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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphopenia is defined as a peripheral lymphocyte count lower than 1500/mm3 in adults and 4500/mm3 in children younger than eight months of age. We propose a classification of lymphopenia according to the mechanism involved: lymphocyte production defects, including primary immune deficiencies and immune deficiencies secondary to malnutrition or zinc deprivation; excess catabolism, due to causes including radiotherapy, chemotherapy, immunosuppressive therapy, HIV infection, and systemic lupus erythematosus; abnormal lymphocyte trapping, including mainly splenomegaly, certain viral infections, septic shock, extended burns, systemic granulomatosis, and corticosteroids; other causes of lymphocytopenia, with mechanisms that remain poorly understood: ethnicity (Ethiopians), lymphoma, renal insufficiency, and idiopathic CD4 lymphocytopenia.
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PMID:[Diagnosis of lymphocytopenia]. 1671 Jan 63

Clinical observations of Babesia canis infection in 63 dogs during a 1-year period are summarised, demonstrating the pathogenicity of the Babesia strain endemic in Hungary. Most patients had babesiosis in the spring and autumn, correlating with the seasonal activity of ticks. Male animals appeared in higher numbers, probably due to an overrepresentation of outdoor dogs. Uncomplicated babesiosis was diagnosed in 32 cases. The disease affected dogs of any age in this study. Symptoms were similar to those published from other parts of the world: lethargy, fever, splenomegaly, pallor, icterus, haemoglobinuria and presence of ticks were the most common observations. Thrombocytopenia, lymphopenia and neutropenia were frequent haemogram changes. Imidocarb appeared to be highly effective in eliminating the Babesia infection. Thirty-one animals demonstrated babesiosis with complications. Most Rottweilers (7/9) developed complicated disease. Old age was a risk factor for multiple complications. Multiple organ manifestations had poor prognosis. Hepatopathy (44%), pancreatitis (33%), acute renal failure (ARF; 31%) and disseminated intravascular coagulation (DIC; 24%) were frequent complications, while immune-mediated haemolytic anaemia (IMHA; 10%), acute respiratory distress syndrome (ARDS; 6%) and cerebral babesiosis (3%) were rarely observed. There was a significant difference between the mean age of dogs having uncomplicated disease, babesiosis with a single complication and babesiosis with multiple complications (3.4, 4.8 and 8.6 years, respectively, p < 0.001). The recovery rate (78, 68 and 25%, respectively, p = 0.005) and mortality rate (3, 21 and 67%, respectively, p < 0.001) also tended to differ significantly in these groups. Systemic inflammatory response syndrome (SIRS) and DIC are two possible pathways leading to multiple organ dysfunction syndrome (MODS) in babesiosis. DIC was found to predict MODS more sensitively in this study than SIRS: there were 6 animals developing MODS out of 11 identified with DIC, while only 5 dogs developed MODS out of 22 having SIRS.
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PMID:Clinical manifestations of canine babesiosis in Hungary (63 cases). 1702 Jan 40

The Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency syndrome caused by mutations in the WAS protein (WASP). This participates in signalling and cytoskeletal homoeostasis, and some of its activities are regulated by its binding to the WASP interacting protein (WIP). WIP deficiency, however, has not yet been shown to be of pathological significance in humans. Here we show that, in WIP null (WIP(-/-)) mice, it produces haematological alterations and anatomical abnormalities in several organs, most probably as a consequence of autoimmune attacks. Granulocytosis and severe lymphopenia are associated with a proportional increase in segmented cells and fewer bone marrow erythrocytes and lymphocytes. Splenomegaly is accompanied by an increase of haematopoietic tissue and red pulp, reduction of the white pulp, and fewer B (B220(+)) lymphocytes (also apparent in the lymph nodes and Peyer's patches). Ulcerative colitis, interstitial pneumonitis, glomerular nephropathy with IgA deposits, autoantibodies, and joint inflammation are also evident. These progressive immunological disorders closely mimic those seen in WAS. WIP deficiency may thus be implicated in some cases in which mutations in the gene encoding WASP are not detected.
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PMID:WIP null mice display a progressive immunological disorder that resembles Wiskott-Aldrich syndrome. 1708 54

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

CD137-mediated signals costimulate T cells and protect them from activation-induced apoptosis; they induce curative antitumor immunity and enhance antiviral immune responses in mice. In contrast, anti-CD137 agonistic mAbs can suppress T-dependent humoral immunity and reverse the course of established autoimmune disease. These results have provided a rationale for assessing the therapeutic potential of CD137 ligands in human clinical trials. In this study, we report that a single 200-mug injection of anti-CD137 given to otherwise naive BALB/c or C57BL/6 mice led to the development of a series of immunological anomalies. These included splenomegaly, lymphadenopathy, hepatomegaly, multifocal hepatitis, anemia, altered trafficking of B cells and CD8 T cells, loss of NK cells, and a 10-fold increase in bone marrow (BM) cells bearing the phenotype of hemopoietic stem cells. These events were dependent on CD8 T cells, TNF-alpha, IFN-gamma, and type I IFNs. BM cells up-regulated Fas, and there was a significant increase in the number of CD8+ T cells that correlated with a loss of CD19+ and Ab-secreting cells in the BM. TCR Valphabeta usage was random and polyclonal among liver-infiltrating CD8 T cells, and multifocal CD8+ T cell infiltrates were resolved upon termination of anti-CD137 treatment. Anti-CD137-treated mice developed lymphopenia, thrombocytopenia, and anemia, and had lowered levels of hemoglobin and increased numbers of reticulocytes.
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PMID:Cytokine-mediated disruption of lymphocyte trafficking, hemopoiesis, and induction of lymphopenia, anemia, and thrombocytopenia in anti-CD137-treated mice. 1737 76

Chronic immune activation is a major cause for progressive immunodeficiency in human immunodeficiency virus type-1 (HIV) infection. The underlying trigger, however, remains largely unknown. HIV single-stranded RNA is a potent immune activator by triggering Toll-like receptor (TLR) 7/8. Thus, we hypothesized that sustained TLR7 triggering induces chronic immune activation and thereby contributes to progressive immunodeficiency. We used the synthetic compound R848 or a mixture of uridine-rich HIV single-stranded (ss) RNA oligonucleotides--both are potent TLR7/8 agonists--to explore the effects of sustained TLR7 triggering on the murine lymphoid system. Sustained TLR7 triggering induced an immunopathology reminiscent of progressive lymphoid destruction in HIV disease; we observed lymphopenia, elevated proinflammatory cytokines, splenomegaly, contracted lymphoid subsets, and lymphoid microarchitecture alteration with reduced marginal zone B-lymphocytes. Upon exposure to inactivated vesiculo-stomatitis virus, antibody production was abolished, although splenic lymphocytes were activated and total IgG was elevated. Our data imply that HIV itself may directly contribute to immune activation and dysfunction by stimulating TLR7. Thus, manipulation of TLR7 signaling may be a potential strategy to reduce chronic hyper-immune activation and, thereby, disease progression in HIV infection.
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PMID:Triggering TLR7 in mice induces immune activation and lymphoid system disruption, resembling HIV-mediated pathology. 1913 56

Lassa virus causes a hemorrhagic fever endemic in West Africa. The pathogenesis and the immune responses associated with the disease are poorly understood, and no vaccine is available. We followed virological, pathological, and immunological markers associated with fatal and nonfatal Lassa virus infection of cynomolgus monkeys. The clinical picture was characterized by fever, weight loss, depression, and acute respiratory syndrome. Transient thrombocytopenia and lymphopenia, lymphadenopathy, splenomegaly, infiltration of mononuclear cells, and alterations of the liver, lungs, and endothelia were observed. Survivors exhibited fewer lesions and a lower viral load than nonsurvivors. Although all animals developed strong humoral responses, antibodies appeared more rapidly in survivors and were directed against GP(1), GP(2), and NP. Type I interferons were detected early after infection in survivors but only during the terminal stages in fatalities. The mRNAs for CXCL10 (IP-10) and CXCL11 (I-TAC) were abundant in peripheral blood mononuclear cells and lymph nodes from infected animals, but plasma interleukin-6 was detected only in fatalities. In survivors, high activated-monocyte counts were followed by a rise in the total number of circulating monocytes. Activated T lymphocytes circulated in survivors, whereas T-cell activation was low and delayed in fatalities. In vitro stimulation with inactivated Lassa virus induced activation of T lymphocytes from all infected monkeys, but only lymphocytes from survivors proliferated. Thus, early and strong immune responses and control of viral replication were associated with recovery, whereas fatal infection was characterized by major alterations of the blood formula and, in organs, weak immune responses and uncontrolled viral replication.
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PMID:Early and strong immune responses are associated with control of viral replication and recovery in lassa virus-infected cynomolgus monkeys. 1929 92

Three dogs from Saskatoon, Saskatchewan were diagnosed with acute granulocytic anaplasmosis. Fever, lethargy, inappetence, vomiting, diarrhea, and lameness were reported. Lymphopenia, thrombocytopenia, and splenomegaly were identified in all dogs. Inclusions were identified within the cytoplasm of blood neutrophils, and infection with Anaplasma phagocytophilum was confirmed by polymerase chain reaction.
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PMID:Granulocytic anaplasmosis in three dogs from Saskatoon, Saskatchewan. 1988 21

This paper reports on a canine angiosarcoma, presenting as an "undifferentiated metastasizing tumor". A 14-year-old female Cocker Spaniel was referred to the University of Extremadura Veterinary Clinic for clinical examination after suffering rapid deterioration, with chronic cough, anorexia and cachexia. One week after clinical examination, the dog died of right congestive heart failure and ventricular arrhythmia. Blood counts revealed lymphopenia and platelet depletion. The biochemistry profile was within normal limits, except for a drop in blood urea nitrogen. Cytological evaluation of liver and spleen biopsies revealed clustered anaplastic cells that lacked convincing tissue differentiation. Major findings at necropsy were enlarged spleen and multiple, beige to dark-red nodules ranging from 0.5 to 3 cm in diameter in the heart, lung, liver and spleen. At histological examination, multiple nests of anaplastic epithelioid cells were found in sections from all affected organs. Immunohistochemistry revealed widespread expression of CD31 and Factor VIII-related antigen. The neoplastic cells were negative for CD 18. The diagnosis of epithelioid angiosarcoma, localized in the myocardium, lung, liver and spleen was made. The primary site of the neoplasm could not be determined.
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PMID:Widespread epithelioid angiosarcoma with ventricular wall involvement in a dog. 2264 42

Lymphocytopenia is defined by a lymphocyte count less than 1500/mm(3) in adults and less than 4500/mm(3) in children before the age of 8 months. Lymphocytopenia can be global or selectively affect a peculiar lymphocyte subpopulation. The patient's age, the context as well as the associated clinical manifestations and treatment prescribed must be taken into account in order to identify the etiology of lymphocytopenia. In adults, lymphocytopenia can be caused by: (1) insufficient thymic output (primary immune deficiencies, corticosteroid treatment, zinc deficiency, etc.), (2) increased lymphocyte catabolism (radiotherapy, chemotherapy, immunosuppressant, HIV infection, systemic lupus, etc.), (3) modified lymphocyte distribution (viral infections, septic shock, extensive burns, splenomegaly, granulomatosis, etc.), (4) multifactorial or unknown etiology (end-stage renal disease, lymphoid malignancies, solid tumor, ethnicity, etc.). In children, in addition to these etiologies, other immune deficiencies may be responsible for severe lymphocytopenia (thymocytes apoptosis, cytokine deficiencies, altered B-cell and T-cell receptor synthesis, signal transduction and cellular interactions deficiencies). Idiopathic CD4(+) lymphocytopenia is a rare disorder. It is defined by a persisting lymphocyte CD4(+) count less or equal to 300/mm(3) or less or equal to 20% of total lymphocytes in the absence of alternative diagnosis. Clinical symptoms can be absent or include opportunistic infections, auto-immune manifestations, lymphoma or solid tumors. Treatment is similar to that of HIV-infected patients and sometimes relies on specific immunotherapy even though clinical benefit has not been evaluated.
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PMID:[Lymphocytopenia: aetiology and diagnosis, when to think about idiopathic CD4(+) lymphocytopenia?]. 2265 64


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