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)

A lymph node was examined from a 4-year-old female child with documented "Mo1" (CR3) deficiency. There was hypoplasia of the lymph node, with small, poorly delineated germinal centers and overall lymphopenia. Retrospective analysis of the clinical course of a decreased elder sister of the index patient indicated that the elder sister probably also had "Mo1" deficiency. Review of findings at autopsy revealed severe hypoplasia of all lymphoid organs with lymphopenia. Our observations suggest that lymphoid tissue hypoplasia may be a feature of CR3 deficiency and is likely a result of the defective lymphocyte adherence functions to endothelium associated with absent lymphocyte function-associated antigen (LFA-1).
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PMID:Severe hypoplasia of lymphoid tissues in Mo1 deficiency. 296 63

This study examined the relationship between exercise-induced changes in the concentration of circulating immunocompetent cells and their surface expression of adhesion molecules: L-selectin (CD62L) and three beta 2-integrins [LFA-1(CD11a/CD18), Mac-1 (CD11b/CD18), and p150/95(CD11c/CD18)]. Eight young male volunteers exercised on a cycle ergometer for 60 min at 60% maximal oxygen uptake. Peripheral blood samples, collected every 30 min throughout exercise and during the 2-h recovery period, were used for flow-cytometric analysis. The experimental results were compared with control data obtained ever 60 min at corresponding times of the nonexercise day. The exercise regimen induced a granulocytosis and a lymphocytosis, mainly due to an elevation of CD8+ and CD16+ cells. During recovery, a further granulocytosis occurred but accompanied by a lymphopenia. The increased CD8+ cell-count during exercise was characterized by a selective mobilization of the CD62L- and CD11ahigh cells, i.e. primed CD8+ cells. A postexercise suppression of CD4+ cell-count was derived only from CD62L+ cells. The CD11b+ and CD11c+ lymphocytes also increased during exercise, largely attributable to an increase in CD16+ cells which co-expressed CD11b and CD11c molecules. The CD62L surface density of granulocytes increased significantly during recovery. This resulted from a selective influx of CD62Lhigh granulocytes into the circulation. There were no significant changes in per-cell density of the three beta 2-integrins on granulocytes and lymphocytes throughout the experimental period. These results suggest that the cell-surface expression of CD62L (and CD11a) molecules is associated with the differential mobilization of CD8+ cells during exercise, the postexercise suppression of CD4+ cell-counts and the granulocytosis following exercise.
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PMID:Exercise-induced changes in the expression of surface adhesion molecules on circulating granulocytes and lymphocytes subpopulations. 758 96

Endotoxin challenge causes metabolic dysfunction mediated by TNF, and sequestration of leukocytes. NPC 15669, N-carboxy-L-leucine, N-[2,7-dimethylfluoren-9-yl)methyl] ester, inhibits leukocyte recruitment into inflammatory lesions in animals, and inhibits endotoxin-induced neutropenia and lymphopenia in mice. This study was carried out to determine whether the ability of NPC 15669 to inhibit leukocyte sequestration is sufficient to promote survival after endotoxin challenge. To inhibit leukocyte sequestration directly, mice were treated with anti-CD11a (LFA-1) or anti-CD11b (Mac-1) before endotoxin challenge. Anti-CD11b partly inhibited neutropenia and lymphopenia in response to challenge with LPS, but anti--CD11a had little effect on leukopenia. At doses of 100 and 1000 micrograms/kg, anti-CD11b increased survival to endotoxin challenge from 0 to 20 and 40%, respectively, whereas anti-CD11a was without effect. These observations, coupled with the finding that NPC 15669 does not inhibit endotoxin-induced TNF release suggest that inhibition of leukocyte sequestration can increase survival after endotoxin challenge, and that NPC 15669 or antibodies to Mac-1 may represent effective therapies for gram-negative sepsis and shock.
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PMID:Mice treated with a leumedin or antibody to Mac-1 to inhibit leukocyte sequestration survive endotoxin challenge. 846 78

The objective was to elucidate the immunological abnormalities underlying polymyositis (PM) and dermatomyositis (DM). The phenotype of peripheral blood mononuclear cell (PBMNC) subsets and cell surface expression of activation (CD25 and HLA-DR) and adhesion (LFA-1) molecules was studied in 12 patients with PM and in 10 patients with DM. PBMNC subsets and expression of T-cell activation molecules were evaluated by cytofluorography. Double immunofluorescence and indirect immunoperoxidase techniques were applied to muscle biopsies to define T-cell phenotype and LFA-1/ICAM-1 expression. In PM, the absolute number of circulating cytotoxic (CD8+CD28+) T cells was selectively reduced. T cells showed increased expression of activation molecules, CD25 and HLA-DR, and increased adhesion capacity as the absolute numbers of CD3+CD25+, CD8+HLA-DR+, CD3+LFA-1+('bright') and CD8+ CD8+LFA-1+('bright') cells were higher than in healthy donors and DM patients. In PM muscle biopsies, T cells were mainly CD3+CD8+ and LFA-1+; additionally, endothelial cells and myofibres surrounded by T cells showed positive staining for ICAM-1. In DM, there was a general lymphopenia that led to a decreased absolute number of all T-lymphocyte subsets. It is proposed that in PM, in contrast to DM, LFA-1/ICAM-1 interactions enable activated CD8+ T cells to migrate selectively into the inflamed muscle and to adhere to myofibres, leading to tissue injury.
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PMID:T-lymphocyte immunophenotyping in polymyositis and dermatomyositis. 881 Jun 66

The immunological effects of recombinant human interleukin 12 (rhIL-12) administration were examined during the conduct of a Phase I clinical trial. Forty patients with advanced cancer received bolus i.v. injections of rhIL-12 in doses ranging between 3 and 1000 ng/kg. Dose-dependent increases in serum IFN-gamma levels were seen during rhIL-12 therapy. Significant lymphopenia was observed 24 h after single i.v. injections of rhIL-12 at each dose level. The degree of lymphopenia was dose dependent, and a plateau effect was seen with rhIL-12 doses of 100 ng/kg and higher. Lymphocyte counts reached nadir levels at approximately 10 h after rhIL-12 injection and returned to baseline within 14 days postinjection. Rebound lymphocytosis, as seen after interleukin 2 therapy, was not observed after recovery from rhIL-12-induced lymphopenia. rhIL-12-induced lymphopenia involved all major lymphocyte subsets, although natural killer (NK) cell numbers were the most profoundly affected, and CD4 T-cell numbers were the least affected. CD2, LFA-1, and CD56 were transiently up-regulated on the surface of NK cells exposed to rhIL-12 in vivo. Peripheral blood mononuclear cells obtained from cancer patients before rhIL-12 therapy exhibited defective NK cell cytotoxicity and T-cell-proliferative responses. Peripheral blood mononuclear cells obtained after lymphocyte recovery following the administration of a single 500 ng/kg dose of rhIL-12 displayed augmented NK cell cytolytic activity in four of four patients tested and enhanced T-cell proliferation in three of four patients tested. These studies confirm that doses of rhIL-12 resulting in significant immunological activity can be administered with acceptable toxicity to cancer patients. Furthermore, rhIL-12 therapy can reverse defects in NK cell and T-cell function that are associated with advanced cancer in humans.
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PMID:Immunological effects of interleukin 12 administered by bolus intravenous injection to patients with cancer. 991 97

One type of emotional behavior called restlessness occurs when the anteromedial hypothalamus is stimulated in cats. We examined the changes in the distribution and surface expression of adhesion molecules in leukocytes accompanied with restlessness. Mature female cats were used for this study. The cats were stimulated with 60 Hz sine wave train pulses (20-90 microA, 10 s in duration, at 5-min intervals) for 60 min. Samples of blood were collected from 30 min before stimulation up to several hours after the final stimulation. The number of granulocytes increased just after stimulation, while at the same time the expression of L-selectin decreased. On the other hand, the number of CD4+ and CD8+ T lymphocytes decreased at 1-2 h after the end of the stimulation, while the expression of L-selectin increased. In addition, the expression of LFA-1 and VLA-4 did not change. These data suggest that hypothalamically elicited restlessness is thus accompanied by a leukocyte distribution change, which might be mediated by changes in the expression of L-selectin on leukocytes. Plasma cortisol increased during stimulation in restlessness. However, during in vitro culture experiments, cortisol did not alter the expression of leukocyte L-selectin which thus indicated that cortisol does not directly affect the surface expression of L-selectin. These results thus suggest that hypothalamically induced restlessness is a useful stress model for psychoneuroimmunological studies.
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PMID:Changes in the leukocyte distribution and surface expression of adhesion molecules accompanied with hypothalamically induced restlessness in the cat. 1075 1