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)

Stress induces an imbalance of neuroimmunomodulation, a phenomenon involving the immune, central nervous and endocrine systems. Receptors to substances involved in stress reactions and anxiety, like adrenaline, acetylcholine, histamine, endomorphines, ACTH and several neuropeptides, are present on lymphocytes and lymphocytes can secrete various hormones and neuropeptides. Peripheral and central, cortical and subcortical nervous structures influence immune response. Steroids play a dose dependent inhibitory role perhaps via GIF (Glucocorticoid Increasing Factor) and cytokines (IL 1). In rats, stress induces an increase of corticosterone levels and a lymphopenia depending on the presence of adrenals and pituitary, whereas functional responses to mitogens appear decreased in animals even after surgical removal of adrenals and/or pituitary. Immune response vary according to the degree of control over stressors, to the type of stressor and the animal species. Chronic or repeated stress tends to stimulate immune reaction, contrary to acute stress. In man grief reactions, terminal illness of a spouse, divorce, examinations, caregiving to Alzheimer patients have been used as models of stress, with immune consequences. Pathological anxiety has been less studied, with only few anomalies reported in DSM III-R panic disorder. The immune system participation in the adaptive response to stress is reviewed.
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PMID:[Stress and panic. Immunologic aspects]. 828 94

We have analysed data from 150 patients initially classified as having CVID. About 10% had laboratory abnormalities suggesting known single gene disorders (eg: hyper-IgM syndrome), and in a few a genetic defect has been confirmed. We have attempted to sub-classify the remaining patients by analysis of their circulating lymphocytes. B lymphocyte markers have been used to estimate the numbers of circulating immature and class switched B cells; there is an association between the presence of high relative numbers of immature circulating B cells, splenomegaly and autoimmune disease. About 25% of CVID patients have a moderate CD4+ T lymphopenia, sometimes with a relative expansion of CD8+ T cells. About 30% of CVID patients have persistent relatively high levels of circulating CD8+ T cells binding immunogenic peptides from EBV or CMV. Many of these patients also have high relative numbers of circulating CD8+ perforin positive T cells, and there is evidence that these cells may be responsible for neutropenia or inflammatory bowel disease in some patients. The clinical spectrum of CVID is diverse, with some patients suffering from few infections, and over 50% have evidence of structural lung damage. About 25% of UK patients have chronic inflammation in various organs, particularly the lungs, liver and spleen, often with granulomatous changes. Steroids are used to treat many of the patients with chronic inflammatory complications, although trials are in progress with anti-TNF agents. The incidence of these inflammatory complications is different between countries, being rare in Sweden. Attempts to correlate clinical phenotypes with the laboratory abnormalities described above have been disappointing, suggesting that unknown genetic factors unrelated to the cause of the immunodeficiency determine the complications; attempts to identify some of these factors will be discussed. Finally a provisional scheme to sub classify CVID patients according to lymphocyte abnormalities will be presented, the purpose being to focus the screening of candidate genes causing CVID to specific subsets of patients.
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PMID:Clinical and Immunological Spectrum of Common Variable Immunodeficiency (CVID). 1730

JC virus (JCV) is a human polyomavirus that infects the central nervous system (CNS) of immunocompromised patients. JCV granule cell neuronopathy (JCV-GCN) is caused by infection of cerebellar granule cells, causing ataxia. A 77-year-old man with iatrogenic lymphopenia presented with severe ataxia and was diagnosed with JCV-GCN. His ataxia and cerebrospinal fluid (CSF) improved with intravenous immunoglobulin, high-dose intravenous methylprednisolone, mirtazapine, and mefloquine. Interleukin-7 (IL-7) therapy reconstituted his lymphocytes and reduced his CSF JCV load. One month after IL-7 therapy, he developed worsening ataxia and CSF inflammation, which raised suspicion for immune reconstitution inflammatory syndrome. Steroids were restarted and his ataxia stabilized.
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PMID:JC virus granule cell neuronopathy in the setting of chronic lymphopenia treated with recombinant interleukin-7. 2742 31