Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic energy intake restriction (CEIR) prolonged the median life span and inhibited autoimmunity and development of autoimmune disease in BXSB mice, as has been established for mice of several other autoimmune-prone, short-lived strains. Whether imposed just after weaning or delayed until manifestations of disease had appeared, CEIR inhibited or reversed development of autoimmunity and immune complex-based renal disease in male BXSB mice. CEIR also prevented the formation of anti-DNA antibodies and prevented the increase in circulating immune complex levels that is typically observed in male mice of this strain. Moreover, CEIR inhibited development of splenomegaly and prevented the normal age-associated decline of a number of immunological functions, including interleukin 2 production, cell-mediated cytotoxic responses, and mixed lymphocyte reactivity. The observed improvement in cell-mediated immune responses was attributed largely to the capacity of CEIR to inhibit development of the splenomegaly that occurs concomitant with expansion of a non-T, non-B lymphoid cell population. These findings emphasize that CEIR, even when imposed relatively late in life in BXSB mice, can influence expression of autoimmunities and autoimmune diseases of different genetic origins and presumed pathogenetic bases.
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PMID:The effects of dietary restriction on immune function and development of autoimmune disease in BXSB mice. 134 65

Chronic energy (calorie) intake restriction (CEIR) prolonged life, inhibited autoimmune disease, and influenced immunologic and hematologic parameters in NZB mice. Abnormalities in numbers and proportions of T and B cells populations were corrected. Deficient responses to phytomitogens, mixed lymphocyte reactions, formation of plaque-forming cells to sheep red blood cells in vitro, production of cytotoxic T lymphocytes after in vitro stimulation, and interleukin 2 production were also corrected. CEIR prevented the extreme splenomegaly that normally occurs with age in NZB mice. This influence was associated with reduction of a greatly expanded non-T, non-B lymphoid cell population. Calorie restriction also prevented in NZB mice the rapid decrease in total numbers of colony-forming B cells in bone marrow that is also characteristic of mice of this strain. The influences of CEIR on immune parameters and hematopoiesis were generally less marked in non-autoimmune-prone DBA/2 mice than in autoimmune-prone NZB mice. CEIR has been shown to produce profound influences on several strains of autoimmune-prone mice (NZB x NZW)F1, MRL/lpr, BXSB, and NZB herein). In each of these strains, the pathogenesis and manifestations of autoimmune disease are dissimilar. Therefore, it seems likely that calorie restriction acts on an as yet elusive mechanism that operates to foster development of the diseases associated with aging common to each of these autoimmune strains as well as autoimmune-resistant mice and rats. Further investigation of the molecular and cellular bases of the benefits of CEIR seems urgent.
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PMID:Effects of calorie restriction on immunologic functions and development of autoimmune disease in NZB mice. 140 33

In this work, plasmodial antigens were examined for their ability to suppress the cellular immune response during lethal Plasmodium berghei infection. Splenic enlargement and the number and function of white spleen cells were assessed after injection of normal mice with irradiated parasitized erythrocytes (IPE) or with parasitized erythrocytes (PE) membranes. Both IPE and PE membranes caused splenomegaly and an increase in the number of splenic white cells with concurrent alteration of the relative proportions of T cells and macrophages. The percentage of T lymphocytes was fractionally diminished, but there was a marked increase in Lyt 2.2 positive (suppressor and cytotoxic) T subsets and in the number of splenic macrophage precursors. The pathological enlargement of the spleen was induced by various plasma membrane-derived antigens containing both proteins and carbohydrates. Splenocytes of mice injected with liposomes containing deoxycholate-treated PE or PE fractions showed both diminished interleukin 2 production and a decreased response to mitogen. It appears that some of the changes in the cellular immune response during P. berghei infection are a consequence of the massive provision of a wide spectrum of antigens, capable of suppressing the immune response. Thus, it may be appropriate to evaluate the possible negative effect of parasite epitopes that are candidates for vaccine.
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PMID:Plasmodium berghei: immunosuppression of the cell-mediated immune response induced by nonviable antigenic preparations. 264 64

The effect of (-)15-deoxyspergualin (15-dsp), a new immunosuppressant which was originally separated from the culture filtrate of a strain of Bacillus laterosporus, was evaluated in this study. Various doses of 15-dsp were subcutaneously administered to New Zealand black/white F1 hybrid mice (B/WF1) four times a week starting at 14 weeks of age, just prior to the onset of nephropathy. The life span of the treated animals, studied at 0.6 to 6.0 mg/kg body weights, compared with the control mice was significantly prolonged by 15-dsp treatment (percent survival of the treated mice at 50 to 70 weeks of age was significantly higher than that of the control mice, except that of the 0.6 mg group at 60 wks of age, P less than 0.05 by Fisher's exact test). In the 6.0 mg group of mice, complete suppression of spontaneously progressive splenomegaly with decreased total spleen cells was observed at 24 through 36 weeks of age compared with the same-aged control group of mice (P less than 0.01). Absolute numbers of L3T4+ splenocytes determined by flow cytometry, as well as L3T4+/Lyt2+ ratio, were decreased, while in vitro interleukin 2 production by splenocytes induced with staphylococcal enterotoxin A was significantly enhanced. Serum IgG anti-ds DNA antibody levels, measured by radioimmunoassay in the treated mice, were significantly lower at 24 through 36 weeks of age than those in the control mice (P less than 0.01), and the incidence of significant proteinuria (greater than or equal to 100 mg/dl) in the 15-dsp group was lower at both 32 and 36 weeks of age (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lupus nephropathy in New Zealand F1 hybrid mice treated by (-)15-deoxyspergualin. 319 66

We investigated the relationship between the increased cell diameter of Lyt-2+ T cells and the development of autoimmune disease in aging NZB and NZB X NZW F1 hybrid (BW) mice. Individual animals were analyzed for Lyt-2+ T cell size (by narrow-angle forward light scatter), anti-erythrocyte autoantibodies, anemia, proteinuria, and splenomegaly. The peak light scatter of the Lyt-2+ T cells correlated with the level of anti-erythrocyte autoantibodies and severity of hemolytic anemia, but not with proteinuria or splenomegaly. The cell size of this T cell subset did not increase in old BW or in NZB mice homozygous for the xid gene (NZB.xid). The in vivo administration of bacterial lipopolysaccharide to young NZB mice did not stimulate the enlargement of Lyt-2+ T cells. Ly-2+ T cells from old NZB mice could be stimulated by concanavalin A (Con A) to express interleukin 2 (IL 2) receptors and to synthesize DNA in vitro. However, in vivo administration of Con A to old NZB mice did not induce the expression of IL 2 receptors on Lyt-2+ T cells. Further, in vivo T suppressor function was impaired in old NZB mice with enlarged Lyt-2+ T cells. Thus, the enlargement of Lyt-2+ T cells in old NZB mice appears related to impaired T cell function in vivo and is associated with the development of anti-erythrocyte autoantibodies and autoimmune hemolytic anemia.
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PMID:Enlargement of Lyt-2-positive T cells is associated with functional impairment and autoimmune hemolytic anemia in New Zealand Black mice. 392 48

This study investigates a new approach to adoptive therapy of glioblastoma using as antitumor effector a potent major histocompatibility complex nonrestricted killer clone (TALL-104) established from a patient with acute T-lymphoblastic leukemia. The human glioblastoma cell line U-87 MG could be successfully engrafted in mice with severe combined immunodeficiency using the i.p., intracerebral, and s.c. routes. The latter model was elected to evaluate therapy based on its high reproducibility. Tumor growth in mice engrafted s.c. was proportionally associated with splenomegaly and leukocytosis. Multiple transfers of lethally irradiated (non-proliferating) TALL-104 cells at the tumor site resulted in about 50-70% inhibition of tumor growth as compared to untreated mice, with concomitant reduction of splenomegaly and leukocytosis. The antitumor effects were inversely proportional to the size of the tumor at initiation of therapy, 90-100% inhibition occurring in severe combined immunodeficiency mice treated from the day of U-87 MG challenge. Neither splenomegaly nor leukocytosis developed in animals in which tumor growth was completely blocked. Stimulation of TALL-104 cells with either interleukin 2 or interleukin 12 prior to irradiation and adoptive transfer increased the antitumor efficacy of the killer cells to about the same extent. The potential usefulness of irradiated TALL-104 cells in adjuvant therapy against glioblastomas and other well-localized tumors is discussed.
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PMID:Treatment of experimental glioblastoma with a human major histocompatibility complex nonrestricted cytotoxic T cell line. 780 48

We describe a case of T gamma lymphoproliferative disease (T gamma LPD) which presented in an uncustomary acute onset in an adult with massive splenomegaly. Morphologically the cells represented monocytic leukemia. Karyotyping and equivocol special stain results suggested hairy cell leukemia. Gene rearrangement indicated a T lymphocytic malignancy. Immunocytochemistry stains were not definitive. Immunophenotyping by flow cytometry defined the cells as consistent with T gamma LPD (CD45+, CD56+, CD2+, CD3+, CD11b+, and CD38+; some cells CD8+; and CD57-). Although the cells did not have spontaneous activity, which is often the situation for most cases of T gamma LPD, the cells could be partially induced with exogenous interleukin 2 to exhibit in vitro cytotoxicity against a natural killer lymphocyte-susceptible target cell line (K562) but not a lymphocyte-activated killer target cell line (HEPG2). This report hopefully continues to increase the awareness of T gamma LPD as well as demonstrates an unusual acute form which could have been misdiagnosed unless a multidisciplinary approach, especially including flow cytometric immunophenotyping, was used to evaluate the patient.
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PMID:An acute form of T gamma lymphoproliferative disease presenting with massive splenomegaly--importance of immunophenotyping for diagnosis. 851 86

Abdominal tuberculous lymphadenitis is very rare. We report a case of pulmonary tuberculosis showing marked abdominal lymphadenopathy and splenomegaly. A 95-year-old man was admitted to our hospital because of abnormal chest X-ray and body weight loss in last 6 months. He had low grade fever with no abdominal pain. He did not have past history of tuberculosis. Laboratory examination showed mild renal dysfunction and mild glucose intolerance. Soluble interleukin 2 recepter was highly elevated (3800 U/ml). Tumor markers, such as carcinoembryonic antigen (CEA), cytokeratin 19 fragment (CYFRA), and progastrin-releasing peptide (Pro GRP) were all within normal limit. Chest X-ray showed multiple nodules in bilateral lung fields. Chest computed tomography showed multiple nodules in bilateral lungs, especially in upper part of lungs, right hilar lymphadenopathy and upper mediastinal lymphadenopathy. Abdominal and pelvic enhanced computed tomography showed marked abdominal lymphadenopathy and splenomegaly (67 x 49 mm). Abdominal lymph nodes were hepatoduodenal (50 x 50 mm), splenic hilar (40 x 25 mm), upper paraaortic (30 x 60 mm), and small superior mesenteric (10 x 10 mm) lymph nodes. FDG-PET showed accumulation in the nodules of right lung field, right hilar lymph nodes, upper mediastinal lymph nodes, and abdominal lymph nodes. Bronchial lavage fluid (BAL) smear for acid-fast bacilli was positive, polymerase chain reaction for Mycobacterium tuberculosis was positive and acid-fast bacilli was cultured. Transbronchial lung biopsy specimen demonstrated non-specific intraalveolar organization and alveolitis. The patient was diagnosed as pulmonary tuberculosis, but about abdominal lymphadenopathy and splenomegaly we had to differentiate malignant lymphoma, and for definite diagnosis, laparotomy was necessary. But considering his age and general condition, we followed up carefully with anti-tuberculosis therapy. Pulmonary tuberculosis, abdominal lymphadenopathy and splenomegaly all showed marked improvement 4 months after starting anti-tuberculosis therapy with isoniazid, rifampicin, and ethambutol, so we clinically diagnosed abdominal tuberculous lymphadenitis and splenic tuberculosis.
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PMID:[A case of tuberculosis with multiple lung nodules, abdominal lymphadenopathy, and splenomegaly]. 1992 50