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)

Mice bearing the immunosuppressive plasmacytoma TEPC-183 exhibit a marked splenic hyperplasia. We have characterized these tumor-reactive splenocytes on the basis of cell surface marker expression, nonspecific esterase activity, and morphology. Although splenocyte numbers increased progressively throughout tumor growth, B- and T-lymphocytes, as defined by surface immunoglobulin and Thy-1 antigen expression, respectively, did not increase significantly. Fourteen days after tumor implantation, T-lymphocytes decreased from 70 million to 50 million per spleen. However, cells expressing Mac-1 antigen or nonspecific esterase activity increased from 10 to 65 million. This constituted a 6-fold increase in splenic macrophages. Further studies utilizing the expression of PC.2 antigen in conjunction with morphological examination indicated that metastatic TEPC-183 cells comprise approximately 5% of the tumor-host splenocyte population 14 days after implantation. Ablation of plasmacytoma by cyclophosphamide inhibited the tumor-associated splenocytosis and led to an increase in splenic T-cells (from 70 to 120 million). In addition, macrophage numbers returned to normal. This study also assessed the ability of splenocytes from animals with either actively growing tumors or those from cyclophosphamide-treated tumor-bearing mice to mediate an antitumor response. Splenocytes, when assessed 1 wk following tumor ablation by cyclophosphamide, demonstrated antitumor activity in Winn neutralization assays. This activity was not detectable in splenocytes from animals with progressively growing tumors. Additional studies revealed that the cell population involved in the antitumor effect was glass nonadherent, nylon-wool nonadherent, and expressed Thy-1 antigen. These observations were consistent with the expansion of the splenic T-lymphocyte population following cyclophosphamide treatment. However, the immune response directed against primary TEPC-183 tumor cells was not inhibitory to metastatic tumor cells.
Cancer Res 1985 Dec
PMID:Cellular changes and antitumor responses in the plasmacytoma-bearing mouse following cyclophosphamide treatment. 286 30

The cell mediated immune (CMI) response was studied by E-rosette formation in vitro and delayed type hypersensitivity (DTH) skin reaction in buffalo calves vaccinated with monovalent type 0 as well as with a polyvalent foot-and-mouth disease vaccine. Up to 35 days post-vaccination there was a significant increase (P less than 0.05) in the number of T-lymphocytes in both animal groups. Thereafter, the number of lymphocytes decreased. Delayed type hypersensitivity (DTH) skin reaction was characterized by a significant increase in skin thickness; histology showed mononuclear infiltration and perivascular cuffing.
Acta Virol 1985 Dec
PMID:Cell mediated immune response following foot-and-mouth disease vaccination in buffalo calves. 286 64

A previously healthy 27-year-old man with class II pulmonary sarcoidosis developed severe humoral immunodeficiency within the course of the disease with an IgG of less than 250 mg/ml and undetectable levels of IgA and IgM. Repeated skin tests were negative for seven common recall antigens. Cellular blood test demonstrated normal numbers of B cells and slight T-cell lymphopenia with a normal T-helper/suppressor subset distribution (ratio 1.6). In contrast, parallel examination of the bronchial alveolar lavage fluid (BAL) demonstrated highly elevated numbers of T cells with a subset ratio of 3.1 and significant numbers of activated T cells as revealed by the expression of Ia and Tac antigens. Functional in vitro assays showed a greatly decreased mitogenic response of blood T cells and diminished production of immunoglobulins. These data indicate that, despite a severely depressed systemic humoral and cellular immune system, T-cell activation can take place at the inflammatory site, potentially causing the lesions characteristic of sarcoidosis.
Clin Immunol Immunopathol 1985 Dec
PMID:Pulmonary sarcoidosis associated with acquired humoral and cellular immunodeficiency. 293 72

Accumulation of inflammatory and immune cells within lung parenchyma would constitute the initial step in producing the alveolar structural abnormalities. It is usually assumed that alveolitis, as assessed by broncho-alveolar lavage (BAL), represents a biological assessment of lung disease activity. The aim of this study, using monoclonal antibodies, is to characterize the T lymphocytes alveolitis in the lung and in peripheral blood in 3 well-defined populations: 1 degree) control subjects (n = 7); 2 degrees) patients with biopsy proven mediastino-pulmonary sarcoidosis (sarc) (n = 73), classified according to their clinical activity as active, inactive, chronic, and treated; 3 degrees) patients with extrinsic alveolar alveolitis (EAA) (n = 19). For the same BAL volume, the % of CD4+ cells and the CD4/CD8 ratio are increased in chronic and active sarc, contrasting with an increase in the % of CD8+ cells and a decrease in the CD4/CD8 ratio in the EAA. In absolute values, there are 2 times as many CD4+ cells and 5 times as many CD8+ cells in EAA than in sarcoidosis. In sarcoidosis, corticotherapy tends to normalize the CD4/CD8 ratio although the intensity of the lymphocytic alveolitis is not affected. In the peripheral blood, lymphopenia is observed only in the active form of sarc. in the CD4+ population, without any significant change in the CD4/CD8 ratio compared to the other groups. The number and distributions of BAL. T lymphocytes subsets may constitute a biological indicator for diagnostic orientation, but they do not distinguish sufficiently between the different groups of sarcoidosis to be of any prognostic value.
Pathol Biol (Paris) 1987 Dec
PMID:[T lymphocyte subsets in alveolar lavage and peripheral blood in sarcoidosis and extrinsic allergic alveolitis]. 296 92

Deficiency in zinc, an essential trace element, is a frequent human dietary problem in the United States and is also associated with such disease states as alcoholism, renal disease, burns, gastrointestinal tract disorders, and acrodermatitis enteropathica. Skin lesions and poor wound healing are observed in severe forms of the deficiency. However, modest deficits in zinc cause lymphopenia and reduced immune capacity among affected humans. With the mouse used as a model because it has an immune system analogues to that of humans, the effects of zinc deficiency on immune function have been well characterized. A suboptimal intake of zinc causes marked atrophy of the thymus, a 50% reduction in leukocytes, a rise in corticosterone levels, and a 40% to 70% reduction in antibody-mediated, cell-mediated, and delayed-type hypersensitivity responses.
Arch Dermatol 1987 Dec
PMID:Zinc deficiency and immune function. 312 Jun 53

The effects of cortisol and adrenaline on natural killer (NK) cell activity and the distribution of circulating lymphocyte subpopulations were studied in twenty volunteers, using a continuous intravenous infusion pattern to simulate some of the hormonal changes induced by major surgery. The participants were allocated to receive either cortisol for 5 h, adrenaline for 1 h, cortisol for 5 h with simultaneous adrenaline during the last hour, or placebo for 5 h. Cortisol induced leucocytosis, neutrophilia, and lymphopenia with marked reduction in the number of T-lymphocyte subsets (OKT3+, OKT4+, and OKT8+ cells). No changes were induced in the activity or number of NK (Leu 11+) cells. Adrenaline produced an instantaneous increase in NK-cell activity accompanied by a selective increase in circulating NK cells. Significant leucocytosis, lymphocytosis and neutrophilia occurred. All measurements returned to preinfusion levels within 15 min after completing infusion. The effects of simultaneous infusion of cortisol and adrenaline were equal to the additive response to the hormones administered separately, except for the leucocytosis, which clearly exceeded this. In the placebo group all measurements remained unchanged. The results confirm the role of adrenaline as a potent stimulator/inducer of NK-cell activity. Adrenaline may be responsible for the increase in NK-cell activity during anaesthesia and major surgery.
Eur J Clin Invest 1987 Dec
PMID:Natural killer cell activity during cortisol and adrenaline infusion in healthy volunteers. 312 49

The kinetics of lymphocyte migration in 12 pre-treatment patients with nasopharyngeal carcinoma (NPC) and three cancer controls in remission were studied with Indium III oxine-labelled autologous lymphocytes. The migratory patterns of the labelled lymphocytes were defined by serial gamma imaging and blood clearance of Indium over 72 h. Once in the systemic circulation the labelled lymphocytes migrated immediately to the liver and spleen. In all the subjects studied the lymphocytes began to migrate out of the liver at 0.5 h, only to return to the organ gradually between 2 and 72 h. In the control subjects the lymphocytes migrated out of the spleen from about 4 h. This coincided with a hump in the peripheral blood clearance curve after about 4 h signifying re-entry of the lymphocytes into the vascular space from the spleen. In the 'early' NPC subjects (Stage I-III) the rate at which the lymphocytes entered the spleen was much reduced from about 4 to 72 h, suggesting a prolonged transit time of the lymphocyte through the organ. However, there were still prominent humps in the blood clearance curves, suggesting significant re-entry of lymphocytes into the vascular space. In the 'late' NPC subjects (Stage IV-V), the activity of the spleen was low between 4 and 72 h and there was continuous sequestration of lymphocytes in the organ. Consequently the humps in the blood clearance curves were much reduced or absent. The activities of the metastatic lymph nodes were intense between 2 and 48 h, suggesting marked sequestration of lymphocytes in the diseased lymph nodes. Migration of lymphocytes in the metastatic area of the liver was notably absent and presented as cold areas on gamma scanning. The sequestration of lymphocytes in the spleen and metastatic lymph nodes in 'early' and 'late' NPC could lead to a contraction of intravascular lymphocyte pool and could explain the stage-dependent lymphopenia reported in NPC.
Clin Exp Immunol 1988 Dec
PMID:A study of lymphocyte kinetics in nasopharyngeal carcinoma with indium III oxine-labelled lymphocytes. 314 79

A kinetic study of lymphocyte subpopulations was performed in 61 dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) patients aged 8 months to 12 years and in 59 age-matched normal controls. There were 36 patients in grade 2 and 25 patients in grade 3 of the disease severity. The studies were performed on febrile stage, the day of subsidence of fever or shock stage, 3 subsequent days after subsidence of fever or shock, and once on the recovery stage (approximately 14-18 days after subsidence of fever or shock). The study revealed that the absolute total lymphocytes, CD3+, CD4+, CD8+ and HNK-1+ cells were decreased on febrile stage and their lowest values were noted on the first day of subsidence of fever or shock, while B1+ cells were in the normal range. Thereafter, all lymphocyte subpopulations were increased. The total lymphocytes, B1+ and CD8+ cells were rapidly increased and were above normal value on day 2 after subsidence of fever or shock (early convalescence), then gradually declined to the normal range. In contrast, CD3+, CD4+ and HNK-1+ cells were increased gradually and reached their normal values on day 2 after subsidence of fever or shock. The T4:T8 ratio began to reverse on the day of subsidence of fever or shock, reached its peak on day 2 after shock and returned to normal ratio rapidly thereafter. Thus, the absolute lymphopenia on the day of shock was due to the decrement or T cells (both CD4+ and CD8+ cells) and HNK-1+ cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Southeast Asian J Trop Med Public Health 1988 Dec
PMID:Kinetics of lymphocyte subpopulations in dengue hemorrhagic fever/dengue shock syndrome. 323 78

Serum and CSF from 32 patients with idiopathic ALS, 30 age-matched controls and 30 MS patients were investigated regarding immunoglobulin concentration and virus-specific antibodies, the lymphocytes in the peripheral blood and lymphocyte subsets were also investigated. ALS patients' results were compared with findings in MS and controls. The ALS patients had significantly higher IgG concentration in serum than the controls, marked lymphopenia, reduction of CD2, CD8 and Leu 7 positive cells and increase of the CD4/CD8 ratio and of SIg-positive lymphocytes. Compared with the MS patients, the ALS patients showed similarity in T-subset distribution with a lower standard deviation. No HTLV-I and HIV antibodies were found in any group and no significant differences in antibody distribution to Toxoplasma G, herpes simplex, cytomegalovirus, measles and mumps viruses were evident. All ALS patients were investigated at an early disease stage, therefore, our findings seem to support the conclusion that the immune alterations are related to the mechanisms of the disease and not to complications of its evolution.
Acta Neurol Scand 1988 Dec
PMID:Immunity assessment in the early stages of amyotrophic lateral sclerosis: a study of virus antibodies and lymphocyte subsets. 326 63

IgG anti-lymphocyte antibodies (ALA) reactive with resting lymphocytes were demonstrated in sera of patients with systemic lupus erythematosus (SLE) by immunofluorescence and flow cytometry and were shown (i) to bind T cells by non-Fc receptor-related mechanisms, (ii) to potentiate antibody-dependent cellular cytotoxicity (ADCC) of lymphocytes in vitro which correlated with binding to T cells, and (iii) to occur at a similar frequency in 29 SLE sera (56%) as IgM ALA (59%). IgG ALA levels in sera negatively correlated with absolute numbers of circulating lymphocytes in patients (r = -0.48, P less than 0.05), as did IgM ALA levels (r = -0.54, P less than 0.05); however, a stronger correlation resulted when levels of both ALA isotypes were considered together (r = -0.61, P less than 0.01). Different groups of SLE patients were distinguished with respect to relative serum content of IgM and IgG ALA and corresponding serum capacity to predominantly mediate ADCC, complement-dependent cytotoxicity (CDC), or both. No correlation existed between serum ADCC and CDC activities in vitro (r = 0.22). However, SLE patient lymphocyte counts negatively correlated with ADCC (r = -0.59, P less than 0.01) and to a lesser but still significant extent with CDC (r = -0.47, P less than 0.05). The latter results suggested that ADCC, induced by serum IgG ALA, was a mechanism of cytoloysis which occurred independently of CDC and which, like CDC, was significantly associated with lymphopenia in vivo.
Clin Immunol Immunopathol 1987 Dec
PMID:Isotype and cytotoxicity spectra of anti-lymphocyte antibodies in patients with systemic lupus erythematosus. 331 37


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