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Notes: Abstract Wide variations in susceptibility to skin tumor development by chronic ultraviolet light (UV) exposure and antigenicity of induced tumors which is estimated by tumor rejection in syngeneic recipients have been recognized among various murine strains. To examine the effect of parent genetic background on latency and antigenicity of UV-induced tumors originating in F1 hybrids, we induced skin tumors in three mouse strains: BALB/c, C57BL/6, (B6), and C3H/HeMs (C3H/He), and their F1, hybrids: (BALB/c×C3H/He)F1, (CC3F1), (BALB/c×B6)F1, (CB6F1) and (C3H/He×B6)F1, (C3B6F1) by exposing mice to UV radiation (0.44 mW/ cm2 for 1 h) three times a week, and analyzed whether the UV-induccd tumors originating in F1 hybrids possess the similar property in latency or antigenicity as seen in the UV-induced tumors derived from the parent strains. The latency of tumor induction by chronic UV exposure in C3H/He, BALB/c and their F1, hybrid CC3F1, was relatively short whereas that of B6 was relatively long, and that of F1, hybrids with B6 (CB6F, and C3B6F1) was intermediate. On the other hand, the low antigenicity as progressive growth behavior of UV-induced tumors in syngeneic recipients was observed not only in tumors derived from C3H/He but also in those from F, hybrids with C3H/He (C3B6F1, and CC3F1) whereas most tumors derived from B6, BALB/c and their F1 hybrid CC3F1 were highly antigenic as to be rejected in syngeneic recipients. These findings suggest that the parent genetic quality regulating the susceptibility to tumor induction by chronic UV exposure is co-dominantly inherited into F1 hybrids. On the other hand, that providing the progressive growth behavior of induced tumors appears to be a dominant effect.

Notes: A 59-year-old woman with multiple myeloma at stage IA exhibited recurrent pyoderma gangrenosum of 13 years’ duration. She also had a history of mitral regurgitation and cerebral infarction, but no significant family history was present. In September 1994, she noted a painful erythematous papule on her left foot, which was treated with a topical injection of triamcinolone. It responded well to this treatment at the time, but a similar eruption developed in the same place in February 1995, and enlarged to form an irregularly shaped, punched-out ulcer with surrounding infiltrative erythema despite topical treatment ( 〈link href="#f1"〉Fig. 1). Further, since November 1994, she had noted pain in the right dorsal foot.〈figure xml:id="f1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD843:IJD_843_f1"/〉Necrotic ulcer with an elevated purulent border and pustules on the left footThe laboratory findings showed an elevated concentration of immunoglobulin A (IgA) (607 mg/dL) in the serum and the presence of Bence-Jones protein in the urine. The following examinations revealed normal or negative values: full blood cell count, rheumatoid factor, complement components, cryoglobulin, Treponema pallidum hemagglutination (TPHA), stool test, and chest radiography. The histology of a biopsy specimen from the elevated border of the lesion showed predominant neutrophilic infiltrates in the upper dermis and a diagnosis of recurrent pyoderma gangrenosum was made. Treatment with salazosulfapyridine (2 mg/day) was started. Two weeks of therapy resulted in a poor response, and so systemic administration of prednisone (30 mg/day) was started. As the bacterial culture examination revealed Mycobacterium tuberculosis growth from the surface exudate of the ulcer and a tuberculin test was strongly positive, rifampicin (RFP) and isoniazid (INH) were added. In spite of these therapies, fever increased, the C-reactive protein (CRP) level and white blood cell (WBC) count became elevated, and bilateral multiple shadows were detected on chest roentgenography. Although ethambutol hydrochloride (EB) was added, the laboratory findings remained and the symptoms did not sufficiently respond. Furthermore, she noted a painful, erythematous and edematous swelling on the dorsum of her right foot ( 〈link href="#f2"〉Fig. 2), where an aspiration test disclosed caseous material in the pus. M. tuberculosis was also positively cultured from the pus. Foot roentgenography showed narrowed joint spaces and destruction of the cuneiform bones, suggesting bone and joint tuberculosis. An additional biopsy specimen from the ulcer of the left foot showed a granulomatous infiltration surrounded by multinucleate giant cells ( 〈link href="#f3"〉Fig. 3), and cutaneous tuberculosis was confirmed by a niacin test; polymerase chain reaction was positive. After administration of RFP 0.45 g/day, INH 0.3 g/day, and EB 0.75 g/day for 15 months, the lung shadow disappeared, the ulcer on the left foot was epithelialized, and the swelling on the right foot with a pus-discharging fistula also disappeared.〈figure xml:id="f2"〉2〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD843:IJD_843_f2"/〉Dorsal aspect of the right foot with erythema, swelling, and pain〈figure xml:id="f3"〉3〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD843:IJD_843_f3"/〉Biopsy of the ulcer showing lymphocyte infiltration with plasma cells and multinucleate giant cells

Notes: : Typical papules obtained from a patient with hyperkeratosis lenticularis perstans (HLP) were examined by light and electron microscopy. Dense cellular infiltrate, which consisted mainly of mononuclear cells, was observed in the dermis underlying the lesion. Electron microscopic studies revealed that these cells were mostly lymphocytic cells. In addition, several Langerhans cells were found in the infiltrate, some of which were apposed to the lymphocytic cells. These findings suggested that immunologic reactions via Langerhans cells might occur in HLP and further raises a possibility that Langerhans cells might be involved in the pathogenesis of HLP.

Notes: A 68-year-old man developed pemphigus foliaceus, myasthenia gravis with a spindle cell thymoma, and later died with red cell aplasia. At autopsy, pemphigus affected the oesophageal mucosa, and this finding was confirmed by direct immunofluorescence.In order to clarify the relationship between pemphigus and myasthenia gravis or thymoma, sera from 38 patients with myasthenia gravis were examined. Intercellular epithelial antibodies (IC-AB) at titres of 10-40 were found in 8, when monkey oesophagus was employed as the substrate. IC-AB in sera of patients with pemphigus and or myasthenia gravis did not react to any part of human thymoma, human hyperplastic thymus or monkey normal thymus. Deposits of immunoglobulins or complement were not demonstrated in the human thymoma.

Notes: Deposition of immunoglobulins, complement and fibrinogen on eosinophilic staining cells was investigated using direct immunofluorescence techniques. Serum factor deposition was detected on benign epidermal eosinophilic cells seen in pityriasis lichenoides et varioliformis acuta, sunburn erythema and, in addition, on subepidermal hyaline bodies in lichen planus; no such deposition occurred on neoplastic eosinophilic cells in Bowen's disease and squamous cell carcinoma. The qualitative findings of immunofluorescence microscopy seem to be different in inflammatory and malignant dermatoses.

Notes: An effect of colchicine on the active Arthus reaction in rabbits was investigated in vivo with simultaneous evaluation of in vitro chemotacdc activity of polymorphonuclear leukocytes. Arthus reactions were induced by intracutancous injection of ovalbumin into rabbits prcimmunized with ovalbumin. Colchicine, 1 mg/kg or 2 mg/kg, injected intraperitoneally one hour prior to the induction of the Arthus reaction, suppressed erythema and induration at 12 h, when histology showed decreased numbers of infiltrated polymorphonuclear leukocytes and no apparent vascular damage. Perivascular deposits of C3, suggestive of the presence of immune complexes, persisted to 24 h. In vitro chcmotaxis of polymorphonuclear leukocytes using Boyden chamber techniques revealed suppression of the activity in the colchicinc–treatcd animals at 6 and 12 h.These findings suggest that colchicine inhibits vascular injury by interfering with directional chemotaxis of polymorphonuclear leukocytes to the lesional sites.

Notes: Abstract Six ultraviolet-light(UV)-induced tumors of (BALB/c×C57BL/6)F1 (H-2d/b) mouse origin were analyzed for the effector T cell subsets involved in tumor rejection the MHC class I to which cytolytic T lymphocytes (CTL) are restricted, and the effect of UV radiation on tumor rejection, to characterize their tumor-rejection antigens (TRA) recognized by CTL. All tumors were rejected in syngeneic normal mice but grew progressively in nude mice. CD8+ T cells mediated the antitumor responses for all tumors and CD4+ T cells could also do so for one tumor 6.1B. Each tumor induced potent CTL that recognized the specific TRA in preferential association with MHC class I haplotypes not from H-2b but from H-2d; that is, Kd, Dd or Ld. Profiles of TRA expression on two tumors were obtained by the analyses of their antigen-loss variants. ♀1A codominantly expressed at least four distinct TRA associated with Kd, all of which induced CTL. On the other hand, UV♂ 1 had at least two distinct TRA, one of which, associated with Kd, exclusively induced CTL. However, in the absence of the dominant TRA, another TRA associated with Ld on R95C, a variant of UV♂, 1, induced CTL. Unlike other tumors, R95C grew progressively in short-term-UV-irradiated syngeneic mice. Nude mice reconstituted with a combination of CD4+ T cells from short-term-UV-irradiated mice and CD8+ T cells from normal mice did not reject R95C. An increase in the former T cell population led the reconstituted mice to reject the tumor. These findings suggest some functional defects of CD4+ T cells rather than the generation of suppressor cells in short-term-UV-irradiated mice. The UV-induced tumors used in the present study provide a unique system for analyzing the preferential sorting of TRA as well as for elucidation of the TRA itself.

Notes: Abstract. Six ultraviolet-light(UV)-induced tumors of (BALB/c×C57BL/6)F1 (H-2d/b) mouse origin were analyzed for the effector T cell subsets involved in tumor rejection, the MHC class I to which cytolytic T lymphocytes (CTL) are restricted, and the effect of UV radiation on tumor rejection, to characterize their tumor-rejection antigens (TRA) recognized by CTL. All tumors were rejected in syngeneic normal mice but grew progressively in nude mice. CD8+ T cells mediated the antitumor responses for all tumors and CD4+ T cells could also do so for one tumor 6.1B. Each tumor induced potent CTL that recognized the specific TRA in preferential association with MHC class I haplotypes not from H-2b but from H-2d; that is, Kd, Dd or Ld. Profiles of TRA expression on two tumors were obtained by the analyses of their antigen-loss variants. ♀1A codominantly expressed at least four distinct TRA associated with Kd, all of which induced CTL. On the other hand, UV♂ 1 had at least two distinct TRA, one of which, associated with Kd, exclusively induced CTL. However, in the absence of the dominant TRA, another TRA associated with Ld on R95C, a variant of UV♂, 1, induced CTL. Unlike other tumors, R95C grew progressively in short-term-UV-irradiated syngeneic mice. Nude mice reconstituted with a combination of CD4+ T cells from short-term-UV-irradiated mice and CD8+ T cells from normal mice did not reject R95C. An increase in the former T cell population led the reconstituted mice to reject the tumor. These findings suggest some functional defects of CD4+ T cells rather than the generation of suppressor cells in short-term-UV-irradiated mice. The UV-induced tumors used in the present study provide a unique system for analyzing the preferential sorting of TRA as well as for elucidation of the TRA itself.

Notes: Abstract The effect of the supernatants obtained from the liquid culture medium ofSporothrix schenkii andCandida albicans on the generation of superoxide anion (O 2 − and hydroxyl radicals OH., the elements of reactive oxygen species (ROS), and chemilimunescence (CL), a measure of several ROS, by polymorphonuclear leukocytes (PMNs) was examined. In our study, it was shown that the supernatant ofS. schenkii increased all types of ROS generation examined and CL, while that ofC. albicans increased OH. generation and CL. The effect of the supernatants ofS. schenkii on OH. generation and CL and that ofC. albicans on CL were most remarkable when the supernatant obtained 8 weeks after the inoculation was used. The supernatant ofS. schenkii was shown to be a much more potent stimulant than the supernatant ofC. albicans. This ROS-stimulating effect of the supernatant ofS. schenkii was heat stable but not dialyzable. These findings suggest the possible role of ROS produced by infiltrated PMNs in the inflammatory skin lesions induced byS. schenkii.