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)

Bone-marrow-derived B lymphocytes and thymus-dependent T lymphocytes were quantitated in a group of 38 patients with histologically confirmed sarcoidosis. B lymphocytes were identified by detecting surface immunoglobulins (Ig, IgG, IgM, and IgA) and complement receptors. T lymphocytes were identified by E-rosette assay. The untreated patients with both limited and disseminated disease had lymphopenia, reduced T-cell number, and low E/Ig cell ratios. Absolute numbers of circulating E-rosette lymphocytes did not show any correlation with cutaneous anergy. The numbers of Ig-bearing lymphocytes or the sum of the numbers of IgG, IgM, and IgA(GMA)-bearing lymphocytes were elevated in patients with disseminated disease, whereas the numbers of complement receptor lymphocytes were normal in all groups. It is proposed that this discrepancy of results on B-lymphocyte subpopulations might be explained by the presence of antibody or extrinsic antigen-antibody complexes bound to lymphocytes, as supported by elevated GMA/Ig ratios. The numbers of circulating B lymphocytes, as detected by any of three markers employed in this study, showed no correlation with the levels of serum immunoglobulins. The mechanisms of T-cell depletion and increase of immunoglobulin-bearing cells remain to be determined.
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PMID:Sarcoid lymphocytes: B- and T-cell quantitation. 78 27

Corticosteroids, well known to increase susceptibility to infection, are often administered to atopic patients. Atopy may be associated with lymphocyte abnormalities and increased susceptibility to infections caused by intracellular organisms. We sought to determine whether atopic and nonatopic subjects respond in a similar manner to corticosteroids administered both systemically and locally. We compared the response of peripheral blood leukocytes of 15 atopic asthmatics and 10 nonatopic control subjects to prednisone or beclomethasone dipropionate. We determined leukocyte number, total eosinophil count, T-cell number, complement receptor lymphocyte number, and concanavalin A (Con A)- and phytohemagglutinin (PHA)-induced lymphocyte proliferation before and 5 hr after administration of 20 mg of prednisone orally or 336 micrograms of beclomethasone dipropionate by aerosol inhalation. Baseline values of the groups differed. The atopic asthmatic group had higher total eosinophil count, lower percent lymphocyte count, and slightly lower Con A- and PHA (high concentration)-induced lymphocyte proliferation. T-cell and complement receptor lymphocyte number were equivalent in both groups. Prednisone caused a profound eosinopenia, monocytopenia, T lymphopenia, depression of mitogen-induced lymphocyte proliferation, and increase in leukocyte number and complement receptor lymphocyte percent. Beclomethasone dipropionate was associated with little or no change in these parameters. We conclude that atopic asthma is not associated with a defect in corticosteroid-sensitive leukocyte populations and that beclomethasone dipropionate aerosol, as opposed to prednisone, does not alter peripheral blood mononuclear cell populations.
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PMID:Corticosteroid-sensitive lymphocytes are normal in atopic asthma. 724 Jun 1

Normal subjects given 60 mg of prednisone orally at 8:00 a.m. developed a transient lymphopenia at 2:00 p.m. To define the populations of lymphocytes affected the number and type of lymphocytes in the peripheral blood were assayed. "Late" and "early" spontaneous sheep red blood cell rosettes were used as markers for thymus-derived (T) lymphocytes and one of its subpopulations, respectively. Receptors for aggregated gammaglobulin and complement identified bursal-equivalent or bone marrow-derived (B) lymphocytes and one of its subpopulations, respectively. 6 h after administration of 60 mg of prednisone, the blood samples showed a decrease in proportion of T cells from 69.2 +/- 2.1% to 55.9 +/- 2.8% (average +/- SE) and an increase in B-cell proportion from 21.3 +/- 2.0% to 44.8 +/- 4.1%. The changes of "early" rosettes and complement receptor lymphocytes also paralleled these. In all cases the absolute numbers of T cells and of B cells were decreased by prednisone. The density gradient distribution of the lymphocytes did not change after prednisone. These data indicate that both T and B lymphocytes are affected by the prednisone but that the T cell lymphopenia was more pronounced. The lymphopenia might reflect either sequestration in the marrow and/or transient arrest of recirculation.
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PMID:Human lymphocyte subpopulations. Effect of corticosteroids. 1134 71

Spinal cord injury (SCI) triggers a robust inflammatory response that contributes in part to the secondary degeneration of spared tissue. Here, we use flow cytometry to quantify the inflammatory response after SCI. Besides its objective evaluation, flow cytometry allows for levels of particular markers to be documented that further aid in the identification of cellular subsets. Analyses of blood from SCI mice for CD45 (common leukocyte antigen), CD11b (complement receptor-3), Gr-1 (neutrophil/monocyte marker), and CD3 (T-cell marker) revealed a marked increase in circulating neutrophils (CD45(high):Gr-1(high)) at 12 hr compared with controls. Monocyte density in blood increased at 24 hr, and in contrast, lymphocyte numbers were significantly decreased. Mirroring the early increase in neutrophils within the blood, flow analysis of the spinal cord lesion site revealed a significant (P < 0.01) and maintained increase in blood-derived leukocytes (CD45(high):CD11b(high)) from 12 to 96 hr compared with sham-injured and naive controls. Importantly, this technique clearly distinguishes blood-derived neutrophils (CD45:Gr-1(high):F4/80(negative)) and monocyte/macrophages (CD45(high)) from resident microglia (CD45(low)) and revealed that the majority of the blood-derived infiltrate were neutrophils. Our results highlight an assumed, but previously uncharacterized, marked and transient increase in leukocyte populations in blood early after SCI followed by the orchestrated invasion of neutrophils and monocytes into the injured cord. In contrast to mobilization of neutrophils, SCI induces lymphopenia that may contribute negatively to the overall outcome after spinal cord trauma.
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PMID:Dynamics of the inflammatory response after murine spinal cord injury revealed by flow cytometry. 1843 14