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)

Cold-reactive lymphocytotoxin (CLT) in the sera of patients with sarcoidosis was investigated by a complement-dependent 51Cr-release cytotoxicity assay. CLT activity was present in 19 out of 34 active sarcoidosis patients, but absent from all 6 resolved sarcoidosis patients and from 19 out of 20 healthy control subjects. CLT activity was not correlated with age or sex, degree of lymphopenia, presence of anergy, or with other clinical parameters, but was correlated with the activity of the disease. Lymphocytotoxic activity was greatest at 15 degrees C and negligible at 4 degrees C and 37 degrees C. The CLT in sarcoidosis sera had higher reactivity to B-lymphocytes than to T-lymphocytes. The CLT purified from sarcoidosis serum was identical with the antibody of IgM class. It was cytotoxic for B-lymphocytes but not reactive to T-lymphocytes. These results suggest that an IgM cold-reactive lymphocytotoxin exists in the sera of patients with active sarcoidosis.
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PMID:IgM cold-reactive lymphocytotoxin from sera in patients with sarcoidosis. 633 80

Sarcoidosis is a multisystem disease characterized by enhanced immune responses at sites of involvement. For this reason, an immunohistological study using monoclonal antibodies against T-cell subpopulations was carried out in order to evaluate the topographic distribution of immunocompetent cells in tissue sections obtained from a variety of involved organs, such as parenchymal lung, lymph nodes, eyes, skin, and liver. Biopsy specimens were also stained for detection of immunoglobulins, complement, and fibrinogen deposits. The data demonstrate a redistribution of T cells from the blood to all the sites of disease activity where they account for the large majority of infiltrating cells, both in the early lesions (merely a lymphocytic infiltrate) and in well-organized granulomas. Moreover, these cells express a helper-related phenotype, as demonstrated by the high Leu-3/Leu-2 ratios, at sites of involvement with respect to the blood (blood, 1.8/1; transbronchial lung biopsies, 10.5/1; lymph nodes, 19/1; skin, 28/1; liver, 22/1; eye, 14/1). In line with this helper infiltration is the presence of plasma cells and immunoglobulin deposits, suggesting a local hyperreactivity of the B-cell immune system. Both the hypergammaglobulinemia and the T lymphopenia usually observed in the blood of sarcoid patients could be explained by these observations. Comparative analysis of immunohistological data and bronchoalveolar lavage (BAL) findings provides further evidence that BAL cellularity reflects the changes already occurring in lung histology. The studies emphasize the importance that immunological phenomena play in the pathogenesis of sarcoidosis and provide new insights into the mechanisms leading to the formation and maintenance of the sarcoid granuloma.
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PMID:Immunohistological study in sarcoidosis: evaluation at different sites of disease activity. 636 83

A quantitative analysis of leukocytes in the peripheral blood of 16 patients with lymphogranulomatosis X revealed the following findings: The number of total leukocytes, monocytes, neutrophils, and eosinophils varied considerably and showed no clear common tendency. Blood basophils were found to be clearly increased with a mean value of 0.17 +/- 0.18 X 10(9)/1 as compared to 55 normal donors (0.04 +/- 0.01 X 10(9)/1). Lymphocyte counts were within the normal range. Lymphopenia was seen in 2 patients. Lymphocytes with azure granules which encompass T-suppressors were found to exceed normal values by a factor of 15. In 14 cases a variable number of hyperbasophil cells were present. Lymphogranulomatosis X seems to present with a characteristic blood picture which might be of diagnostic aid.
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PMID:Blood findings in lymphogranulomatosis X. 669 1

Lymphocyte counts in the peripheral blood were performed in 123 patients with thoracic sarcoidosis and in 33 healthy subjects. A significant decrease in the number of lymphocytes as compared to controls was observed, at least in patients of Caucasian origin. This lymphopenia was more pronounced when the disease was of more than 10 years' duration, was accompanied by extrathoracic manifestations and belonged to radiological groups II or III. The only parameter of pathological activity with which it correlated was serum angiotensin converting enzyme activity. Patients from the french Caribbean had scattered lymphocyte counts which precluded any firms conclusion.
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PMID:[Clinical value of the blood lymphocyte count in thoracic sarcoidosis in adults. Apropos of 123 cases]. 671 44

The percentage and the absolute numbers of T lymphocytes Fc receptors for IgG and IgM (T gamma and T mu lymphocytes, respectively) were evaluated in fourteen patients with active sarcoidosis and in a group of controls. A marked increase in the percentage of T gamma cells and a net decrease of T mu cells were found. Although sarcoidosis patients present a T lymphopenia, the absolute number of T gamma lymphocytes was still increased whereas the T mu decrease was even more pronounced. The possible causes of this imbalance in view of the recent interpretations of T suppressor and T helper lymphocytes are discussed.
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PMID:Imbalance in T gamma and T mu lymphocyte subpopulations in patients with sarcoidosis. 696 13

Patients with active sarcoidosis have a depression in systemic cell-mediated immunity manifested by lymphopenia, a reduction in circulating T cells, and impaired responses of these cells to polyclonal mitogens and recall antigens. Studies of bronchoalveolar cells (BA) have disclosed characteristic changes in lymphocyte populations that are opposite to what is found in peripheral blood. Since previous lavage studies have not specifically addressed endobronchial disease, we present results of peripheral blood (PB) and BA lymphocyte studies in a patient with acute pulmonary sarcoidosis who had gross endobronchial nodules. The lymphocytosis in the BA air space of this patient was greatly increased compared with patients with newly diagnosed sarcoidosis but no overt endobronchial disease. Cell surface markers, morphology, and in vitro proliferative response indicated that the BA lymphocytes were stimulated and more reactive than PB lymphocytes, suggesting a local immune inflammatory response. Bronchial biopsy specimens showed mononuclear cell infiltration of the epithelium overlying the inflammatory nodules. The biopsy examination and great increase in lymphocytes recovered from the airways suggest that the bronchi were a source of the BA lymphocytes. Since clinically inapparent bronchial involvement is frequent in sarcoidosis, inflamed bronchi may also be a source of BA lymphocytes in the absence of conspicuous endobronchial nodules.
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PMID:Nodular endobronchial sarcoidosis: a study comparing blood and lung lymphocytes. 722 7

The authors report a case of sarcoidosis associated with protein losing enteropathy. The diagnosis of intrathoracic stage I sarcoidosis was based on x-ray and biopsy of mediastinal lymph nodes. Enteric protein loss was suspected because of edema lasting for 2 yr, hypoproteinemia, decreased concentrations of serum immunoglobulins, and lymphopenia involving mainly T-cells and proved by 51CrCl3 test (21%/120 hr). Lymphography was consistent with granulomatous involvement of retroperitoneal lymph glands while small bowel biopsy showed blunt villi and dilated lacteals. All the pathological parameters normalized after 6 mo of prednisone treatment. In some cases of sarcoidosis, when abdominal lymph glands are involved, cellular and humoral immunologic derangements may be caused or potentiated by excessive enteric protein and lymphocyte loss.
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PMID:Sarcoidosis and protein losing enteropathy. 735 18

We report the occurrence of cutaneous sarcoid-like granulomas in one patient with common variable immunodeficiency and another with 'thymoma and hypogammaglobulinaemia'. To our knowledge, this is the first time that such skin lesions have been described in patients with primary immunodeficiency. These granulomas may be attributed to a combination of interleukin-2 deficiency and a profound CD4 lymphopenia. The lesions are similar to the non-infectious 'papular eruption' associated with human immunodeficiency virus infection, and might reflect a common pathogenic mechanism.
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PMID:Cutaneous sarcoid-like granulomas in primary immunodeficiency disorders. 830 1

72 clinical and laboratory features were analyzed on the IBM PC 486 for 126 new cases of lymphogranulomatosis prior to treatment. Myelograms were found to vary with sex and age of the patients demonstrating close relations between hemopoiesis and processes in the lymph nodes. In males maturation of myeloid elements KM was inhibited, though they had more monocytes KM. These monocytes got more numerous in unfavorable histological variants and generalization. Lymphopenia and monocytosis were more pronounced in patients under 30 becoming more severe in generalization and intoxication. Age-related changes in cholesterol in lymphogranulomatosis patients were abnormal: in older patients cholesterol was low. This phenomenon is extremely unfavorable. The findings elucidate prognostic value of sex and age in lymphogranulomatosis and suggest a hypothesis that monocytes (macrophages) and secreted by them monokines are responsible for specific intoxication, neutrophilia and lymphopenia. Berezovsky-Sternberg cells may be hybrids of macrophages and B-lymphocytes.
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PMID:[Lymphogranulomatosis: a systems analysis of the age- and sex-related characteristics of hemopoiesis and metabolism]. 917 75

Because of its association with cutaneous anergy, sarcoidosis was originally viewed as a defect of cellular immunity. Supporting that misperception were early studies of peripheral blood lymphocytes that found lymphopenia and impaired lymphocyte responses to mitogens and recall antigens. The clue to a vast underlying network of complex hyperactive cellular immune functions was discovered in the paradoxical finding of in vitro spontaneous lymphoblastic transformation and lymphokine production. Subsequently, investigative focus shifted to the activated, proliferating T-helper lymphocytes, the lymphokines of which were found to function in the recruitment and retention of monocytes for granuloma development. T-helper lymphocytes also contributed to the mechanism of hypergammaglobulinemia through their influence on B cells. The most intriguing question about sarcoid immunology is the initiating factor that triggers the T-lymphocyte activation and proliferation in the first place. There is much to suggest that antigen processing and presentation launches the process. Because lymphocyte activation and proliferation antedate granuloma formation at K-S skin test sites and in the lung, we combined the harvesting technique of BAL with the K-S bioassay to show that granulomagenic antigen is being processed by monocyte-macrophages. The finding of autologous monocyte-macrophage granulomagenicity raises the distinct possibility that sarcoidosis is a unique cell-mediated type of autoimmune process. The isolation and identification of the granulomagenic factor is the exciting research frontier ahead.
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PMID:Immunology of sarcoidosis. 941 55


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