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)

In 23 subjects of different ages with Down's syndrome a number of parameters of non-specific defense of humoral and cellular immunity were investigated. While in all age groups complement factors C3, C4 and C5 as well as phagocytosis and NBT indices were in the normal range, a dysgammaglobulinaemia increasing with age with a hyperglobulinaemia of the IgG, IgA and IgD types was found, sparing immunoglobulins IgM and IgE. In addition the transformation capacity of peripheral blood lymphocytes decreased with age. This is understood as the consequence of premature aging of the thymus-dependent immune system.
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PMID:On the influence of age on immunity in Down's syndrome. 13 10

Two cases of combined immunodeficiency with lymphopenia, thymic dysplasia, and defective immunoglobulin production are reported. Both show selective hypo-gammaglobulinemia (IgG and IgA respectively) and selective hyper-gammaglobulinemia (both IgE, IgA, and IgM respectively). The cases are classified, by correlation of clinical and histopathological data as a variant of Fireman's disease.
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PMID:Combined immune deficiency syndromes with primary T-cell defect and partial B-cell reactive hyperactivity. Immunological and morphological analysis of two unusual cases. 15 Jan 19

Host defenses were evaluated in 70 healthy aged volunteers. Individuals who had diseases or who were taking medication known to affect the inflammatory and immune responses were excluded from the study. Volunteers were followed for 24 months to correlate their state of health with the evaluation of host defenses. Polymorphonuclear leukocyte function and the serum opsonic capacity for Escherichia coli and Staphylococcus aureus were normal. Assays of complement components and activity revealed unexplained elevations in native C3 and properdin, normal concentrations of factor B, normal conversion of C3 by inulin, and normal levels of hemolytic complement. The levels of IgG and IgA did not differ from levels noted in younger controls, but the concentration of IgM was decreased and that of IgE increased. The prevalence of autoantibodies was low. None of the volunteers were anergic, but lymphocyte responses to mitogens were depressed in three-day cultures. The number and percentages of E-rosette-forming cells and cells bearing surface IgD or IgM were normal. No lymphopenia was noted.
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PMID:Host defenses in the aged: evaluation of components of the inflammatory and immune responses. 35 76

A six-year old boy who had suffered from the age of two with chronic diarrhea has been found to be severely retarded in statural growth. Examinations discovered marked lymphopenia with a T lymphocyte defect accompanied by absent IgA and IgE. In contrast with other cases described in literature, in this case the immunodeficiency was not accompanied by bone or cartilage alterations. The only factor apparently responsible for his lack of growth was the malabsorption.
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PMID:Harmonic dwarfism, lymphopenia, deficit of IgA and IgE in a 6-year old boy. 61 Apr 13

Absolute T and B lymphocytes, total eosinophil counts (TEC), and serum IgE levels were studied in twenty-three asthmatic subjects. Compared to a mean peripheral T-lymphocyte count of 1620+/-486/mm3 in twenty control subjects, the mean value in the asthmatic patients was depressed significantly at 1192+/-4 12 (P less than 0-005). T lymphopenia was observed in ten of twenty-three patients (43%). The serum IgE was elevated above the upper limits of 507 mug/ml in six of seventeen patients. TEC above 250/mm3 was observed in twelve of seventeen subjects. T lymphopenia and hyper-immunoglobulinaemia E were each associated with hypereosinophilia. No correlation was observed between T lymphopenia and hyperimmunoglobulinaemia E.
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PMID:Lymphocyte subpopulations, serum IgE and total eosinophil counts in patients with bronchial asthma. 108 84

A longitudinal investigation has been conducted into the cell-mediated immune responses of onchocerciasis patients after a single-dose treatment with ivermectin. Untreated patients tested for delayed cutaneous hypersensitivity (DCH) to seven recall antigens showed lower responses than infection-free control individuals (P less than 0.01), but 6 and 14 months after treatment DCH reactions increased to similar levels to those seen in the controls. The in vitro cellular reactivity to Onchocerca volvulus-derived antigen (OvAg) was reduced in untreated patients as compared with controls, and the lymphocyte blastogenic responses to OvAg and streptolysin-O clearly improved up to 14 months after treatment. Peripheral blood mononuclear cells (PBMC) from untreated patients produced IL-1 beta, tumour necrosis factor-alpha (TNF-alpha) and IL-6 in response to mitogenic stimulation with phytohaemagglutinin (PHA), only low levels of IL-1 beta, IL-2 and TNF-alpha in response to OvAg, but higher amounts of IL-4 and interferon-gamma (IFN-gamma) in response to OvAg than control individuals. After ivermectin treatment, the OvAg-induced production of IL-1 beta and TNF-alpha increased significantly 1 and 14 months after treatment. The PHA-induced production of IL-2 and IL-4 increased 1 month after treatment and remained significantly elevated until 14 months after treatment, whereas the OvAg-specific secretion of IL-2, IL-4 and IFN-gamma did not change after ivermectin treatment. Flow cytometric analysis of lymphocyte-subsets in the peripheral blood of untreated patients revealed a relative and absolute (P less than 0.01) diminution of CD4+ cells and a significantly smaller CD4+/CD8+ cell ratio as compared with controls. By 4 weeks after treatment and thereafter, CD4+ T cells increased relatively and absolutely (P less than 0.01); likewise there was an absolute increase in T-helper-inducer cells (CD4+CD45RO+) and a temporarily improved CD4+/CD8+ cell ratio (P = 0.001). The expression of the low-affinity receptor for IgE (CD23) on total lymphocytes decreased from 14% to 7% by 14 months after treatment. The CD8+ cells and CD3+TCR gamma delta + cells were higher in patients than in controls and both remained elevated until 14 months after treatment. These results suggest a distinctly improved cellular immunity in human onchocerciasis that was facilitated by ivermectin therapy.
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PMID:Ivermectin-facilitated immunity in onchocerciasis. Reversal of lymphocytopenia, cellular anergy and deficient cytokine production after single treatment. 151 57

Immune function in patients with hairy cell leukemia (HCL) was examined serially during treatment with alternating monthly cycles of recombinant interferon alpha-2a and 2'-deoxycoformycin (dCF). At presentation, most patients had normal numbers of T lymphocytes and their cells had normal proliferative responses to mitogens [phytohemagglutinin (PHA) and concanavalin A (Con A)] and alloantigens. Patients had severe monocytopenia, decreased delayed-type hypersensitivity (DTH) reactions, and decreased peripheral blood natural killer (NK) activity. Treatment caused a profound decrease in all lymphocyte subpopulations. T cells were more affected than B cells or NK cells. Numbers of CD4+ and CD8+ lymphocytes decreased to levels less than 200 cells/microliters in all patients during treatment. This decrease in T cell number was associated with a marked decrease in proliferative responsiveness to PHA, Con A, and alloantigens. These abnormalities persisted throughout the 14 months of treatment and have continued for up to 6 months beyond discontinuation of treatment. NK cell activity increased during treatment, but cycled depending on the phase of treatment; highest activities were observed after interferon (IFN)-alpha and lower levels of activity were observed after dCF. DTH responses generally did not improve during therapy. Levels of IgM, IgG, IgA, and IgD did not change during treatment, but IgE levels rose in most patients. All immunosuppressive effects were attributable to dCF since patients receiving IFN-alpha 2a alone did not exhibit these same immunosuppressive effects, and patients receiving dCF alone after IFN failure exhibited similar abnormalities. Despite this severe immunosuppression from dCF, life-threatening opportunistic infections have not been observed in our patient population. Six patients developed localized Herpes zoster infection among 21 patients who had received dCF. Pending the results of long-term follow-up, we recommend that dCF be reserved for patients who have failed splenectomy and IFN therapy.
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PMID:Deoxycoformycin-induced immunosuppression in patients with hairy cell leukemia. 278 73

We report four cases of Omenn's syndrome (OS), an autosomal recessive disease characterized by early erythrodermia, protracted diarrhea, severe infections, lymphadenopathy, hepatosplenomegaly, failure to thrive, and leukocytosis with marked eosinophilia. The immunological investigations revealed B lymphopenia with increased levels of serum IgE and marked depression of T-cell activation, not restored by the addition of exogenous interleukin 2 (IL-2). IL-2 and interferon-gamma (IFN-gamma) production in vitro were very low or absent. One patient was treated with HLA-identical bone marrow transplant with a complete remission of the clinical picture and the immunological defect. The infant died of graft versus host disease 4 months after the graft. For the remaining three infants the outcome was also fatal within the first year of life. In conclusion, OS should be considered a severe combined immunodeficiency disease with peculiar clinical, immunological, and histological findings.
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PMID:Clinical and immunological findings in four infants with Omenn's syndrome: a form of severe combined immunodeficiency with phenotypically normal T cells, elevated IgE, and eosinophilia. 311 64

We investigated the influence of human growth hormone (hGH) on mitogen-stimulated lymphoproliferation, in vitro IgM production, serum levels of immunoglobulins, somatomedin-C (Sm-C) values and serum growth-promoting activity (Thymidine Activity, TA) in 18 short children, aged between 6.6-14.5 years, undergoing a 3-month course of hGH therapy. Blood was collected the day before treatment (Group A), on the 5th day after patients were administered hGH daily (0.1 U/kg) i.m. for 4 days (Group B), after a 3-month course of hGH injected three times weekly, and finally before (Group C) and 24 h after an extra injection (Group D). In vitro IgM production from the patients' unstimulated lymphocytes decreased from 277 +/- 41 (Group A) to 168 +/- 38 (Group B), to 119 +/- 43 (Group C) and then to 119 +/- 28 ng/ml (Group D) (p less than 0.05). Using PWM-stimulated lymphocytes in vitro IgM production decreased from 2,015 +/- 464 (Group A) to 1,116 +/- 316 (Group B), then to 511 +/- 170 (Group C) and 968 +/- 295 ng/ml (Group D) (p less than 0.02). The variation of this decrease could be correlated with the variation of growth velocity during treatment (r = 0.619, p less than 0.05). In contrast, no significant changes were found following therapy either in serum levels of IgA, IgE, IgG, IgM, Sm-C and TA, or in phytohemagglutinin, concanavalin A and pokeweed mitogen-stimulated lymphoproliferation. Our data suggest that there is some relationship between growth hormone, growth and immunity.
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PMID:Immunological and endocrinological response to growth hormone therapy in short children. 320 73

We report a 5-year-old girl with adenosine deaminase (ADA) deficiency who was asymptomatic during the first years of life. At 3 years of age, she developed chronic and recurrent sinopulmonary infections, and at 4 1/2 years of age she had one major infection with Streptococcus pneumoniae (bacteremia and septic arthritis of the hip). Immunologic evaluation at 5 years of age revealed persistent lymphopenia, decreased helper-suppressor T cell ratios, and low proliferative responses to mitogens. The IgG, IgM, and IgA levels were normal; the IgG2 level was low normal or below normal. The patient had specific antibodies against toxoids and viral antigens but failed to produce antibodies against Haemophilus influenzae type b and pneumococcal polysaccharides. Although no symptoms of allergy were present, she had persistent eosinophilia and elevated IgE levels. The patient had 0.6% of normal ADA activity in erythrocytes and approximately 1% of normal ADA activity in peripheral blood mononuclear cells. Beginning at 6 years of age, she was treated with weekly injections of polyethylene glycol-modified bovine ADA. This treatment was well tolerated and effectively reversed the biochemical consequence of ADA deficiency. Concomitantly, she improved clinically and her T lymphocyte numbers and blastogenic responses to mitogens in vitro became normal. The late onset of clinical symptoms and relatively benign clinical course in this patient emphasize the need to consider ADA deficiency in a broad spectrum of immunodeficient children.
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PMID:Adenosine deaminase deficiency with late onset of recurrent infections: response to treatment with polyethylene glycol-modified adenosine deaminase. 326 Sep 44


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