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Biomedical subjects

J D Bos

Publications and source records attributed to J D Bos.

At least 181 records · Page 10Linked to original sources
PubMed1989

Immunology of contact dermatitis.

Allergic contact dermatitis is a classical type IV delayed hypersensitivity immune response. This cell-mediated response is also known as hapten-type delayed hypersensitivity. Allergic contact dermatitis may be viewed as hyperreactivity of the skin immune system. In the present view of allergic contact dermatitis, individuals are born in a state of tolerance to environmental haptenic allergens. During life, sensitization to any hapten(s) may occur. Subsequent elicitation of a sensitized individual then leads to dermatitis, often accompanied by severe pruritus. Human epidermal Langerhans cells play a central role during the sensitization stage. These antigen presenting dendritic cells, loaded with environmental haptens, continuously leave the epidermis through the lymph vessels and, upon arrival in the paracortical T-cell areas of the skin draining lymph nodes, they differentiate into interdigitating cells. There is now in-vitro evidence for such a maturation of human Langerhans cells into interdigitating cells. Any given individual may be sensitized to any particular hapten by this route. Allergic contact dermatitis is probably a skin-specific disease because of the capacity of Langerhans/interdigitating cells to induce relatively naive T-cells to become memory T-cells. Factors determining the ultimate outcome in this continuous hapten presenting process, i.e. whether or not the original state of tolerance will persist, are still enigmatic. During elicitation, when the allergenic hapten is applied epicutaneously to a sensitized individual, a focal accumulation of immune response associated cells producing a wide variety of cytokines and inflammatory mediators ultimately results in the clinical condition of allergic contact dermatitis. Langerhans cells do not seem to play a major role during this stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The allergens in cosmetics.

The ingredients responsible for allergy to cosmetics were determined in 119 patients suffering from cosmetic-related contact dermatitis. Most reactions (56.3%) were caused by skin care products, followed by nail cosmetics (13.4%), perfumes (8.4%), and hair cosmetics (5.9%). Preservatives were most frequently implicated (32.0%), followed by fragrances (26.5%) and emulsifiers (14.3%). By far the most important cosmetic allergen was Kathon CG, (a preservative system containing, as active ingredients, a mixture of methylisothiazolinone and methyl chloroisothiazolinone) reacting in 33 patients (27.7%). Other frequent causes of cosmetic-related contact allergic reactions were toluenesulfonamide/formaldehyde resin in nail hardener and/or nail lacquer (15 patients [12.6%]), and oleamidopropyl dimethylamine, an emulsifier in baby body lotion (13 patients [10.9%]).

Adolescent↗
PubMed1988

Direct and indirect nickel-specific stimulation of T lymphocytes from patients with allergic contact dermatitis to nickel.

Fourteen T lymphocyte clones (TLC) specific for the contact allergen nickel were prepared either from lesional tissue biopsies or from peripheral blood of patients with allergic nickel-contact dermatitis. Two nickel-specific TLC, obtained from lesional tissue, responded to nickel without the participation of antigen-presenting cells (APC). This direct stimulation by nickel was not restricted by major histocompatibility complex-encoded molecules, since antibodies against HLA class I and II molecules did not block nickel-specific proliferation. Proliferation of other nickel-specific TLC was dependent on the presence of APC and was diversely restricted by HLA class II molecules. With one exception, the restriction determinants were present on HLA-DR and HLA-DQ molecules. Four TLC recognized nickel in association with subtypes of these serologically defined molecules. Five TLC seemed to recognize nickel in the context of highly unusual restriction determinants, since their restrictions could not be explained by the function of single polymorphic HLA class II epitopes. The absence of HLA class II restrictions and the occurrence of deviant HLA class II restrictions in part of the nickel-specific TLC are suggested to result from direct interactions of nickel with critical immune response molecules.

Antigen-Presenting Cells↗
PubMed1988

Central nervous system involvement in early and late syphilis: the problem of asymptomatic neurosyphilis.

Patients with syphilitic infections are at risk of development of symptomatic neurosyphilis. Adequate treatment with 2.4-7.2 x 10(6) units benzyl penicillin-G intramuscularly within 1 year after infection will rule out this risk. However, more than 1 year after infection this treatment is not fully reliable. In asymptomatic CNS involvement (asymptomatic neurosyphilis) only intravenous penicillin treatment is considered to be adequate in the prevention of neurosyphilis. In this study we redefined criteria for this condition by comparing serum and cerebrospinal fluid (CSF) samples of symptomatic neurosyphilitic patients with those of latent syphilitic patients without CNS involvement. Diagnostic criteria of the World Health Organization and of Centers of Disease Control for asymptomatic neurosyphilis (positive CSF Venereal Disease Research Laboratory (VDRL) test, combined with raised CSF cell count and/or protein content) were studied and compared with some newer parameters such as signs of intrathecal treponemal antibody production (Treponema pallidum haemagglutination assay and intrathecal Treponema pallidum assay index), immunoglobulin G (IgG) and M (IgM) index. The results of this study in 203 syphilitic patients revealed that either a positive CSF-VDRL or combination of a raised IgG and/or IgM index with an elevated CSF cell count both are useful criteria for "ruling-in" asymptomatic neurosyphilis.

Humans↗
PubMed1988

Enrichment of unlabeled human Langerhans cells from epidermal cell suspensions by discontinuous density gradient centrifugation.

In this report we introduce an alternative procedure for enrichment of human epidermal Langerhans cells (LC) from epidermal cell suspensions of normal skin. By means of discontinuous Ficoll-Metrizoate density gradient centrifugation, a fraction containing high numbers of viable, more than 80% pure LC was recovered, as judged by CD1a expression. The purity of the LC-enriched fraction appeared to be dependent on the percentage LC in the crude epidermal cell suspension. LC enriched by this method retained their accessory and antigen-presenting capacities, as determined in the Concanavalin-A induced T-cell response, in the allogeneic mixed leukocyte reaction and in the antigen-specific T-cell proliferation assay in vitro. The great advantage of this method is that it is simple and rapid and that the isolated LC are unlabeled.

Antigen-Presenting Cells↗
PubMed1988

Low-dose cyclosporin A in severe psoriasis. A double-blind study.

Twenty patients with severe plaque psoriasis were selected to receive either low-dose cyclosporin A (CyA) or placebo (CyA vehicle) in a double-blind randomized trial at two centres. Within 4 weeks the mean reduction in the Psoriasis Area and Severity Index (PASI) in 10 patients receiving CyA (mean dose 5.5 mg/kg/day) differed significantly from the mean reduction in 10 patients receiving placebo. In eight patients given placebo a switch to CyA therapy resulted within 4 weeks in a mean reduction in PASI of 90%. In a total 15 out of 18 patients given CyA (83%) (mean dose 5.6 mg/kg/day) there was an improvement of greater than or equal to 75% in PASI within 4 weeks. In a 2-month tapering off phase a lower mean CyA dose (3 mg/kg/day) was effective in maintaining the reduced PASI scores in seven of nine patients. Four out of five CyA treated patients who entered a post-treatment observation phase had a relapse (PASI score greater than or equal to 50% of score at baseline) after a mean interval of 6.5 weeks. The most important side-effects were mild reversible hypertension in 5 of 18 patients (28%), and reversible elevated serum creatinine levels in 7 of 18 patients (39%). We consider that further studies are justified in severe chronic psoriasis to establish suitable regimens for maintenance of remission in psoriasis with low-doses of CyA or a combination of CyA with other anti-psoriatic agents.

Adult↗
PubMed1988

Patch test reactivity to DMDM hydantoin. Relationship to formaldehyde allergy.

The relationship between contact allergy to formaldehyde and positive patch test reactions to DMDM hydantoin was investigated. 35 formaldehyde-allergic patients were patch tested with serial dilutions of formaldehyde (0.1%-0.3%-1.0% aq.) and DM hydantoin (the non-formaldehyde-containing parent compound of DMDM hydantoin). 21 were also patch tested with MDM hydantoin (1 molecule formaldehyde) in serial dilutions: 7 (33%) reacted to 1 or more concentrations. The other 14 were also tested with DMDM hydantoin (2 molecules formaldehyde) in serial dilutions: 8 (57%) reacted to 1 or more concentrations. Patients patch-test-positive to formaldehyde 0.1% and/or 0.3% tended to show more patch test reactivity to (D)MDM hydantoin than those who reacted only to 1%. Aqueous solutions of (D)MDM hydantoin in concentrations as used in cosmetic products therefore contain enough free formaldehyde to cause dermatitis in a patch test system in some formaldehyde-allergic patients: 12 such patients applied a cream containing 1% DMDM hydantoin to the flexor aspect of the lower arm twice daily for 1 week; 4 (33%) developed dermatitis. The use of a cream containing 0.25% DMDM hydantoin in these 4 patients still caused dermatitis in 1 and provoked itching in another. An increase in the use of DMDM hydantoin in cosmetic products will also inevitable increase the risk of cosmetic dermatitis in consumers allergic to formaldehyde.

Cosmetics↗
PubMed1988

Cross-reaction pattern of the cationic emulsifier oleamidopropyl dimethylamine.

13 patients allergic to the cationic emulsifier oleamidopropyl dimethylamine were tested with a series of related amide-amine type surfactants in order to investigate its cross-reaction pattern. With 1 exception, all patients reacted to at least 4 of the test materials. Most reactions were observed to ricinoleamidopropyl dimethylamine lactate and tallowamidopropyl dimethylamine (11 patients, 85%); 9 patients (of 12 tested, 75%) reacted to lauramidopropyl dimethylamine and 6 (46%) to myristamidopropyl dimethylamine. A certain pattern of cross-reactivity was recognised.

Adolescent↗
PubMed1988

T-lymphocyte and Langerhans cell distribution in normal and allergically induced oral mucosa in contact with nickel-containing dental alloys.

An in vivo comparison was made between the contact allergic stomatitis-inducing capacity of nickel, nickel-containing dental alloys and a non-corrosive precious metal. Fifteen patients with a positive allergic skin reaction to nickel were divided into 3 groups (A, B and C). The patients in Group A (n = 4) were fitted with an intra-oral corrosion-resistant nickel-chromium Alloy A; the patients of Group B (n = 5) received a more corrosion prone nickel-chromium Alloy B and in Group C (n = 6) strongly corroding pure nickel was used. A corrosion-resistant foil of pure palladium was placed on the contralateral side. Reactivity of pure nickel foil was also tested on the skin in Group C. Immunohistological examination of the oral mucosa on the test and reference sides was performed with monoclonal antibodies directed against T-lymphocyte subsets and Langerhans cells (LC). The results showed that at the pure nickel site the LC did increase significantly in the connective tissue (approx. 4X) of the oral mucosa. However, statistical analysis of all 6 patients of Group C together showed no corresponding increase of LC in the epithelium at the site with the pure nickel, although a numerical increase of LC was noted in the epithelium adjacent to the pure nickel foil in 2 patients, which was remarkable. It can be concluded from statistical analysis that both the reference foils and the test foils can influence the number of suppressor/cytotoxic T-lymphocytes in the connective tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Count↗
PubMed1988

Cerebrospinal fluid IgG and IgM indexes as indicators of active neurosyphilis.

Serological and non-serological tests were performed in matched samples of cerebrospinal fluid and serum from 236 syphilitic patients. An increased IgG or IgM index, or both, was found about 70 times more often in symptomatic neurosyphilis than in latent syphilis without involvement of the central nervous system. An increased Ig index, together with a cell count greater than 5/microL, was only found in symptomatic neurosyphilis. Although the numbers of data are small, we conclude that the IgG and IgM indexes are valuable tests in the diagnosis of syphilitic involvement of the central nervous system.

Adult↗
PubMed1987

Nickel-specific T lymphocyte clones derived from allergic nickel-contact dermatitis lesions in man: heterogeneity based on requirement of dendritic antigen-presenting cell subsets.

Inflammatory skin T cells were cloned in an antigen-independent way from lesions of patients with experimentally induced nickel-contact dermatitis. In three experiments 7-15% of the CD4+8- T lymphocyte clones (TLC) appeared to be specific for nickel in a proliferation assay. These proliferative response of nickel-specific TLC required the presence of antigen-presenting cells (APC) and were restricted by HLA class II molecules. All TLC recognized nickel presented by APC from epidermal skin. Remarkably, 5 out of 8 nickel-specific TLC exclusively recognized nickel when presented by these skin-specific APC whereas 3 out of these 8 clones could also recognize nickel presented by APC from peripheral blood. The critical APC within the fractions of epidermal cells and peripheral blood appeared to belong to the family of dendritic cells, i.e. Langerhans cells and circulating dendritic cells, respectively.

Antigen-Presenting Cells↗
PubMed1987

The crucial role of human dendritic antigen-presenting cell subsets in nickel-specific T-cell proliferation.

In the majority of patients, allergic nickel contact dermatitis is associated with a proliferative response of peripheral blood T lymphocytes to nickel sulfate. Optimal proliferation was found in a concentration range of 1-2 X 10(-4) M nickel sulfate. Nickel-specific response of purified peripheral blood T cells requires the presence of antigen-presenting cells (APC). Both peripheral blood monocytes and skin-derived epidermal cells could function as APC, but epidermal cells were shown to be more potent than monocytes. By testing FcR+ monocytes and FcR- circulating dendritic cells for their antigen-presenting capacities, it was found that the critical APC within the fraction of monocytes is the circulating dendritic cell. Testing highly purified T6+ (CD 1) skin-specific dendritic cells (Langerhans cells, LC) and T6- epidermal cells as APC, the critical APC within the fraction of epidermal cells appeared to be the LC. The crucial role of LC was stressed in experiments using T cells from patients exhibiting a positive patch test to nickel but a low or absent proliferative response to nickel by unpurified peripheral blood cells. Whereas addition of peripheral blood APC was ineffective, addition of LC to purified peripheral T cells was shown to overcome this low responsiveness to nickel. These results indicate the crucial role of dendritic APC subsets in nickel-specific T-cell proliferation.

Antigen-Presenting Cells↗
PubMed1987

The skin immune system (SIS): distribution and immunophenotype of lymphocyte subpopulations in normal human skin.

The complexity of immune response-associated cells present in normal human skin was recently redefined as the skin immune system (SIS). In the present study, the exact immunophenotypes of lymphocyte subpopulations with their localizations in normal human skin were determined quantitatively. B cells were not found to be present in normal human skin. Lymphocytes were always of T-cell type, and 90% of these T cells were clustered in 1-3 rows around postcapillary venules of the papillary vascular plexus or adjacent to cutaneous appendages. In such perivascular localizations, they were found to differ from their circulating counterparts in three ways. First, skin perivascular cells were found to be approximately evenly distributed over CD4+ inducer and CD8+ suppressor-cytotoxic T-cell subsets (mean CD4/CD8 ratio: papillary layer 0.96, reticular layer 0.99). Second, within the category of CD4+ inducer T cells, most were phenotyped as CD4+, 4B4+ helper inducer T lymphocytes, whereas CD4+, 2H4+ suppressor inducer T lymphocytes were found to be relatively rare (less than 5%). Third, the majority of skin perivascular T cells were activated as they expressed HLA-DR and interleukin 2 receptors. Intraepidermal, directly subepidermal, and other ("free") lymphocytes were mostly of the CD8+ suppressor-cytotoxic T-cell subset but accounted for less than 10% of the total number of lymphocytes. Intraepidermally localized T cells accounted for less than 2% of the total number of lymphocytes present in normal skin. Our results indicate that preferential perivascular localization of activated T lymphocytes is the characteristic of normal human skin. This might be a reflection of continuous antigen recognition upon endothelial cell presentation and/or continuous T cell-mediated endothelial cell activation thereby inducing enhanced antigen clearing by the skin's endothelium.

B-Lymphocytes↗