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

Alemtuzumab is a humanized monoclonal antibody directed against the CD52 antigen, which is abundantly expressed on all normal and most malignant T-lymphocytes. We summarize the results of our experience using alemtuzumab to treat a range of clinically aggressive, mature, post-thymic, T-cell malignancies, including T-cell prolymphocytic leukemia (T-PLL), cutaneous T-cell lymphoma (CTCL), T-cell large granular lymphocyte (T-LGL) leukemia, and human T-cell lymphotropic virus I (HTLV-I) associated adult T-cell leukemia-lymphoma (ATLL). Alemtuzumab was administered at a dose of 30 mg, three times a week until maximum response. Apart from first-dose reactions, which were common, treatment was well tolerated, the main complication being infection and viral reactivation associated with the prolonged lymphopenia. Overall response rates were 76% (60% complete response) in 39 patients with T-PLL and 100% in 3 patients with CTCL, of duration up to 4 yr. Experience in T-LGL and ATLL is limited to single cases only and further studies are required to better define the role of alemtuzumab in these subgroups. Our results indicate that alemtuzumab has activity in T-cell malignancies, particularly in T-PLL and in patients with predominantly blood and bone marrow disease. It may be possible to prolong response duration by the use of high-dose therapy and stem cell transplantation. Alemtuzumab may also have a role in purging minimal residual disease following other chemotherapy and prior to transplantation. We conclude that treatment with alemtuzumab may offer new hope to patients who otherwise have a bleak prognosis.
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PMID:Alemtuzumab in T-cell malignancies. 1218 Apr 89

Individual variability in the central control of the cellular immune responses is the main subject of the study. Previously, it was found that destruction of the lateral hypothalamus (LH) produced long-term depression of the cytotoxicity of NK cells (NKCC) and their number (LGL). In the present experiment we compared changes in the peripheral blood NKCC, LGL number, as well as leukocyte and lymphocyte number, their mitogenic activity and plasma corticosterone level evoked by electrolytic LH lesions in rats which were categorized as either high (HR) and low (LR) responders according to their locomotor response to a new environment. It was found that: (1) before the lesion NKCC (measured by 51Cr release assay) was higher in the HRs than in LRs; (2) LH damage caused a drop in NKCC and LGL number (21st postlesion day) preceded by a transient enhancement (5th postlesion day) significant for HRs only. As a result of a greater decrease in the HRs than LRs the baseline differences between groups disappeared by 21st postlesion day; (3) NKCC and LGL depression was not accompanied by changes in lytic activity of a single NK cell (agarose assay) which indicates that NKCC decrease concerned the population level and was dependent on LGL redistribution and/or recycling rate; (4) on the 21st postlesion day there was a significant leuko- and lymphopenia in the lesioned groups both HRs and LRs; (5) proliferative lymphocyte response to PWM (colorimetric assay) and plasma corticosterone level were not affected either by the motility level or by the lesion. The results emphasize the importance of individual differences in behavioral reactivity for NKCC regulation and a possible involvement of LH in the mechanism which connects high locomotor activity with stimulation of NKCC.
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PMID:The effects of lateral hypothalamic lesions on peripheral blood natural killer cell cytotoxicity in rats hyper- and hyporesponsive to novelty. 1458 37

The effect of i.p. administration of 1mg/kg of amphetamine (AMPH) on natural killer cells cytotoxicity (NKCC) and number of large granular lymphocytes (LGL-NK) together with plasma corticosterone (CORT) level and WBC was evaluated in male Wistar rats differing in two behavioral features: locomotor reactivity to novelty (high, HR and low, LR responders) and social position (dominants, D and subordinates, S). In the majority of animals AMPH evoked (30 min after administration) an increase in NKCC and LGL (NK) number accompanied by lymphopenia, neutrocytosis, monocytosis, and an increase in CORT level. Changes in NKCC (LU20) showed substantial individual variability: in HR group approximately 513Delta%, p <0.01 (relative to the control); LR group approximately 56Delta%, p >.05; D group approximately 441Delta%, p >0.001; S group approximately 216Delta%, p >0.05; HR/D group approximately 643Delta%, p <.001; HR/S group approximately 414Delta%, p <.001; LR/D group approximately 191Delta%, p >.05; and LR/S group approximately -19Delta%, p .05. The increase in CORT level, lymphopenia, and neutrocytosis indicated a stress-like reaction to AMPH. No significant correlation between NKCC and CORT level was found. The results obtained indicate that AMPH can evoke an increase in NK-related cytotoxic activity quantitatively related to high behavioral reactivity to novelty and social dominance, however NKCC is not related to the AMPH-induced CORT changes.
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PMID:Effects of amphetamine on NK-related cytotoxicity in rats differing in locomotor reactivity and social position. 1558 40

Although addiction to amphetamine (AMPH) is a serious social and medical problem, the data concerning AMPH - immune interactions are still not numerous. To analyze the mechanism of AMPH-induced changes in the function of the immune system, rats were pretreated with beta-adrenergic receptor antagonist propranolol (PROP; 5 mg/kg, i.p.) prior to AMPH (1 mg/kg, i.p.) administration. Natural Killer cells cytotoxicity (NKCC) ((51)Cr-release assay), the number of LGLs (NK cells) (Timonen method), leukocytes, lymphocytes and monocytes, and plasma corticosterone level (CORT) (RIA) were evaluated in the peripheral blood and spleen. In the peripheral blood increases in NKCC (+331 Delta %), as well as in LGL (+33 Delta %) and monocyte (+65 Delta %) number observed after AMPH were partially inhibited by PROP (respectively by 30%, 19%, and 30%) in contrast to lymphopenia (-19 Delta %) and granulocytosis (+65 Delta %) which were not affected by beta-blockade. In the spleen AMPH-induced decreases in NKCC (-25 Delta %) and in all the leukocyte populations number (approximately -30 Delta %) were completely blocked by PROP. Plasma CORT level, highly elevated by AMPH (+337 Delta %), was attenuated nearly by 50% under beta-adrenergic blockade. These data indicate that AMPH-induced enhancement of cytotoxic activity of NK cell is related to beta-adrenergic mechanism.
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PMID:Amphetamine enhances natural killer cytotoxic activity via beta-adrenergic mechanism. 1724 44