with pimozide: a follow-up study.

Fourteen patients with monosymptomatic delusions of infestation were followed-up 19-48 months after treatment with pimozide was terminated. Seven patients had remained in remission since the treatment. Three had developed relapses, but were without symptoms with intermittent treatment. Four patients responded poorly to pimozide and had still symptoms at the follow-up. The study indicates, that a large proportion of patients with monosymptomatic delusions of infestation treated with pimozide will be able to discontinue the medication for years without recurrence of their delusions.

Aged↗