Differential expression of D-type cyclins in HaCaT keratinocytes and in psoriasis.

In this study, we show that the G0-G1/S phase of HaCaT keratinocyte cell cycle is characterized by D1-type cyclin expression, whereas during the repeated rapid turnover of highly proliferating cells, the expression of cyclins D2 and D3 dominates. Knocking down cyclin D1 mRNA resulted in no change of cell proliferation and morphology, indicating that D2 and D3 cyclins could substitute for D1 in driving the cell cycle. Increased numbers of cyclin D1-expressing keratinocytes were found in the basal layers of the lesional psoriatic epidermis compared to both normal and non-lesional epidermis without increased expression of cyclin D1 mRNA, suggesting a possible dysfunction in the degradation of cyclin D1 protein.

Haloperidol attenuates beta-amyloid-induced calcium imbalance in human fibroblasts.

Background: Antipsychotics are widely used in the treatment of behavioral and psychological symptoms of dementia. A low frequency of Alzheimer's disease in patients with schizophrenia is reported, and it has been proposed that antipsychotic medications, such as haloperidol, may be responsible. Disruption of intracellular calcium levels is considered to play a key role in beta-amyloid-induced neurotoxicity in Alzheimer's disease.

A mannose-binding receptor is expressed on human keratinocytes and mediates killing of Candida albicans.

Human keratinocytes are known to kill Candida albicans in vitro, but the mechanism of killing is not yet understood. Here, we demonstrate that spontaneous, ultraviolet-B-light-induced, alpha-melanocyte-stimulating-hormone-induced, and interleukin-8-induced Candida killing by keratinocytes can be inhibited with mannan and mannosylated bovine serum albumin (Man-BSA). A polyclonal goat serum raised against the human macrophage mannose receptor stained suprabasal keratinocytes, but no staining was observed on keratinocytes with a monoclonal antibody (mAb15) specific for the human macrophage mannose receptor.

Identification of a soluble interleukin-8 inhibitor in the supernatant of polymorphonuclear leukocytes.

Interleukin-8 (IL-8) plays a crucial role in the pathogenesis of inflammatory and hyperproliferative diseases in various organs. The purpose of the present investigation was to establish whether there is any naturally occurring inhibitor of IL-8. Here we demonstrate that an IL-8 inhibitor (IL-8INH) is present in the supernatant of polymorphonuclear (PMN) leukocytes.

Human herpesvirus 8 in classic Kaposi sarcoma.

Recent studies suggest the role of a new human herpesvirus (HHV8) in the pathogenesis of different forms of Kaposi sarcoma (KS). In the present work we investigated the presence of HHV8 sequences in KS tumour tissues from patient with classic KS. Since clear evidences point to the role of immune suppression in the development of AIDS-associated KS or patients receiving immunosuppressive therapy, immunological investigations were also performed.

Interleukin-8 induces HLA-DR expression on cultured human keratinocytes via specific receptors.

Recent studies suggest that interleukin (IL)-8 exerts a direct influence on several functions such as the chemotaxis or proliferation of human keratinocytes (HK). Since the effects of IL-8 in skin are mediated through specific receptors, we have studied the characteristics of the keratinocyte IL-8 receptor. We could identify specific binding sites for IL-8 in cultured HKs by flow cytometry.

The interleukin-8 receptor: a potential target for antipsoriatic therapy?

Interleukin-8 is assumed to play a central role in the pathogenesis of psoriasis. Since an increased expression of the interleukin-8 receptor has been observed both in polymorphonuclear leukocytes and in affected psoriatic epidermis, we were interested in whether the interleukin-8 receptor could be a molecular target of antipsoriatic compounds. Cyclosporine, calcitriol, calcipotriol or dithranol caused a dose-dependent decrease in interleukin-8 binding to cultured human keratinocytes, while interleukin-8 binding to granulocytes was not affected.

The lymphocyte transformation test with sulphadiminidum and with prealbumin-sulphadiminidum complex in patients with drug allergy.

Earlier results (the absence or a decreased level of prealbumin [PA] in the serum, a higher proportion of PA-bearing lymphocytes as antigen-binding cells, and the presence of PA in the eluate of lymphocytes in patients with drug allergy) permitted the conclusion that, besides its other relevant functions, PA may also behave as a hapten carrier protein. The lymphocyte transformation test (LTT) involving measurement of 3H-thymidine uptake was therefore carried out with sulphadiminidum (SA) alone, with the PA-SA complex, and with the albumin-SA complex in patients with proven (3 cases) or suspected (63 cases) sensitivity to SA. In all 3 cases with proven drug allergy to SA and in 5 of the 63 suspect cases, the LTT was positive in response to both the drug alone and to the PA-SA complex (The albumin-SA complex gave positivity in only one case).

Expression of monocyte/macrophage markers (CD13, CD14, CD68) on human keratinocytes in healthy and diseased skin.

The results of several investigations proved that, in special circumstances, human keratinocytes (HKs) synthesize and express cell surface moieties characteristic of effector and/or accessory cells of the immune system, such as CD16, CD36, HLA-DR, and intercellular adhesion molecule-1 (CD54), which are all detectable on the surfaces of macrophages. In the present study, skin biopsies from healthy volunteers, from positive tuberculin skin tests, and from patients with acute urticaria (AU), lichen planus (LP), psoriasis vulgaris (PV), mycosis fungoides (MF), and purpura pigmentosa chronica (PPC) were investigated by means of a multistep immunoperoxidase method to examine the reactivity of the HKs with a panel of monoclonal antibodies (MABs) characteristic of monocyte/macrophage cell lines. In biopsies obtained from positive tuberculin tests and from clinically involved skin of patients with LP, PV, MF, or PPC, a multifocal, positive peroxidase reaction was observed on the membranes of HKs of the basal and suprabasal cell layers when the MABs OKM13 (CD13), OKM14 (CD14), and Dako-Macrophage (CD68) were used.

Platelet-activating factor antagonists (BN 52021 and BN 50730) inhibit tumor necrosis factor-alfa-mediated cytotoxicity on murine L929 tumor cells.

Tumor necrosis factor (TNF)-alfa has been described as a mononuclear phagocyte-produced cytotoxin that causes the necrosis and regression of some tumors. The mechanism of the cytotoxicity and the basis for the differential cytotoxic effects of TNF against cells of various origin remains unclear. It has also been reported, that murine TNF stimulates the production of platelet-activating factor (PAF) by cultured peritoneal macrophages, and that PAF enhances TNF production by alveolar macrophages.

Expression of complement receptor CR2 (CD21) on human subcorneal keratinocytes in normal and diseased skin.

Human keratinocytes are able to synthesize and express cell surface moieties characteristic of effector and/or accessory cells of the immune system (CD16, CD36, HLA-DR, intercellular adhesion molecule-1). In the present study, skin biopsies from healthy volunteers, from patients with psoriasis vulgaris (PV), mycosis fungoides (MF), purpura pigmentosa chronica (PPC), acute urticaria (AU) and from positive tuberculin skin tests were investigated with regard to the reactivity with the monoclonal antibodies to complement receptors CR1 CR2 and CR3 by means of a multistep immunoperoxidase method. In the clinically involved skin of all patients with PV, MF or PPC, and in biopsies obtained from positive tuberculin tests, specific epidermal intercellular staining with OKB7 and Leu anti-CR2 was seen on subcorneal keratinocytes.

The mouse erythrocyte binding receptor is expressed on human keratinocytes.

Immunocytes and different types of epidermal cells share cell surface antigen characteristics e.g. keratinocytes react specifically with the Leu 11 (CD16) monoclonal antibody and they express MHC class II and OKM5 (CD36) antigens after gamma-interferon stimulation.

Enhancing effect of whole-body ultraviolet light irradiation on Candida albicans activity of human polymorphonuclear leukocytes.

In an irradiation dose-dependent manner, the whole-body ultraviolet irradiation of healthy volunteers enhances the Candida albicans killing activity of the circulating polymorphonuclear granulocytes. This enhancing effect can be inhibited by oral indomethacine treatment. The sera of the irradiated subjects enhances the killing activity of the granulocytes of untreated individuals.

Enhancement of Candida albicans killing activity of separated human epidermal cells by ultraviolet radiation.

Ultraviolet irradiation enhanced the Candida albicans killing activity of freshly separated human epidermal cells in vitro. The stimulation was dose-dependent and was not due to soluble extracellular factors acting on non-irradiated epidermal cells. The enhancement of the killing activity remained unchanged when epidermal cells were depleted of Langerhans cells.

Enhancement of mouse erythrocyte rosette formation of human lymphocytes by interferon gamma.

Interferon-gamma enhances the mouse erythrocyte rosette formation of human peripheral blood mononuclear cells in a dose-dependent way. Pretreatment of the cells with colchicin abolishes the enhancing effect. An increased expression of the mouse erythrocyte binding receptor may underlie the phenomenon.

The effect of mouse erythrocyte rosette forming lymphocytes on lymphokine production in T-cell cultures.

An enhancement effect of mouse erythrocyte rosette forming (MERF) cells on the production of migration inhibitory factor, chemotactic factor for neutrophils and skin reactive factor in T-lymphocyte cultures stimulated with the purified protein derivative of tuberculin was observed. We consider it likely that the MERF cells, possessing the appropriate cell surface constituents to construct an immunogenic moiety, present antigen on their surfaces to elicit lymphokine production.

Relationship of mouse erythrocyte binding receptor on peripheral blood mononuclear cells to receptors for IgG Fc and C3.

When peripheral blood mononuclear cells separated at 4 degrees C were incubated at 37 degrees C, they shed their surface receptors. Total absorption of the released mouse erythrocyte binding receptors from the supernatant of the cell suspension with mouse erythrocytes did not lead to a change in the IgG Fc and C3 receptor content of the supernatant. On removal of the C3 or IgG Fc receptors, the quantity of mouse erythrocyte binding receptor remained unchanged.

A comparative study of the inhibitory effect of trypan blue on mouse erythrocyte and C3 binding receptors of peripheral blood mononuclear cells from healthy donors and patients suffering from chronic lymphocytic leukaemia.

Trypan blue has previously been shown to interact with the C3 receptor, but not with the Fc receptor. In the present work the effects of Trypan blue on mouse erythrocyte (ME) and C3 binding receptors of the peripheral blood mononuclear cells have been studied in healthy individuals and in patients with chronic lymphocytic leukemia (CLL). The resulting dose-response curves have been compared with each another.

Inhibitory effect of C3b on rosette formation of peripheral blood mononuclear cells with mouse erythrocytes.

The inhibitory effect of C3b on the mouse erythrocyte and C3 binding receptors of peripheral blood mononuclear cells have been studied. The results of statistical analysis indicate that there is not a significant difference between the effects of C3b on the two receptors.

Regulation of lymphokine production in peripheral blood mononuclear cell cultures.

An increase in the production of macrophage migration inhibitory factor, chemotactic factor for neutrophils, and skin reactive factor, was observed in lymphocyte cultures if the cells were allowed to age in culture for 24 h. The increased lymphokine production was reduced by adding concanavalin A-stimulated and mitomycin C-treated suppressor cells. It is suggested that the lymphokine production could be regulated by suppressive mononuclear cells.