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B Moncada

Publications and source records attributed to B Moncada.

At least 19 recordsLinked to original sources
PubMed1993

Autoeczematization is associated with abnormal immune recognition of autologous skin antigens.

BACKGROUND: The pathogenesis of autoeczematization (AE) is not well understood; however, previous studies suggest that AE is an autoimmune condition. OBJECTIVE: Our purpose was to assess whether AE is associated with an abnormal immune recognition of autologous skin antigens. METHODS: Eight patients with AE, six healthy control subjects, and three patients with localized contact dermatitis (LCD) were studied. Activation markers were detected on peripheral blood T lymphocytes. Autologous mixed epidermal cell-lymphocyte reaction (AMECLR) was performed for each subject and cell proliferation was assessed by tritiated thymidine incorporation. RESULTS: Many activated T cells were detected in patients with AE (5.2% +/- 4.5% vs 0.2% +/- 0.4% in control subjects, p < 0.05). AMECLR showed a significantly higher cell proliferation in AE compared with both healthy subjects and patients with LCD (6372 +/- 3217 cpm vs 2638 +/- 1788 cpm, and 2471 +/- 1389 cpm, respectively; p < 0.05). Peripheral blood mononuclear cells cultured in the presence of an autologous skin homogenate also showed a significantly increased cell proliferation in patients with AE than in control subjects. CONCLUSION: Our results suggest that an abnormal immune response against autologous skin antigens occurs in AE that could be related to the pathogenesis of this disease.

Autoantigens↗
PubMed1993

Lack of expression of intercellular adhesion molecule ICAM-1 in lepromatous leprosy patients.

It is conceivable that an abnormal expression of cell-adhesion molecules can contribute to the poor inflammatory response seen in some inflammatory skin diseases. Adhesins are cell-surface molecules that are expressed by many cell types. The main function of adhesins appears to be the promotion of cellular interactions, such as those occurring between immune cells. The epidermis of patients with inflammatory skin diseases exhibits an increased expression of ICAM-1, and it has been postulated that such increased expression can be important in the genesis of cutaneous inflammation. The expression of cell-adhesion molecules (LFA-1, LFA-2, LFA-3 and ICAM-1) in skin lesions of leprosy patients was studied, as well as the in vitro expression of these molecules induced with gamma interferon (IFN-gamma). A lack of expression of ICAM-1 in the epidermis of lepromatous patients was noted; in addition, no expression of ICAM-1 was seen in the nearly normal skin from these patients incubated with IFN-gamma. A similar expression of the four molecules studies was noted in the dermis of both the lepromatous and tuberculoid types of leprosy. The epidermis of the lepromatous leprosy patients appears to have a defective expression of ICAM-1.

Antigens, CD↗
PubMed1991

Immune sensitization against epidermal antigens in polymorphous light eruption.

To get further insight into the pathogenesis of polymorphous light eruption, we studied nine patients with polymorphous light eruption and six healthy persons. Two skin biopsy specimens were obtained from each person, one from previously ultraviolet light-irradiated skin and another one from unirradiated skin. An epidermal cell suspension, skin homogenate, or both were prepared from each specimen. Autologous cultures were made with peripheral blood mononuclear cells combined with irradiated or unirradiated skin homogenate and peripheral blood mononuclear cells combined with irradiated or unirradiated epidermal cell suspension. Cell proliferation was assessed by 3H-thymidine incorporation assay. The response of peripheral blood mononuclear cells to unirradiated epidermal cells or unirradiated skin homogenate was similar in both patients and controls. However, peripheral blood mononuclear cells from patients with polymorphous light eruption showed a significantly increased proliferative response to both irradiated epidermal cells and irradiated skin homogenate. Our results indicate that ultraviolet light increases the stimulatory capability of polymorphous light eruption epidermal cells in a unidirectional mixed culture with autologous peripheral blood mononuclear cells. This suggests that an immune sensitization against autologous ultraviolet light-modified skin antigens occurs in polymorphous light eruption.

Adolescent↗
PubMed1988

Evidence of cell-mediated immune contrasuppression in lepromatous leprosy: modulation of a putative T contrasuppressor cell-subset.

Some lepromatous leprosy (LL) patients are characterized by the presence of activated suppressor T cells that specifically inhibit the immune response to Mycobacterium leprae antigens. Immune contrasuppressor (CS) cell activity antagonize suppressor function. Whereas the former function has been extensively studied in leprosy, the latter has not been explored. We studied the peripheral blood mononuclear cells (PBMNC) of 20 patients with leprosy (10 lepromatous and 10 tuberculoid) and six healthy contacts. We found CS-like activity in the PBMNC from some LL patients when assayed in vitro using lepromin as antigen. This CS-like function was found in CD8+, vicia villosa adherent (VV+) T cells. CS-like activity was not detected in PBMNC from either tuberculoid patients or healthy contacts. Pre-treatment of CD8+, VV+ cells with either recombinant IL-2 (5 u/ml) or recombinant interferon-gamma (1,000 u/ml) did not modify significantly their putative CS function. However, in 50% of lepromatous patients the pre-incubation of CD8+, VV+ cells with both lymphokines together increased significantly the CS-like activity. These data suggest that the in vitro immune response to M. leprae in some LL patients can be augmented by either modifying numerically the contrasuppressor T cells or activating them with lymphokines.

Antigens, Bacterial↗
PubMed1987

Quantitative analysis of contrasuppressor T lymphocytes in leprosy; induction of Ia antigens with gamma interferon.

Lepromatous leprosy is characterized by immune anergy and abnormal suppressor T-cell function. Contrasuppressor cells are a subset of CD8+, vicia villosa-adherent T lymphocytes. T-contrasuppressor (Tcs) cells act on T-helper cells to cause them to become unresponsive to the action of T-suppressor cells. In 8 lepromatous (LL) and 7 tuberculoid (TT) patients, and 6 healthy contacts we studied the percent of the following lymphocyte subsets: CD3+, CD4+, CD8+, Ia+, vicia villosa+ (VV+), CD8, VV+, VV, Ia+, and Ia, Tac+. This was done in baseline status as well as post-stimulation with recombinant gamma interferon (rIFN-gamma). We found that peripheral blood mononuclear cells from LL and TT patients and controls exhibit a similar number of putative contrasuppressor lymphocytes (CD8, VV+ cells). However, in the contrasuppressor subset from LL patients we found a low percent of Ia+ (p less than 0.05 compared to controls or TT). In the three groups studied, the rIFN-gamma enhanced the percent of Ia+ lymphocytes in the CD8, VV+ cell subpopulation. However, the CD8, VV+ lymphocytes from LL patients, despite the effect of rIFN-gamma, continue to have a low percent of Ia+ cells (p less than 0.05 compared to controls or TT). These findings suggest that LL patients might have abnormalities in the contrasuppressor immune circuit. Future functional studies on the role of Tcs cells in the anergy seen in LL will be required in order to define the apparent dysfunction occurring in this disease.

Antigens, Surface↗
PubMed1985

Thalidomide--effect on T cell subsets as a possible mechanism of action.

Thalidomide is the drug of choice in the erythema nodosum leprosum (ENL) type of lepra reaction. Lately it has been used successfully in other diseases, such as discoid lupus erythematosus, actinic prurigo, Behcet's disease, etc. However, its mechanism of action remains unknown. In patients for whom thalidomide provided relief in their disorder, the proportions of T lymphocytes and their subsets in peripheral blood were assessed by means of monoclonal antibodies. Three lepromatous leprosy patients with ENL had their T helper populations significantly increased after thalidomide therapy. A 14-year-old girl with Behcet's syndrome showed a consistent decrease in Ia+ cells throughout her three-month course of thalidomide therapy. The same findings were observed in two patients with the actinic prurigo type of polymorphous light eruption. From these results, we conclude that thalidomide may act as an immunomodulating agent on T cell subsets.

Adolescent↗
PubMed1984

Immunopathology of polymorphous light eruption. T lymphocytes in blood and skin.

Polymorphous light eruption (PLE; actinic prurigo) is a relatively common dermatologic disease. People suffering from it have a pruritic skin eruption on exposed areas. PLE may be an immunologically mediated disease. Sixteen patients with PLE were studied. T lymphocytes and the helper and suppressor-cytotoxic subsets were assessed in peripheral blood by an indirect immunofluorescent method with the use of monoclonal antibodies. Total T lymphocytes were significantly increased as compared to controls. By an indirect immunoperoxidase technic with the use of monoclonal antibodies, characterization of the dermal cell infiltrate was done. Predominance of T total, T helper, and cells marked with Ia antigen were found. These findings suggest that an abnormal immune response is responsible for the tissue damage in PLE.

Adolescent↗
PubMed1983

T-lymphocyte subsets in leprosy.

Immunologic abnormalities in T cells have been reported in patients with lepromatous leprosy. Ten patients with leprosy (eight lepromatous, one dimorphous, one tuberculoid) were studied in order to detect the proportions of total T lymphocytes and helper as well as suppressor subsets, using monoclonal antibodies in an indirect immunofluorescence test. Percentages of total T cells, suppressor cells, as well as helper subsets were similar in leprosy patients as compared with age-matched controls. This study could be considered a preliminary one to be followed by functional assays.

Adolescent↗
PubMed1983

Actinic prurigo.

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Diagnosis, Differential↗
PubMed1982

Neonatal pemphigus vulgaris: role of passively transferred pemphigus antibodies.

A neonate with oral lesions of pemphigus vulgaris is described. The diagnosis was confirmed by cytological examination of lesions, positive intercellular IgG staining of the acantholytic cells, and presence of pemphigus antibodies in his serum. At the time of delivery, the child's mother had active pemphigus vulgaris, and it is suggested that this was a case of passively transferred disease.

Adolescent↗