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[Investigation of CD68 positive monocytes/macrophage(CD68+ Mo/M phi) in urine and infiltrated tissue of various kidney diseases in children].

In order to investigate the participation of monocytes/macrophages(Mo/M phi) in the progression of various kidney diseases of children, Mo/M phi in urine and that infiltrating renal tissue were both measured as the number of CD68 positive Mo/M phi (CD68+ Mo/M phi), using anti-CD68 antibody. The number of CD68+ Mo/M phi infiltrating in one glomerulus was significantly higher in Henoch-Schönlein purpura nephritis(HSPN) (p < 0.01) in comparison with that in minimal change nephrotic syndrome(MCNS) (p < 0.01), and a high tendency was found in IgA nephropathy (IgAN), proliferative glomerulonephritis (non-IgAN), focal segmental glomerulosclerosis(FSGS) and membranoproliferative glomerulonephritis (MPGN), respectively. The number of CD68+ Mo/M phi infiltrating one mm2 of tubulo-interstitium area was significantly higher in HSPN(p < 0.05), FSGS(p < 0.01), Alport's syndrome(p < 0.01), respectively, than that in MCNS. The number of CD68+ Mo/M phi in one milliliter of urine correlated significantly with both that infiltrating the glomerulus and the tubulo-interstitium(both p < 0.01). Moreover the number of urine CD68+ Mo/M phi in a clinically active stage was significantly higher than that in an inactive stage in the AGN(p < 0.05), IgAN(p < 0.05), HSPN(p < 0.05), non-IgAN(p < 0.01) and MPGN groups(p < 0.05), respectively. From these results, 1) It was suggested that the Mo/M phi infiltrating renal tissue participated in the development of various kidney diseases. 2) It was predicted that CD68+ Mo/M phi in urine reflected both the number of Mo/M phi infiltrating the glomerulus and that in the tubulo-interstitium. 3) It was suggested that the number of CD68+ Mo/M phi in urine indicated clinical activity in proliferative glomerulonephritis groups of children.

Adolescent↗

Increased mast cell infiltration in familial varicose veins: pathogenetic implications?

AIM: Increased infiltration of activated mast cells has been recently implicated in the pathophysiology of varicose veins. The aim of the present study was to investigate a possible association between mast cell infiltration of primary varicose veins and clinical features, which could clarify further varicose vein pathophysiology. METHODS: Seventeen patients, operated on for primary varicose veins and greater saphenous vein incompetence, participated in the study. Mast cells, distributed within the adventitia of grossly abnormal segments of the greater saphenous vein and calf varicosities removed during surgery, were identified and measured in stained tissue sections. The mast cell count, expressed as mast cells per 10 high-power fields, was subsequently associated with clinical features, including age, gender, body mass index, familial varicose veins, duration of varicose vein disease and relation to previous pregnancies, leg symptoms and findings on physical examination, clinical class and score of chronic venous insufficiency (CEAP classification). RESULTS: Patients with family history of varicose veins (n=7) had a significantly increased mast cell infiltration (median, interquartile range) of the abnormal venous segments (16, 8.4) in comparison with those (n=10) without such a history (9.2, 7.3), p=0.005. Mast cell infiltration had a significant inverse association with age (r= -0.49, p=0.046), but not with the remaining clinical features. CONCLUSION: Our findings support the hypothesis that the increased mast cell infiltration in varicose veins is not a consequence of venous hypertension. Furthermore, the increased mast cell infiltration in familial varicose veins implies a rather primary role and therefore the presence of a distinct pathophysiology. Further investigation testing the activity of mast cells in cases of family history might reveal another step in the pathogenic mechanism of varicose veins, leading to a more rational treatment.

Adult↗

[Effect of a leukotriene B4 antagonist on substance P-induced granulocyte infiltration in mouse skin].

Substance P causes granulocyte (neutrophil and eosinophil) infiltration in mouse skin by inducing mast cell degranulation. However, the mediator responsible for this granulocyte infiltration has not been determined. In this study, we examined the effect of a leukotriene B4 (LTB4) antagonist ONO-4057 on substance P-induced granulocyte infiltration in the skin of BALB/c mice. Pretreatment with the LTB4 antagonist decreased substance P-induced neutrophil and eosinophil infiltrations in mouse skin at 6 h to the same extent that an inhibitor of mast cell degranulation disodium cromoglycate decreased those responses. The LTB4 antagonist also decreased substance P-induced neutrophil, but not eosinophil, infiltration in mouse skin at 24 h. We conclude that LTB4 is a major mast cell-derived chemotactic mediator for initiating substance P-induced neutrophil and eosinophil infiltrations in mouse skin.

Animals↗

[A study on the thermal expansion characteristics of Alumina-zirconia nano-composite infiltrated ceramic].

OBJECTIVE: To study the characteristics of thermal expansion of the alumina-zirconia nano-composite infiltrated ceramic. METHODS: The thermal expansion coefficients of alumina-zirconia composite matrix, infiltrating glass and infiltrated ceramic were determined by various methods, respectively. RESULTS: The coefficients of thermal expansion of composite matrix with 10 wt%, 20 wt% and 30 wt% zirconia were 7.607, 7.690 and 8.111 microns/(m. degree C) respectively. The thermal expansion coefficients of AZ-8 and AZ-10 infiltration glass were 6.867 and 7.333 microns/(m. degree C), respectively. The thermal expansion coefficient of infiltrated ceramic was 8.413 microns/(m. degree C). CONCLUSION: The thermal expansion coefficients of the glass and composite matrix matched well. The thermal expansion coefficients of the alumina-zirconia nano-composite infiltrated ceramic and several common veneering porcelains matched well, too.

Aluminum Oxide↗

Lymphocytic infiltration and expression of inducible nitric oxide synthase in human duodenal and colonic mucosa is a characteristic feature of ankylosing spondylitis.

OBJECTIVE: In patients with ankylosing spondylitis (AS), inflammatory processes have been detected in the ileal and colonic mucosa. The inducible isoform of nitric oxide synthase (iNOS) may be expressed early in the inflammatory process. We investigated iNOS activity and lymphocytic infiltration in the duodenum and colon in patients with AS and ulcerative colitis compared with controls. METHODS: Gastroscopy with duodenal biopsies and/or colonoscopy with biopsies were conducted in 42 patients with AS treated or not treated with nonsteroidal antiinflammatory drugs (NSAID), in 15 with ulcerative colitis, and in 46 controls. Lymphocytic infiltration in the lamina propria and intraepithelial infiltration were quantified by histological score. iNOS expression was assessed by immunohistochemistry with monoclonal antibodies, and iNOS activity was determined by radiochemical assay. RESULTS: Endoscopic examination of the gastroduodenal or colonic mucosa did not reveal macroscopic lesions in the AS patients. In the duodenum, mucosal lymphocytic infiltration was found in 83.3% of the AS group compared to 48.6% of controls (p = 0.02), and was independent of the NSAID intake. Intraepithelial lymphocyte infiltration was increased in both duodenum and colon in AS patients compared to controls. iNOS activity in duodenum and colon and expression of iNOS protein in lamina propria inflammatory cells was increased in AS patients compared to controls. CONCLUSION: Lymphocytic infiltration and iNOS expression and activity were detected in duodenal and colonic mucosa from patients with AS. Such findings may indicate an inflammatory process in the small intestine and colon of patients with AS.

Adult↗

Eosinophil infiltration and enhancement of airway reactivity by leukocyte chemotactic factor, formyl-methionyl-leucyl-phenylalanine (fMLP), in guinea pigs.

N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) is a bacterial-derived chemotactic factor for eosinophils and neutrophils. This study is aimed to examine whether or not eosinophil infiltration induced by intra-airway administration of fMLP causes the damage of the bronchial epithelium and results in airway hyperresponsiveness in normal non-sensitized guinea pigs. In normal guinea pigs fMLP administered by aerosol inhalation or intratracheal injection caused significant infiltration of eosinophils in the tracheal mucosa and enhanced bronchial reactivity to inhaled histamine 6 and 24 hours after exposure. Electron microscopic examination showed damage of the alignment of the epithelial cells in the bronchial mucosa in fMLP-treated guinea pigs. PAF antagonists CV3988 and WEB2086 and a 5-lipoxygenase inhibitor (AA-861) did not prevent fMLP induced eosinophil infiltration, which suggests that fMLP caused eosinophil infiltration mainly by its chemotactic activity, not by the release of platelet activating factor (PAF) or leukotrienes in this experimental condition. These results showed that in normal guinea pigs a bacteria-derived chemoattractant of fMLP could reproduce a sequence of eosinophil infiltration and airway hyperresponsiveness, similar to the inflammatory pathophysiology after antigen challenge in sensitized animals. We concluded that eosinophil infiltration induced by either immunological or non-immunological mechanisms can cause airway damage and airway hyperresponsiveness.

Administration, Inhalation↗

CA-125 and placental protein 14 concentrations in plasma and peritoneal fluid of women with deeply infiltrating pelvic endometriosis.

OBJECTIVE: To investigate the plasma and peritoneal fluid (PF) concentrations of CA-125 and placental protein (PP14) in women with deeply infiltrating endometriosis. DESIGN: Plasma and PF were collected during 384 consecutive laparoscopies for pelvic pain or infertility. MAIN OUTCOME MEASURE: The presence and extent of endometriosis were carefully assessed, including the area, depth of infiltration, and volume of subtle lesions, typical lesions, and endometriomas. The day of the menstrual cycle was ascertained by endometrial biopsy and/or basal body temperature charts. RESULTS: Peritoneal fluid concentrations were some 100 and 10 times higher than plasma concentrations for CA-125 and PP14, respectively. Cyclic variations of CA-125 concentrations were only found in women with endometriosis showing increased plasma concentrations at the end of the cycle and increased PF concentrations in the early follicular phase. Cyclic variations of PP14 concentrations were found in women with and without endometriosis both in plasma and PF showing increased concentrations in the late luteal and early follicular phases. In women with endometriosis the increased plasma concentrations of PP14 and CA-125 correlated with the presence and volume of endometriomas and of deeply infiltrating endometriosis. The increased concentrations in PF correlated only with the pelvic area of subtle endometriotic lesions. The diagnostic sensitivity and specificity of CA-125 for endometriosis were 25% and 87%, respectively, and for endometriomas and/or deeply infiltrating endometriosis 36% and 87%, respectively, for a cutoff concentration of 25 U/mL. CONCLUSION: Superficial pelvic endometriosis secretes PP14 and CA-125 mainly toward the PF, whereas endometriomas and deeply infiltrating endometriosis secrete mainly toward the plasma. The increased plasma concentrations of CA-125 are most pronounced during the late luteal phase, and endometriomas and/or deeply infiltrating endometriosis can be detected with a sensitivity of 36% and a specificity of 87%.

Analysis of Variance↗

Surface biosolids application: effects on infiltration, erosion, and soil organic carbon in Chihuahuan Desert grasslands and shrublands.

Land application of biosolids is a beneficial-use practice whose ecological effects depend in part on hydrological effects. Biosolids were surface-applied to square 0.5-m2 plots at four rates (0, 7, 34, and 90 dry Mg ha(-1)) on each of three soil-cover combinations in Chihuahuan Desert grassland and shrubland. Infiltration and erosion were measured during two seasons for three biosolids post-application ages. Infiltration was measured during eight periods of a 30-min simulated rain. Biosolids application affected infiltration rate, cumulative infiltration, and erosion. Infiltration increased with increasing biosolids application rate. Application of biosolids at 90 dry Mg ha(-1) increased steady-state infiltration rate by 1.9 to 7.9 cm h(-1). Most of the measured differences in runoff among biosolids application rates were too large to be the result of interception losses and/or increased hydraulic gradient due to increased roughness. Soil erosion was reduced by the application of biosolids; however, the extent of reduction in erosion depended on the initial erodibility of the site. Typically, the greatest marginal reductions in erosion were achieved at the lower biosolids application rates (7 and 34 dry Mg ha(-1)); the difference in erosion between 34 and 90 dry Mg ha(-1) biosolids application rates was not significant. Surface application of biosolids has important hydrological consequences on runoff and soil erosion in desert grasslands that depend on the rate of biosolids applied, and the site and biosolids characteristics.

Conservation of Natural Resources↗

Metal concentrations in soil and seepage water due to infiltration of roof runoff by long term numerical modelling.

The qualitative effects of stormwater infiltration on soil and seepage water are investigated with long term numerical modelling. The retention behaviour of different soils and materials used in infiltration devices is determined with batch and column tests. Results of the laboratory tests are adsorption isotherms which represent input data for numerical transport modelling. The long term simulations are performed with combinations of different solutions (types of roof runoff) and infiltration devices (swale and trench) under different hydrogeological conditions. The presented results contain the infiltration of low polluted roof runoff, runoff from a roof with zinc sheets and from a roof with copper sheets concerning the heavy metals zinc, copper and lead. The increase of concentrations in the infiltration body is high. For the infiltrated water, the results show a migration to groundwater only for the low adsorbing soil.

Adsorption↗

Early ocular chemokine gene expression and leukocyte infiltration after high-risk corneal transplantation.

PURPOSE: To determine the differential gene expression of chemokine species and leukocyte infiltration of grafts in the early pre-rejection postoperative period after high-risk (HR) compared to normal-risk (NR) corneal transplantation. METHODS: Fully mismatched and syngeneic corneal grafts were performed in NR (avascular) and HR (vascularized) recipient beds of BALB/c murine hosts. Gene expression levels of a panel of chemokines were determined by a multiprobe ribonuclease protection assay system. The profiles of infiltrating cells into the corneal grafts at the same times were determined immunohistochemically. RESULTS: Compared to NR transplantation, HR eyes exhibited significantly higher mRNA levels for macrophage inflammatory protein (MIP)-2 and monocyte chemotactic protein-1 (MCP-1) on day 1, and for eotaxin on days 1 and 3 after transplantation. By day 6 after transplantation, still well before graft rejection, significantly higher levels of RANTES, eotaxin, MIP-1alpha, MIP-1beta, MIP-2, and MCP-1 were detected in HR eyes. The overexpression of MIPs in HR eyes correlated with a significant increase in the number of infiltrating macrophages (p<0.01), and neutrophils (p<0.05) in HR compared to NR recipients. Low levels of eosinophil and mast cell infiltration were observed in all grafts, with a modest increase in mast cell infiltration (p<0.05) in HR compared to NR grafts. CONCLUSIONS: These results suggest that increased expression of gene products for select chemokines, in particular those that mediate recruitment of innate immune cells, in the early period after HR corneal transplantation is related to the enhanced leukocytic infiltration of grafts observed in HR keratoplasty.

Animals↗

[Is intracavernosal corticosteroid infiltration really useless in Peyronie's disease?].

UNLABELLED: The value of intracavernosal corticosteroid infiltration remains controversial or may even be contraindicated in Peyronie's disease, as it is considered to be ineffective and a source of morbidity. OBJECTIVE: To retrospectively analyse the efficacy and safety of intracavernosal corticosteroid infiltration in a selected population only presenting clinical criteria of the acute phase of Peyronie's disease (pain and/or recent onset < 6 months). MATERIAL AND METHOD: Intracavernosal corticosteroid infiltration (weekly or twice-weekly) was performed in or around the plaque. Evaluation was based on clinical criteria according to the course of pain, the nodule and curvature and the rates of improvement, resolution, stabilization and deterioration of these criteria were studied. RESULTS: In a series of 271 patients, 123 presented criteria of the acute phase of Peyronie's disease. Forty five of these patients were treated exclusively by intracavernosal corticosteroid infiltration. The mean age was 52 +/- 8 years. The number of intracavernosal infiltrations was usually less than 10 (n = 40) with less than 8 injections in the majority of patients (n = 36). Follow-up was 6 months. There were no cases of clinical deterioration. The best results were observed on pain, which decreased (13.6%) or totally resolved (61.4%). Curvature was decreased (20.5%), the plaque decreased (25%) or disappeared (9%). When intracavernosal corticosteroid infiltration is ineffective, it appears useless to administer more than 3 injections. No morbidity was observed. CONCLUSION: In our population, the reputation of inefficacy and morbidity of local corticosteroid therapy appears to be unjustified. There were no cases of deterioration, but, on the contrary, stabilization and especially very marked and rapid efficacy on pain, but a lesser efficacy on curvature and plaque. Local steroid therapy appears justified during the acute phase, as the injection allows corticosteroids to exert their anti-inflammatory action in situ in line with the pathophysiology of the disease. A standardized, multicentre, prospective, randomized, placebo-controlled study could confirm our impressions.

Adrenal Cortex Hormones↗

Cellular infiltrate, major histocompatibility antigen expression and immunopathogenic mechanisms in cardiac myosin-induced myocarditis.

Immunization with cardiac myosin induces severe myocarditis in genetically predisposed mice. The disease closely parallels that seen after infection with Coxsackievirus B3 and is characterized by a diffuse interstitial cellular infiltrate. To analyze the immunopathologic events in the heart tissue of cardiac myosin-immunized A/J and A.SW mice, the phenotype of inflammatory cells and the expression of class I and class II major histocompatibility (MHC) antigens (Ag) was examined at different time points using the immunoperoxidase method. On day 14 after the initial immunization, very few inflammatory cells were seen, whereas on day 21 the lesions were severe and extended over the whole ventricular wall. At both time points tested, the inflammatory infiltrate was composed of Mac-1+ cells, representing 70 to 80% of the infiltrate, and Thy-1.2+ cells, representing 20 to 25%. These Thy-1.2+ cells consisted of CD4+ cells and to a lesser extent of CD8+ cells. Essentially, no B cells were found on day 14, and on day 21 their frequency was only 1 to 2%. Furthermore, massive Ig deposits were observed along the infiltrated myofibers. Both on day 14 and 21, MHC class II Ag expression was associated with cells of the inflammatory infiltrate, but no aberrant I-A Ag expression was found on endothelial cells of coronary vessels or on myofibers. Similarly, no increased MHC class I Ag expression was seen on myofibers on day 14. However, on day 21 the infiltrated myofibers did show an increase in surface MHC class I Ag expression, thereby suggesting that this phenomenon is a consequence of the inflammatory process. Furthermore, in vivo administration of monoclonal antibodies to either CD4 or CD8 protected cardiac myosin-immunized mice from myocarditis, and a similar effect was achieved by monoclonal antibody to I-A Ag. Thus, cardiac myosin-induced myocarditis is mediated by a cooperation between CD8+ cells and MHC class II restricted, i.e., CD4+ cells.

Animals↗

[Pathology of the placenta. VIII. Asphyxial infiltrates of the placenta].

Asphyxial infiltrates of the afterbirth (umbilical cord and placenta) are believed to be non-inflammatory round-cell to leucocytic infiltrates on the following sites: wall of greater vessels of umbilical cord, chorionic membrane, and, less often, stem villi as well as in the chorionic membrane proper. There has also been cellular to primarily leucocytic subchorial demarcation, usually between chorionic plate and Langhans fibrin or even in Langhans fibrin. Also recorded were parietal thrombi in greater arteries of chorionic membrane and stem villi, usually in concomitance round-cell infiltration of the arterial wall in the sense of asphyxial infiltrates. Those alterations are considered to be an entity associated to intra-uterine foetal asphyxia, with extended duration of parturition being though to play a particular role as a trigger factor of asphyxia. The author's own investigations of such alterations to afterbirths from high-risk pregnancies as well as to a consecutive series of newborns without increased risk have shown for either group that no statistical relationship existed between high-risk factors of asphyxia prior to or during labour, on the one hand, and such asphyxial infiltrates, on the other, not even in cases of prolonged labour. While we are not in a position at present to clearly define this complex in terms of genetic causality, we should like to maintain it under the heading of "asphyxial infiltrates" for the purpose of placental diagnosis.

Chorion↗

Interleukin 2 and granulocyte-macrophage colony-stimulating factor induce a perivascular lymphocytic infiltrate in a skin explant model.

Cutaneous eruptions displaying perivascular inflammatory cell infiltrates histologically may develop with the intravenous administration of cytokines. Similar findings are seen spontaneously in some patients on recovery of peripheral blood lymphocytes after profound marrow aplasia. To investigate the production of a cutaneous perivascular infiltrate further, the ability of several cytokines to induce a perivascular lymphocytic infiltrate was studied in vitro using a skin explant model. A skin biopsy specimen obtained at the time of peripheral blood lymphocyte recovery after chemotherapy-induced marrow aplasia (n = 10) was divided and incubated for 3 days with and without a series of cytokines plus various peripheral blood mononuclear cell populations. Skin incubated with interleukin 2 and granulocyte-macrophage colony-stimulating factor induced a perivascular lymphocytic infiltrate, while control samples did not. Immunophenotypic analysis revealed that the lymphocytes were predominantly CD3+/CD4+. An infiltrate was not observed when skin was incubated with cytokines alone, without the addition of simultaneously isolated peripheral lymphocytes. A perivascular pattern was not observed with the addition of interferon gamma. Only interferon gamma induced keratinocyte intercellular adhesion molecule 1 expression in experimental tissue. Certain cytokines that affect a range of cell types are capable of inducing a common cutaneous histologic pattern, the perivascular lymphocytic infiltrate.

Adult↗

[Clinical course of infiltrative tuberculosis in adolescents].

The course of infiltrative tuberculosis making up 53.2% in the pattern of clinical forms was investigated in 64 adolescents. Infiltrative tuberculosis morbidity among the girls is 3 times higher. The main detection method is represented by a planned roentgenofluorographic examination, since in the region in question infiltrative tuberculosis tends to have limited symptoms in 56.2% of the adolescents, including 30.5% of them even with disseminated process. In 60.9% of the cases, infiltrative tuberculosis is observed to have a decomposition phase which is 4.5 times more frequently traced in patients living in contact with a bacillary ++carrier . In 8% of the patients, infiltrative tuberculosis was complicated by hemoptysis. Infiltrative tuberculosis in 32.8% of the adolescents manifests itself in a pulmonary form of primary tuberculosis. Due to a complex treatment hemodynamic indices are normalized by the end of the first month in addition to the removal of the intoxication signs by the third month. Cavity closure was achieved in 71.8% of the patients. Despite the given therapy, transformation into the destructive forms of tuberculosis took place.

Adolescent↗

[Characterization of lymphocytic infiltrate cells in bullous pemphigoid and pemphigus vulgaris].

By means of monoclonal antibodies (mab) and alkaline phosphatase anti-alkaline-phosphatase (APAAP) technique, the distribution and characteristics of lymphocytic infiltrates were studied in biopsies from 15 patients with bullous pemphigoid (b.P.) and 5 patients with pemphigus vulgaris (P.v.). The biopsies were obtained from freshly developed blisters along with perilesional tissue. The lymphocytic infiltrates in b.P. as well as in P.v. were located in the area of the fresh lesions and consisted almost exclusively of T cells (CD3 positive lymphocytes). In b.P., the discrepancy between a decreased number of CD2 positive lymphocytes (10-20%) and markedly higher number of CD3 staining cells (50-60% of all infiltrate cells) was striking. The characterization of the T cell subpopulations in both dermatoses showed mainly T helper cell infiltrates (CD4), while only up to 10% of T suppressor cells (CD8) were detected. CD45R positive (CD4+/CD45R+: suppression inducing) as well as CD29-positive (CD4+CD29+: cells which provide help for antibody production) T-cell subpopulations were detected in both dermatoses particularly adjacent to blister in up to 10% of the cell infiltrates. Epidermal staining with CD29 mab in b.P. up to the stratum spinosum and in P.v. within intraepidermal blisters was detected. By means of CD19 and CD21 mab B lymphocytes were minimal. Perivascular individual cell staining occurred with CD7 CD16, CD56 and CD57 mab (K/NK cells) in b.P. as well as in P.v. patients. The predominance in T cell infiltrates, particularly T helper cells, suggests the role of cellular immune mechanism in the pathogenesis of these diseases, in b.P. the CD2 antigen (SE receptor) appears to be of particular importance.

B-Lymphocyte Subsets↗

Flow cytometric enumeration of mononuclear cell populations infiltrating the islets of Langerhans in prediabetic NOD mice: development of a model of autoimmune insulitis for type I diabetes.

Type I, insulin-dependent diabetes (IDD) in man and the NOD (non-obese diabetic) mouse is believed to result from an autoimmune destruction of pancreatic beta (beta) cells. In both species the pathologic correlate of this destruction is a peri- and intra-islet immune cell infiltrate, referred to as insulitis, easily recognized histologically. Although histologic studies of insulitis have established the autoimmune nature of IDD, controversy remains concerning the phenotypes and especially function of the islet-infiltrating immune cells. In the present study, we reveal a new protocol which permits enumeration of islet-infiltrating leukocytes using flow cytometry (FACS). Using this technique, we have analyzed systematically the changes in major leukocyte phenotypes during the development of the insulitis lesion. Results indicate that: 1) the first islet-infiltrating leukocytes are class II+, Ig- monocytes and CD8+ T lymphocytes, 2) after a slight decrease in the CD8+ cell population, an influx of CD4+ T lymphocytes occurs, accompanied by increasing numbers of CD8+ T cells, as well as IgM+ and IgG+ B lymphocytes, 3) whereas all the IgM+ B cells appear to be CD5+, between 70-95% of IgG+ B cells express CD5, and 4) throughout the response, the class II+, IgG-cell population remains relatively constant. These data, together with our previous work showing that autoantibody binds to pancreatic beta cells prior to leukocytic infiltration, permit construction of a working model for the natural history of insulitis in the NOD mouse. Briefly, the initial cellular response against the beta cell, which begins between 5-7 weeks of life, appears to be a local inflammation in which class II-positive macrophages and CD8-positive cells (possibly with antibody-dependent cell-mediated cytotoxic potential) infiltrate the islet. Finally, T helper cells are activated, traffic briefly through the islet, and elicit a B lymphocyte and T killer cell invasion of the islet that ultimately leads to beta cell necrosis.

Animals↗

CD8+ cutaneous T-cell lymphoma with pagetoid epidermotropism and angiocentric and angiodestructive infiltration.

A 68-year-old woman had a peculiar clinical course of cutaneous lymphoma. She first developed nonpuritic erythematous macules with fine scales followed by development of erythematous infiltrated plaques. The clinical course could be interpreted as that of mycosis fungoides. Histologically, the lesions showed pagetoid infiltration of atypical lymphoid cells. Suddenly, with high fever, numerous purpuric, ulcerated, or crusted plaques with underlying infiltration or nodules began to appear on most areas of the patient's body. Biopsy specimens of the lesions revealed angiocentric and angiodestructive infiltration by neoplastic T cells and marked epidermotropism of these cells. These atypical cells immunohistochemically had CD8+ surface phenotype. The patient died of respiratory insufficiency due to acute pulmonary infiltration. Autopsy demonstrated angiocentric and angiodestructive lymphomatous infiltration in the lung.

Aged↗