Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To estimate the influence of topical treatment with DMBA and induced tumors on delayed hypersensitivity, the response of spleen lymphocytes to PHA in vitro and macrophage migration inhibition with PHA were studied in DMBA-treated hairless mice. DNA synthesis and blastic transformation of cultured lymphocytes decreased after 6-12 weeks of DMBA application. Lymphocyte response to PHA gradually diminished during the experiment, as compared with control animals. Since the malignant transformation of skin tumors was not observed before 16 weeks of DMBA carcinogenesis, it seems that derangements in cellular immunity preceded the malignant proliferation. The increase in spleen weight and the absence of PHA-induced inhibition of macrophage migration in hairless mice with malignant tumors may also be related to the influence of the tumor itself on the lymphatic system of experimental animals.
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PMID:Immunological phenomena in harmless mice during experimental carcinogenesis induced with long-term topical application of 7, 12-dimethylbenzanthracene (DMBA). 4 67

Blood lymphocytes from nineteen patients with Hodgkin's disease were tested in vitro before and after treatment. The patients were retested in complete and unmaintained remission at least 15 months after termination of radiotherapy. All patients except two had been treated with total nodal irradiation. The lymphocyte-DNA synthesis induced by concanavalin A (Con A) and PPD was poor and the spontaneous DNA synthesis was increased in untreated patients. Most patients had a T lymphocytopenia before treatment. After irradiation the total lymphocyte counts were reduced drastically. The number of T lymphocytes was particularly low, though the number of B lymphocytes decreased as well. However, the lymphocyte response to Con A and PPD remained low and unchanged. The results may suggest a persisting immunodeficiency in Hodgkin's disease as reflected by the lymphocyte response to Con A and PPD.
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PMID:Persisting lymphocyte deficiences during remission in Hodgkin's disease. 30 64

In untreated patients with Hodgkin's disease the percentage of T-lymphocytes was significantly reduced in comparison to healthy controls independent of the stage of the disease. The absolute number of T-lymphocytes was also reduced in most patients. The response of lymphocytes after PHA-stimulation was diminished parallel with the skin reactivity: Normal results were obtained in early stages and with favorable histological types whilst low values were found in stages III and IV and in unfavourable histological types. A correlation between the percentage of T-lymphocytes and the PHA-stimulation was found in early stages, but not in stages III and IV. There was also a correlation between the absolute number of T-lymphocytes and skin reactivity. The percentage of DNA-synthesizing lymphocytes was significantly higher than in normal blood. The highest values were found in stages III and IV and in unfavourable histological types. After radiation therapy the T-lymphopenia, the diminished PHA-stimulation as well as anergy was more pronounced than after chemotherapy.
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PMID:[T-lymphocytes and their function in Hodgkin's disease]. 30 21

This review of recent and new directions in clinical immunologic studies of systemic lupus erythematosus (SLE) is restricted to the areas of lymphocyte surface markers, antigen binding lymphocytes, immune complexes, and lymphocyte hyporesponsiveness in lupus patients. First, it is not clear whether the T-lymphopenia observed in SLE is related to viral destruction of T cells, anti-lymphocyte antibodies, or tissue sequestration. Second, the increase in DNA-binding B lymphocytes observed in active lupus patients may be related to minor alterations in the balance of immunoregulatory T cells or to a bypass of DNA-specific helper T cells. Third, it is speculated that the removal of immune complexes which play a role in lupus glomerulitis by various extracorporeal immune absorbents may be important in the future therapy of SLE. Fourth, the mechanisms of T-lymphocyte hypofunction are unexplained. It is postulated from studies done in other diseases that this hypoactivity may be mediated by the secretion of prostaglandin or other humoral agents from one leukocyte subpopulation suppressing another potentially responsive lymphocyte subpopulation. Also an investigation into the lymphocyte subpopulation reactive with virus-infected fibroblasts may be useful in delineating immunoregulatory lymphocytes important in the pathogenesis of SLE.
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PMID:Clinical immunologic studies in systemic lupus erythematosus. 35 65

The effects of the intravenous administration of triazinate by single and multiple injections were studied in beagle dogs and rhesus monkeys. In dogs, dose levels ranging from 0.3125 to 40 mg/kg were given either as single doses daily for 5 days, or once weekly for 6 weeks. The 5-day regimen was also studied in monkeys with dose levels from 2.5 to 40 mg/kg/day. Prominent drug-related and drug-dependent effects which appeared in both species were piloerection, muscular weakness, and respiratory difficulty which occurred during and immediately after the administration of dose levels of 10 mg/kg or greater. Gastrointestinal toxicity was severe in dogs but mild in monkeys. Lymphoid tissue toxicity was manifested by a circulating lymphopenia and localized cellular depletion in the germinal centers of lymphoid tissues. In dogs, signs of bone marrow toxicity consisted of a circulating neutropenia and, at necropsy, a reduction in the number of erythroid and myeloid elements plus megaloblastosis. Only the latter change was observed in monkeys. This difference in the hematopoietic toxicity between the beagle dog and the rhesus monkey was corroborated by the findings from in vitro studies with bone marrow. DNA synthesis in beagle bone marrow cells was depressed significantly by triazinate as compared with cells from rhesus marrow. A direct renal toxic effect was observed in monkeys given high doses of triazinate (20 and 40 mg/kg/day or 240-280 mg/m/day) for 5 days.
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PMID:Preclinical studies with triazinate (NSC-139105), an antifolate drug, in beagle dogs and rhesus monkeys. 81 4

Several parameters of cell-mediated immunity were assessed in thirty patients with chronic renal failure treated with long-term haemodialysis. Lymphopenia was uncommon, and only two patients showed diminished numbers of thymus-derived peripheral blood lymphocytes. Skin test energy to three antigens was documented in only one patient. No serious infections with intracellular organisms were noted in any of the patients. Phytohaemagglutinin (PHA) induced DNA synthesis in eleven patients was lower than that shown by normal subjects. This poor responsiveness to PHA was not corrected by haemodialysis, and in only two patients was the response improved by substituting normal human plasma for uraemic plasma in the lymphocyte cultures. Thus with the exception of PHA response, other parameters of cell-mediated immunity were intact in this group of chronic stable haemodialysis patients.
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PMID:Cell-mediated immunity in patients on long-term haemodialysis. 108 96

Peripheral blood lymphocyte subpopulations determined in 40 patients with systemic lupus erythematosus, revealed significant lymphopenia in comparison to normal controls. The lymphopenia was caused by decreases in the absolute numbers of both T cells and surface immunoglobulin bearing (SIg) cells. There were significant percentage decreases in T cells and normal percentages of SIg cells, resulting in an increased percentage of "null" cells. The lymphopenia was significantly greater in patients considered to have active disease on the basis of clinical parameters, and was strongly correlated with lymphocytotoxic antibodies, DNA antibodies, and hypocomplementemia. The lymphocytotoxic antibodies were reactive with both T and B lymphocytes from normal and ill donors, human organs, and various lymphoblastoid cell lines. In 30 patients who were followed for up to 22 months, the lymphopenia was clearly seen to develop during, but not before, periods of clinical disease activity, independent of changes in therapy.
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PMID:Relationship of lymphocytotoxic antibodies to lymphopenia and parameters of disease activity in systemic lupus erythematosus. 108 29

The lymphocyte transformation test with phytohemagglutinin as mitogen estimated according to the incorporation of 2-(14)C-thymidine in DNA was used as an indicator of cell-mediated reactivity in 53 healthy subjects. Three age groups were examined: up to 20 years (21 subjects), 21-40 years (10 subjects) and over 70 years (22 subjects). The responsiveness of lymphocytes decreased significantly with age. In the highest age group 12 pathologically low values were found.
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PMID:Ageing and cell-mediated immunity. 118 28

The cause of angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) remains unknown. It is characterized by acute onset, severe constitutional symptoms, cervical or generalized lymphadenopathy, lymphopenia, and polyclonal hypergammaglobulinemia, all of which are highly suggestive of a viral origin. Using immunohistochemical methods, employing murine monoclonal antibody as the primary antibody, we detected human cytomegalovirus antigen in the lymph nodes of eight of 11 patients with AILD. Cytomegalovirus DNA was also detected in the peripheral blood mononuclear cells by DNA dot hybridization in all five of the patients with AILD who were tested using this technique. None of the lymph nodes from the 11 patients stained positive for the rubella virus antigen. Based on the above evidence and the similarity of the immunologic abnormalities found in both AILD and cytomegalovirus infection, the possible role of cytomegalovirus as one of the causative agents for AILD is proposed.
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PMID:Detection of human cytomegalovirus antigen and DNA in lymph nodes and peripheral blood mononuclear cells of patients with angioimmunoblastic lymphadenopathy with dysproteinemia. 131 12

The antiviral nucleoside analogue 2',3'-dideoxycytidine (ddC) is a DNA chain terminator and/or inhibitor of human immunodeficiency virus (HIV) reverse transcriptase. We evaluated the effects of ddC in 36 New Zealand white rabbits. Three/sex were assigned to a control group and 5 treatment groups (10-250 mg/kg/day) for 13 or 18 weeks. Blood samples were taken 1 week prior to treatment and weekly thereafter to termination with the exception of the 2 highest dose groups, where blood sample collection was terminated at week 13. Selected hematological analytes were measured weekly with the exception of prothrombin time (PT) and activated partial thromboplastin time (APTT). PT and APTT and selected biochemical analytes were measured prior to treatment, at 7 weeks, and after 13 weeks of treatment. All rabbits were necropsied. Giemsa and hematoxylin and eosin sections were prepared from methacrylate-embedded marrow. Hematological effects included decreases in red blood cell count, hemoglobin, hematocrit, and white blood cell count and increases in mean corpuscular volume and red cell distribution width. Platelets, platelet volume, PT, APTT, and mean corpuscular hemoglobin concentration values were variable or unchanged. Effects were dose-related, most were seen at 1 week, and they persisted to term. Bone marrow histopathologic changes included megalocytosis, erythroid hypoplasia, bizarre erythroid nuclear morphology, nuclear-cytoplasmic asynchrony, and increased mitotic figures. Lymphopenia caused by ddC plateaued at 2 weeks and persisted until termination. Heteropenia (neutropenia) was sporadic. Biochemical values for serum analytes were unchanged by treatment. The principal hematological effect of ddC upon the erythron was characterized as a nonregenerative macrocytic anemia with erythroid hypoplasia and megaloblastic erythropoiesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematological effects of 2',3'-dideoxycytidine in rabbits. 133 36


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