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D V Belsito

Publications and source records attributed to D V Belsito.

At least 37 records · Page 2Linked to original sources
PubMed1997

The rise and fall of allergic contact dermatitis.

When a simple chemical hapten contacts the skin, it triggers a complex cellular and molecular reaction that eventuates in the cutaneous reaction clinically recognized as allergic contact dermatitis. This review summarizes the crucial role of the cytokines and adhesion molecules that direct the traffic of cells into, and out of, the skin after contact with an allergen. Particularly stressed are the molecular interactions between antigen-bearing Langerhans cells and responding CD4(+) T cells: this interaction results in the amplification of the memory cells that add specificity to the immune response. Finally, negative feedback mechanisms for dampening the response are briefly discussed.

Allergens↗
PubMed1996

Aeroallergen patch testing for patients presenting to contact dermatitis clinics.

BACKGROUND: The role of aeroallergens in the production of allergic contact dermatitis or "allergic contact dermatitis-like" atopic dermatitis is controversial. Although techniques and allergens lack standardization, most studies find positive patch test results in 30% to 40% of patients with atopic dermatitis. OBJECTIVE: Our purpose was to determine the prevalence and clinical significance of positive aeroallergen patch tests in patients undergoing standard patch testing for suspected "nonaeroallerge" allergic contact dermatitis. METHODS: One hundred three consecutive patients referred to three university patch test clinics for patch testing were alos patch tested with six common aeroallergens in glycerine-dust, mold, cat epithelium, tree, grass, and weed-as well as with a glycerine control. Patches were removed at 48 hours. Readings were performed at this time and at 3 to 7 days after initial application. RESULTS: As determined by history, these 103 patients included 16 patients with both atopic dermatitis and mucosal atopy, 10 patients with atopic dermatitis only, 22 patients with mucosal atopy only, and 55 patients with neither atopic dermatitis nor mucosal atopy. Allergic reactions were seen to one aeroallergen in five patients (three with atopic dermatitis and mucosal allergy, and two with no history of atopy). The prevalence (3 of 16 [18.8%]) of reactions in patients with both atopic dermatitis and mucosal allergy was significantly greater than the prevalence (2 of 87 [2.3%]) in patients with only one or neither of these two atopic disorders (p = 0.02). None of these aeroallergen contact hypersensitivities were deemed significant in the patients' current dermatitis. However, reactions were of past relevance in two of the three patients with atopic dermatitis and mucosal allergy. CONCLUSION: In this referral group, none of the six common aeroallergens tested was relevant in the origin of suspected "nonaeroallergen" allergic contact dermatitis. This study suggests that aeroallergen patch testing is of little use in the evaluation of patients referred for routine patch testing for suspected "nonaeroallergen" allergic contact dermatitis. Similar but larger studies inclusive of the assessment of relevance, as well as masked controlled clinical trials assessing the effect of aeroallergen exposure and avoidance, are needed to evaluate this issue more fully.

Adult↗
PubMed1995

Relationship between humoral immunoaugmenting properties of DHEAS and IgD-receptor expression in young and aged mice.

IgD-receptors are associated with augmented antibody production in vivo and are induced on CD4+ T cells by aggregated IgD in young but not in aged mice. In the current study orally or intraperitoneally administered DHEAS was found to enhance antibody production, as measured in a plaque-forming cell assay, and also to cause an increased expression of IgD-R on T cells in both young and aged mice. IgD-R+ T cells are enumerated by rosette cell formation with IgD-coated SRBC. Since, as shown previously, the immunoaugmenting effect of IgD-R+ T cells is blocked by injection of monomeric IgD, the effect of monomeric IgD was also examined in DHEAS-pretreated mice. The inhibitory effect obtained with monomeric IgD in these studies indicates that upregulation of IgD-R by DHEAS plays an important role in the immunoenhancing effect of this hormone. In addition, no significant effect of DHEAS was obtained on contact hypersensitivity to DNCB or on proliferative responses of T cells from young or aged mice. Aged but not young mice showed increases in the numbers of Ia+ epidermal Langerhans cells after DHEAS treatment.

Adjuvants, Immunologic↗
PubMed1995

Synergism between interferon-gamma and cytokines or lipopolysaccharide in the activation of the HIV-LTR in macrophages.

Macrophages (møs) obtained from transgenic mice carrying the HIV long terminal repeat-chloramphenicol acetyl transferase (LTR-CAT) sequence were used to study the influence of various biologic response modifiers (BRMs) on the activation of LTR-directed CAT expression. It was found that LPS or IL-6 alone induced moderate levels of CAT expression, whereas IFN-gamma or TNF-alpha had no significant effect. Co-exposure of møs to IFN-gamma and either LPS, IL-6, or TNF-alpha led to significant synergistic increases in CAT levels. Levels were also synergistically augmented when møs were exposed first to IFN-gamma (priming), washed, and then exposed to either LPS, IL-6, or TNF-alpha. Although IL-6 was synergistic with subsequently added IFN-gamma, the reverse sequence of addition was more effective. LPS and TNF-alpha were inactive when added before IFN-gamma. Initial priming signals were rapid as exposure for 3 h to IFN-gamma was sufficient to prepare the cells for subsequent activation by other BRMs. These results suggest that the duration of latency and progression of HIV infections may be greatly influenced by events such as intercurrent infections that cause IFN-gamma production, thereby priming møs to respond to other cytokines that have been reported to be constitutively elevated during the course of infection with HIV (e.g., IL-6 and/or TNF-alpha).

Animals↗
PubMed1993

Allergic contact dermatitis to topical glucocorticosteroids.

During the past decade, the reported incidence of allergic reactions to topically applied glucocorticosteroids has increased significantly. The two cases reported here typify the presenting symptoms of the glucocorticosteroid-allergic persons. These cases also illustrate the extensive cross-reactivity among the different topical corticosteroids, as well as the potential for systemic contact dermatitis to occur following parenteral exposure. These cases are reviewed in the context of the many other reports in the literature of similar allergic reactions.

Administration, Topical↗
PubMed1992

Allergic contact dermatitis from formaldehyde resins in permanent press clothing: an underdiagnosed cause of generalized dermatitis.

BACKGROUND AND METHODS: Formaldehyde resins have been used to impart wrinkle resistance to clothing fabrics since 1926. After several patients with positive patch tests to formaldehyde resins had been examined, a study was undertaken of the records of all patch tests performed at the University of Louisville Patch Test Clinic and the Allergy Section of the Skin and Cancer Clinic of New York University Medical Center from January 1988 through April 1990 to determine the prevalence of positive patch-test reactions to formaldehyde-based textile resins and the clinical and demographic patterns associated with textile resin allergy. RESULTS: Seventeen patients were identified at the two centers. Twelve were allergic to formaldehyde as well as to formaldehyde textile resins. Several clinical patterns were found, including accentuation of dermatitis in areas of tight clothing, primary occurrence in clothing-covered areas, and a chronic recalcitrant course. Ethylene urea melamine formaldehyde resin was the best screening agent with 14 definite positive reactions and one equivocal reaction. CONCLUSION: Formaldehyde textile resin allergy is more common than has been previously recognized. Patch testing with one or more formaldehyde textile resins is indicated in patients with a particular pattern of dermatitis.

Adult↗
PubMed1991

Immunosuppressive effects of transforming growth factor beta: inhibition of the induction of Ia antigen on Langerhans cells by cytokines and of the contact hypersensitivity response.

Recent reports show that transforming growth factor (TGF)-beta exerts a variety of immunosuppressive activities. The present study focuses on the effects of TGF-beta 1 on expression of Ia antigen by Langerhans cells. Although TGF-beta 1, in concentrations from 0.001 to 100 micrograms/ml, has no effect on constitutive expression of Ia antigen on these cells, the in vitro up-regulation of Ia antigen on the surface of LC by interleukin (IL)-1, tumor necrosis factor-alpha, interferon-gamma, IL-3, and granulocyte/macrophage-colony stimulating factor is inhibited by the concomitant addition of 1 microgram/ml TGF-beta 1. In contrast, TGF-beta 1 has no effect on the up-regulation induced by IL-2 or IL-6. In this report, the activity of TGF-beta closely resembles that of Cyclosporine A (CsA). Similar results are seen in vivo when either TGF-beta 1 (5 micrograms, intraperitoneally [ip], daily on days 0-3) or CsA (1 mg, subcutaneously [sc], twice daily on days 0-3) are given together with IL-2 (500 U, intraperitoneally [ip], twice daily on days 1-3) or interferon-gamma (4,000 U, ip, twice daily on days 1-3). Given the important role of Ia expression in cell-mediated immune reactions, the effect of TGF-beta on contact sensitivity was next investigated. In doses of 5 micrograms, ip, daily on days 6-8, TGF-beta inhibits the expression of contact reactivity in animals sensitized on day 0 and challenged on day 7. In contrast, no effect is observed on the induction of contact sensitivity in mice given TGF-beta 1 on days--1 to 2, sensitized on day 0, and challenged on day 7. The possible importance of antagonism between TGF-beta and other cytokines, especially IFN-gamma, involved in the elicitation of contact hypersensitivity reactions is discussed.

Animals↗
PubMed1991

Effect of triggering epidermal Fc gamma receptors on the interleukin-2- and interleukin-6-induced upregulation of Ia antigen expression by murine epidermal Langerhans cells: the role of prostaglandins and cAMP.

Following incubation of murine epidermis in medium containing either interleukin-2 or interleukin-6, there is significant upregulation in the density of Ia+ epidermal Langerhans cells (to 159% and 175% of control, respectively). This cytokine-induced upregulation is abrogated by either rabbit or human IgG due to triggering of Fc gamma receptors. In contrast, human IgA does not inhibit the effect of interleukin-2 or interleukin-6. Using different isotypes of murine IgG, we have demonstrated that all subclasses are capable of inhibiting the cytokine-induced enhancement of Ia antigen, although IgG1 and IgG2b must be heat aggregated to be effective. The IgG-mediated events are dependent on prostaglandin synthesis because they can be blocked by the cyclooxygenase inhibitor indomethacin, 10 micrograms/ml. The responsible PG appears to be PGD2; in contrast to its known inhibitory effect on macrophages, PGE2 does not inhibit the upregulation of Ia antigen on Langerhans cells. In addition, these IgG-mediated events are dependent upon the generation of cAMP because they can be blocked by the adenylate cyclase inhibitor 2',5'-dideoxyadenosine, 1 mM. Despite the apparently central role of PGD2 and cAMP in this process, triggering of the Fc gamma R by different isotypes of IgG blocks upregulation of Ia via at least two different pathways. The inhibition caused by aggregated IgG1 or IgG2b, which bind to Fc gamma RII on Langerhans cells, is abrogated by para-bromophenacylbromide, an inhibitor of phospholipase A2. In contrast, the inhibition caused by monomeric IgG2a, which binds to Fc gamma RI most likely on keratinocytes, or monomeric IgG3, which probably binds to this same Fc gamma RI, is abrogated by staurosporine, an inhibitor of protein kinase C, as well as by W7, a calmodulin antagonist. Finally, 1,2 dioctanoyl-rac-glycerol, an activator of protein kinase C, mimics the Ig-mediated events. Based on these findings, as well as studies using monoclonal antibodies to the murine Fc gamma receptors I and II, we conclude that, as is the case in murine macrophages, triggering of an epidermal Fc gamma RI, most likely on keratinocytes, results in the generation of cAMP via a Ca(++)-dependent protein kinase C pathway, whereas triggering of an epidermal Fc gamma RII, most likely on Langerhans cells, results in the elevation of cAMP via a phospholipase A2-mediated pathway. In contrast to the situation for macrophages, PGD2 is a vital intermediate in both pathways, perhaps because Langerhans cells have receptors for only this prostaglandin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Cimetidine-induced augmentation of allergic contact hypersensitivity reactions in mice.

BALB/c mice were treated with cimetidine (100 mg/kg) or saline, intraperitoneally, twice daily, from days 0-2 or days 7-9 after sensitization with 0.1%, 2,4,6-trinitro-1-chlorobenzene (TNCB) on day 0. On day 7, the mice were challenged with 1% TNCB to one ear. Ear swelling responses (as an index of sensitization), serum histamine levels, and biopsy specimens of challenged ears were evaluated in groups of cimetidine- or saline-treated mice at 0, 0.5, 1, 1.5, 2, 4, 6, 8, 12, 24, and 48 h after challenge. Additional controls included mice injected with saline or cimetidine and challenged with, but not sensitized to, TNCB (irritant controls). Treatment with cimetidine during the induction but not the elicitation of allergic contact hypersensitivity (ACH) produced a significant enhancement of the response throughout the first 48 h. There was no effect of cimetidine on antigen-presenting cells within the epidermis which might account for this enhancement. Similarly, no difference in mast cell morphology or serum histamine levels between cimetidine- and saline-treated groups was observed. Histologically, the cimetidine-treated animals showed a more intense cellular infiltrate, which was most noticeable at 24 to 48 h, at which time numerous subcorneal and perifollicular neutrophilic abscesses were observed. To further investigate the mechanism of action of cimetidine, mice were injected with cyclophosphamide (150 mg/kg) 2 d prior to sensitization. Mice treated with cyclophosphamide alone or in combination with cimetidine showed no additive or synergistic effect upon the ear swelling response. We conclude that enhancement of ACH by cimetidine is independent of any effect on mast cells or antigen-presenting cells, but may relate to a cimetidine-induced inhibition of the induction of T-suppressor cells at the time of sensitization.

Animals↗
PubMed1990

Contact urticaria caused by rubber. Analysis of seven cases.

Prior to 1979, there had been no reports of contact urticaria to rubber products. Since that time, many cases have been reported. At New York University, the first case, secondary to cornstarch allergy, was seen in 1985. Since that time, we have seen an additional six cases, five of them in the last year. Of these six cases, three were attributable to H. brasiliensis and three to the accelerators. Although the use of latex products has increased dramatically within the past 9 years in response to the epidemic of human immunodeficiency virus infections, it is not clear whether increased exposure alone accounts for the sudden increase in the number of patients with contact urticaria. Four of the patients presented here are hospital personnel involved in surgical procedures, in which, for decades, latex gloves have been used. Furthermore, two of our seven patients are paraplegics, who, as a group, have long had frequent exposure to rubber products. Two possibilities seem most likely: either the diagnosis has been missed by physicians for decades, or in response to the worldwide demand for latex products, the manufacture of latex has become altered in such a fashion that more products from which the allergens (accelerators and H. brasiliensis) are easily leached are now reaching the marketplace.

Adult↗