Rippled-pattern trichomatricoma

A hair matrix tumor showing an unusual tumor cell arrangement was found at the base of a solitary trichoepithelioma. Coexisting with solid epithelial islands and immature hair follicle-like stroma resembling the Verocay bodies of neurilemmoma or "ripplemarks" on waves were found. In other areas myxomatous degeneration of the stroma changed the rippling into a cribriform pattern. In some parts of the tumor there was a dense melanin pigment associated with MEL5 stained melanocytes. S-100 and CD1 (OKT6) antigen stains demonstrated Langerhans cells scattered in the parenchyma and less frequently in the stroma. The majority of tumor cells were considered immature pilar cortical cells because of the following: 1. HKN-6 was strongly positive; 2. a large number of melanocytes were associated with tumor cells in some foci; 3. ultrastructurally immature tumor cells, which had electron-dense tonofilaments and many desmosomes, were transformed without production of trichohyalin granules into semikeratinized cells which showed nuclear degeneration and loss of electron density in tonofilaments. This tumor, however, has not attained the degree of differentiation observed in trichoblastoma (1) another example of an immature cortical cell tumor. Squamous eddy-like or horn pearl-like foci of incomplete keratinization and large keratin-filled cysts were also present within the immature parenchyma, indicating that some immature cells were differentiating toward non-cortical cells, as found in the outer sheath. We would like to designate this tumor "rippled pattern trichomatricoma", a new entity.     

Immunologic immaturity, but high IL-4 productivity, of murine neonatal thymic CD4 single-positive T cells in the last stage of maturation

To determine the levels of maturation and differentiation ofmurine CD4 single-positive (SP) T cells, we compared the secondaryresponses of staphylococcal enterotoxin A (SEA)-induced neonatalthymic, adult thymic and adult splenic CD4 SP T cell blastsprepared from whole or heat-stable antigen^low CD4 SP T cells.Proliferative responses upon re-stimulation with SEA were strongin adult splenic CD4 SP T cell blasts, but quite weak in neonatalthymic and adult thymic CD4 SP T cell blasts. SEA-induced IL-2production was weaker in neonatal thymic blasts than in theadult splenic CD4 SP T cell blasts. In contrast, SEA-inducedIL-4 production was high in neonatal thymic CD4 SP T cell blasts,and low in adult splenic and thymic CD4 SP T cell blasts. Expressionof GATA-3, that directs production of IL-4 in T cells, examinedat protein and mRNA levels, was higher in neonatal thymic cellsthan in adult thymic and splenic cells. These results suggestthat neonatal and adult thymic CD4 SP T cells in the final stageof maturation are relatively immature compared with adult splenicCD4 SP T cells. The cytokine production profile of neonatalthymic CD4 SP T cells suggests that they are inclined towardsa T_h2 response.     

Antibody-dependent cellular cytotoxicity (ADCC)-mediated destruction of human immunodeficiency virus (HIV)-coated CD4+ T lymphocytes by acquired immunodeficiency syndrome (AIDS) effector cells

The acquired immunodeficiency syndrome (AIDS) is defined in clinical terms by the development of Kaposi's sarcoma and/or severe opportunistic infections in persons without predisposing conditions. A hallmark of the syndrome has been a decrease in the number of CD4⁺ T helper cells. The reduction in the frequency of the CD4⁺ lymphocytes has been postulated to be primarily the result of human immunodeficiency virus (HIV) tropism and cytophathogenicity for the T-cell subset. Yet only a small percentage of cells is actually infected with HIV. Recently, we provided evidence indicating that AIDS patients' natural killer cells can mediate normal levels of antibody-dependent cellular cytotoxicity (ADCC) despite exhibiting a defect in natural killer (NK) effector function (J Immunol 139:55, 1987). This finding prompted us to investigate whether AIDS patients' effector cells could mediate ADCC against circulating CD4⁺ T cells infected with or expressing HIV antigen. The findings reported herein demonstrate that AIDS effector cells can mediate lysis of CEM (CD4⁺ T-cell line) coated with HIV protein in the presence of HIV-specific antibody. Lysis was specific, as non-HIV-coated CEM or the addition of HIV-negative serum resulted in no lysis. We then examined HIV-coated peripheral blood-derived CD4⁺ T lymphocytes as targets in ADCC. We demonstrate that in the presence of HIV-specific antibody, HIV-coated CD4⁺ T lymphocytes serve as targets for ADCC by AIDS effector cells. The lytic activity obtained with AIDS effector cells was comparable to that obtained with normal effector cells. These results demonstrate that AIDS effector cells can mediate ADCC against HIV-coated CD4⁺ T lymphocytes and suggest that ADCC may play a rolein vivo in the pathogenesis of AIDS.     

Granuloma formation and hemopoiesis induced by C36-48-mycolic acid-containing glycolipids from Nocardia rubra

As previously reported (I. Yano, I. Tomiyasu, S. Kitabatake, and K. Kaneda, Acta Leprologica 2:341-349, 1984), Nocardia rubra, one of the nonpathogenic actinomycetes, possesses three classes of mycolic acid-containing glycolipid, i.e., glucose mycolate, trehalose dimycolate, and trehalose monomycolate. The carbon chain length of their mycolic acids is shorter (C36-48) than that in mycobacteria (longer than C70), and the glycolipid consists of only alpha-mycolic acid. One intravenous administration of 500 micrograms of each purified glycolipid to ICR mice in the form of water-in-oil-in-water emulsion without any protein antigens caused prominent granuloma formation in the lungs, spleen, and liver. The lung index in the treated mice was about 3.5 times larger than that in the control mice (given water-in-oil-in-water emulsion only) at 1 week after the injection and then rapidly declined, while spleen and liver indices peaked at 2 weeks after the injection and persisted longer. The granuloma consisted of macrophages, some of which phagocytized glycolipid micelles, lymphocytes, monocytes, and neutrophils. In addition, many small hemopoietic islands were observed in the liver sinusoids, where various immature blood cells were trapped by the prominent cytoplasmic projections of Kupffer cells. The granuloma formation and hemopoiesis observed here are considered to be the most characteristic morphological expression of macrophage activation in these organs. This is the first report to show that such histological changes can be induced by chemically defined and homogeneous mycolic acid-containing glycolipids other than those of mycobacteria.     

Investigation of initial changes in the mouse olfactory epithelium following a single intravenous injection of vincristine sulphate

To investigate initial changes in the olfactory epithelium, vincristine sulphate (VCR) was administered intravenously once to male BALB/c mice on day 1 in comparison with unilateral bulbectomy (UBT). The light and electron microscopy of the olfactory epithelium, nerve and/or bulb with BrdU-morphometry was performed sequentially. Further, whole-body radioluminography was conducted at 1 and 24 hours postdose. Apoptosis and an increased number of mitotic cells with a tendency toward decreasing BrdU-positive olfactory epithelial cell counts were observed in olfactory epithelial cells at 6 hours postdose of VCR and became more pronounced at 24 hours postdose. These changes disappeared on days 4 or 15, but minimal axonal degeneration was seen in the olfactory nerve from day 4 onward. Semiquantitative measurement of VCR levels in the ethmoturbinals elicited high drug retention even 24 hours after administration. In contrast, UBT showed no effect on mitosis and BrdU-positive cell counts at 6 hours postdose, but severe lesions in the olfactory epithelium and nerve were seen on days 2, 4, and/or 15. The above results suggest that the initial event of VCR-induced apoptosis in the mouse olfactory epithelium would be mitotic arrest with high drug retention, unlike that evoked by UBT.     

Case of minocycline-induced pneumonitis with bilateral pleural effusion]

A 51-year-old man was admitted to our hospital with fever, dry cough and dyspnea. He had taken minocycline for 11 days because of urinary tract infection. Chest X-ray on admission showed diffuse reticular shadows in bilateral lung fields with bilateral pleural effusion. Cessation of minocycline led to spontaneous improvement of symptoms and radiographic findings. The lymphocyte stimulation test for minocycline with peripheral blood and pleural effusion were negative. After provocation test with minocycline, he developed fever and dry cough and bilateral ground glass opacity appeared on his chest X-ray. He was diagnosed as minocycline-induced pneumonitis and recovered rapidly following corticosteroid therapy.     

Development of enrofloxacin ELISA using a monoclonal antibody tolerating an organic solvent with broad cross-reactivity to other newquinolones

Antibacterial reagents, especially quinolones, are widely used in animals and humans, and have caused serious problems to human health because of their residual contaminants in food. In order to screen for different kinds of newquinolones at the same time, a sensitive and specific enzyme-linked immunoassay (ELISA) has been developed. The anti-enrofloxacin monoclonal antibody was selected because of its ability to react with structurally related newquinolones in organic solvent. The antibody has 100% cross-reactivity with norfloxacin, ciprofloxacin and other newquinolones at 50% inhibition of control values IC₅₀, but not with nitroflazone, sulphadimethoxine. The lowest detection limit of this ELISA was 0.7 ng/ml (ppb) when enrofloxacin was used as the calibrator. Eel extracts were spiked with enrofloxacin and the average recoveries at 10, 50, 100 ng/ml were 98, 102 and 91%, respectively. The proposed ELISA is a useful method for the practical microquantitation of various newquinolones in biological and environmental specimens.