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)

The effects of gallium arsenide (GaAs) exposure on immunocompetence of B6C3F1 female mice were investigated. GaAs was administered as a single intratracheal instillation at doses of 50, 100, and 200 mg/kg. Fourteen days after exposure, various cellular and humoral immune parameters were assessed. GaAs exposure increased spleen cellularity in a dose-dependent manner. However, the percentages of Thy 1.2 positive and Ig positive cells were decreased and that of F4/80 positive cells was increased dose dependently. The IgM and IgG antibody-forming cell response of the spleen to the T-dependent antigen sheep erythrocytes was reduced by 66 and 48%, respectively, at 200 mg/kg. Levels of the serum complement protein, C3, were increased by as much as 16% with no significant change in CH50 levels. The mitogenic response of splenic T cells to Con A and PHA was unaffected by GaAs, but that of B cells to LPS was increased by 52%. The delayed hypersensitivity response to keyhole limpet hemocyanin and mixed lymphocyte response were significantly reduced in a dose-dependent manner by GaAs exposure. Natural killer cell activity against the YAC-1 mouse lymphoma was enhanced in treated mice. Analysis of peritoneal exudate cells (PEC) revealed a dose-dependent decrease in number and a shift in the composition of PECs. The percentage of PEC monocytes increased from 53% of the population to 81%, while the lymphocytes decreased from 46 to 20%. The adherent PEC population demonstrated decreased phagocytosis of covaspheres and increased phagocytosis of chicken erythrocytes (CRBC). GaAs exposure had no effect on host resistance to Plasmodium yoelii or Streptococcus pneumoniae, but dose dependently increased resistance of the mouse to Listeria monocytogenes. Treated mice demonstrated a significantly decreased resistance to the B16F10 melanoma with a sevenfold increase in tumor burden at 200 mg/kg. GaAs affects both humoral and cellular immune parameters in mice and impairs the ability of the immune system to protect against B16F10 tumor challenge.
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PMID:Immunotoxicity of the semiconductor gallium arsenide in female B6C3F1 mice. 269 79

The incidence of tuberculosis is very high in patients treated by hemodialysis particularly in the early stage of hemodialysis. The diagnosis of tuberculosis in dialysis patients was obscured as symptoms were nonspecific and extrapulmonary involvement was seen frequently. We investigated cell mediated immunity in dialysis patients in relation to the period of dialysis. The data indicate that dialysis patients show the following immunological impairments; 1) lymphopenia, 2) decreased B cell, 3) alteration of T cell subset, 4) decreased reaction of PPD skin test, 5) decreased T cell activity, 6) decreased IL-2 production, 7) decreased PHA induced lymphocyte blastogenesis, 8) decreased NK cell. Decreased immunologic host defence mentioned above may contribute to the high incidence of tuberculosis in the early stage as well as in the maintenance phase of dialysis.
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PMID:[Tuberculosis in patients undergoing hemodialysis]. 281 Oct 1

A 2 month-old Japanese girl with hereditary orotic aciduria type I was treated with oral uridine supplement. The activities of orotate phosphoribosyltransferase (OPRT) and orotidine-5'-phosphate decarboxylase (ODC) in erythrocytes were 2.7 and 0.4%, respectively, of those in the controls. Megaloblastic anemia, excessive urinary excretion of orotic acid, lymphopenia and decreased number of OKT3 positive lymphocytes on admission were corrected after the uridine supplement. Peripheral blood lymphocytes (PBL) were cultured for 24 hr in RPMI 1640 medium with 10% heat-inactivated fetal calf serum and further stimulated with PHA-P, ConA or PWM in the presence of 10 to 1000 microM uridine. EB virus-transformed B cell line (LCL) maintained with an optimal concentration of uridine was cultured for 48 hr in uridine free medium and cultured for an additional 48 hr with 1 to 1000 microM uridine. The incorporations of leucine in to PHA-, ConA- and PWM-stimulated PBL and into LCL of the patient increased in the presence of uridine over 10 microM, although they did not increase in controls. These data suggest that low protein synthesis might correlate with an immune deficiency in hereditary orotic aciduria type I.
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PMID:Increase of protein synthesis by uridine supplement in lectin-stimulated peripheral blood lymphocytes and EB virus-transformed B cell line of hereditary orotic aciduria type I. 282 87

In 20 cases of head and neck carcinomas, we have studied the immunological alternation by combined chemotherapy with Cisplatin, Vincristine, and Peplomycin (COP therapy). After COP therapy, the number of peripheral lymphocytes decreased, but the OKT4/8 ratio, the PHA-blastogenesis and the positive rate of skin tests increased. The cellular immunity was distinctly augmented by COP therapy. When compared with results from radiation therapy and operation. This augmentation was suspected to have been caused by the suppressive change of the suppressor T cells.
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PMID:[Alternation of the cellular immunity of patients with head and neck carcinomas under chemotherapy]. 362 31

Assays of lymphocyte subpopulations and function have been performed on patients with acute lymphoblastic leukaemia still in remission after 18 months' treatment. The patients were subjects of a trial of the value of craniospinal irradiation in the third month of treatment in preventing central nervous system relapse. Effects of both irradiation and chemotherapy were observed. Lymphopenia was much more marked in those patients who had received irradiation over a year previously. Assays of response to phytohaemagglutinin (P.H.A.) and staining for surface immunoglobulin indicated that this difference was due to a deficiency in thymus-dependent lymphocytes in the irradiated children. Chemotherapy had a particularly marked depressant effect on lymphocytes with antibody-dependent cytotoxic activity and a proportion of PHA-responsive cells were also depressed. It may be relevant that four of the patients depleted of thymus-dependent lymphocytes by radiation died of infection during remission, while none of those treated with chemotherapy alone died in remission.
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PMID:Immunosuppressive consequences of radiotherapy and chemotherapy in patients with acute lymphoblastic leukaemia. 457 43

Sixteen patients with mycosis fungoides (MF) were given either active transfer factor (TF) or heat-inactivated TF as additional therapy to topical nitrogen mustard or PUVA. The TF was prepared from non-selected healthy blood donors. The clinical evaluation after 2 years of therapy showed that among 8 patients treated with active TF, none went into complete remission of their disease 4 patients had partial remission, one was unchanged, 2 progressed, and one died of active MF. In the placebo-treated group, 5 patients achieved complete remission and 2 partial remission. One patient died early in the trial due to cardiac disease. Immunological studies during the first year of therapy revealed cutaneous anergy towards tuberculin in most patients. This anergy did not change during TF therapy and differed from normal lymphocyte reactivity in vitro after tuberculin stimulation. At the start of treatment the patients had diminished levels of T lymphocytes in peripheral blood. A temporary increase was observed in the total number of T lymphocytes in patients after one month of treatment with active TF. After one year the T lymphopenia had disappeared in both groups. The mitogen reactivity of lymphocytes was found to be normal (PHA, PWM) or somewhat reduced (Con A). It is concluded that under the conditions employed in this trial, TF was not able to prevent progression of early mycosis fungoides, when viewed over a period of 2 years.
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PMID:Transfer factor therapy in mycosis fungoides: a double-blind study. 617 37

A placebo-controlled trial of Levamisole in 47 black children with measles is reported. The children were of satisfactory nutrition but at risk from severe disease as judged by a lymphopenia of less than 2000 X 10(-9)/m3 (less than 2000/mm3) early in the exanthem. A placebo or Levamisole (2.5 mg/kg/dose) were given orally weekly for six weeks. Death or persistence of radiological pneumonia at six weeks occurred in 74% of the Levamisole and 92% of the placebo group. No side effects of the drug were noted. The immune responses that were monitored for six weeks were total lymphocyte and lymphocyte subpopulation counts, PHA stimulated lymphocyte transformation, leucocyte migration inhibition, measles antibody titres and serum levels of immunoglobulins and complement components. In none of these was a significant difference found between the two groups. While there was a trend clinically towards complete recovery in the group that received Levamisole, statistically it was not significant, and therefore Levamisole cannot be recommended for treatment of measles.
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PMID:Levamisole therapy in children at risk from severe measles. 618 87

The rare disorder of chronic mucocutaneous candidiasis is described in a two-year-old African girl who had a moderate lymphopenia due to fewer T and B cells, impaired lymphocyte transformation to PHA and candida antigen, decreased leucocyte migration inhibition to candida antigen and a defective cutaneous delayed hypersensitivity reaction to candida antigen and dinitrochlorobenzene. The patient's serum had a marginal inhibitory effect on the transformation of normal lymphocytes to candida antigen and no effect on PHA stimulation of these cells, as measured by stimulation index. In addition, IgA was deficient in her serum. No associated endocrinopathy was detected and she had a mild iron deficiency anaemia. There was a rapid and excellent response to ketoconazole with all lesions clearing within two months of treatment.
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PMID:Chronic mucocutaneous candidiasis with IgA deficiency in a two-year-old African girl who responded well to ketoconazole. 619 18

Deoxyadenosine (AdR) appears to be central to the molecular events mediating immunodeficiency in children born with adenosine deaminase (ADA) deficiency but it is still uncertain whether lymphotoxicity is due to AdR directly inhibiting transmethylation reactions in which S-adenosylmethionine is the methyl group donor, or is due to phosphorylation of AdR to deoxyadenosine triphosphate (dATP) which then inhibits ribonucleotide reductase or is due to other mechanisms. Using AdR and the ADA inhibitor deoxycoformycin (dCF) and assessing cell viability, nucleoside incorporation into RNA and DNA, as well as measuring deoxyribonucleoside triphosphate (dNTP) concentrations and S-adenosylhomocysteine (SAH) hydrolase activity, we have studied various types of human lymphoid cells and demonstrated in them the relative importance of the above two mechanisms of AdR toxicity. Treatment of normal resting peripheral blood lymphocytes in culture with AdR and dCF resulted in impaired viability. Although elevated dATP levels as well as decreased SAH hydrolase activities were both observed, the failure of a known inhibitor of ribonucleotide reductase (hydroxyurea) to produce toxicity, and the inability of deoxycytidine (CdR) to achieve a rescue effect, point to another mechanism, possibly inhibition of trans-methylation or ATP depletion being the more likely causes of toxicity in resting lymphocytes. The same mechanism may well account for the rapid and severe lymphopenia in patients treated with dCF. On the other hand, in cultured lymphoblasts in the exponential phase of growth. AdR and dCF produced marked inhibition of growth and cell death both in a Thy-ALL line and in a c-ALL line, in the absence of significant inhibition of SAH hydrolase, but with a substantial elevation in dATP concentrations and depressed levels of the other dNTP. Minor toxicity occurred in a proliferating B lymphoblast line despite almost complete inactivation of SAH hydrolase. These observations indicate inhibition of ribonucleotide reductase as the more likely mechanism of toxicity in rapidly proliferating lymphocytes. Other T-cells actively synthesizing DNA, such as PHA-stimulated or MLC activated lymphocytes and T-lymphoid colony forming cells, are also likely to be affected by the same mechanism. Indeed in PHA-stimulated lymphocytes, deoxycytidine caused significant although incomplete rescue from toxicity due to dCF and AdR. In patients with ADA deficiency or treated with ADA inhibitors, both mechanisms could be operative. These observations are also relevant to the possible use of dCF and AdR as immunosuppressive agents and for the removal of T-cells or residual Thy-ALL blasts from bone marr
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PMID:Mechanisms of deoxyadenosine toxicity in human lymphoid cells in vitro: relevance to the therapeutic use of inhibitors of adenosine deaminase. 623 Oct 47

We have carried out a longitudinal study of human polyomavirus infection in 71 pregnant women and correlated the virological findings with changes in the defence system in the same patients. As reactivation of human polyomaviruses generally occurred late in the second trimester it was possible to distinguish between the immunological changes which preceded the onset of reactivation and those which were secondary to the infection. Evidence of reactivation was detected in 26 women; all had high or rising antibody titres against BK or JC virus, but only five of these developed viruria. A positive correlation was observed between a high monocyte count in early pregnancy and subsequent virus reactivation. The virus excretors had significantly lower neutrophil counts than the women who had no evidence of virus reactivation. In contrast, women with serological evidence of virus activity but no viruria has significantly higher neutrophil counts than the non-activators. They also had stronger lymphocyte responses to PHA than the virus excretors. Virus activators were found to have a significant lymphopenia in the third trimester compared to the non-activators. High antibody levels did not appear to inhibit virus excretion. These findings suggest that monocytosis may predispose to reactivation of human polyomaviruses in pregnancy. On the other hand, ability to contain the virus once it has been activated, was associated with neutrophilia, and relatively vigorous in vitro reactivity of lymphocytes to PHA. Persistent lymphopenia was probably secondary to virus reactivation. The model on which this study is based could be adapted to investigate the causes of reactivation of other viruses. It may also help to identify risk factors in patients who are particularly susceptible to infection with opportunistic viruses.
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PMID:Human polyomavirus in pregnancy. A model for the study of defence mechanisms to virus reactivation. 630 42


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