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)

To test the hypothesis that host resistance factors may be abnormal in Guamanians in whom amyotrophic lateral sclerosis and Parkinsonism-dementia develop, cellular immunity was evaluated in both diseases and compared to that of Guamanians with other nervous-system diseases, normal adult Guamanians and non-Guamanians with amyotrophic lateral sclerosis and Parkinsonism. Diminished responses to skin-test antigens, lymphopenia, diminished per cent and total T cells and, less frequently, decreased mitogen responses were seen in Guamanian patients with amytorophic lateral sclerosis and Parkinsonism-dementia but not in the other patient or normal groups. Guamanian patients with amyotrophic lateral sclerosis and diminished cellular immunity had an increased frequency of HLA-Bw35 (P less than 0.005) and shorter mean duration of disease (P less than 0.05) than those with normal cellular immunity. In Parkinsonism dementia diminished cellular immunity was less strongly associated with HLA-BW35 (P less than 0.05) and was not associated with differences in duration of disease. Normal Guamanians and those with other nervous-system diseases showed no association of diminished cellular immunity with HLA-Bw35. The association appeared disease-related, with onset concomitant with the neurologic expression of Guamanian amyotrophic lateral sclerosis and Parkinsonism-dementia.
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PMID:Cellular immunity in Guamanians with amyotrophic lateral sclerosis and Parkinsonism-dementia. 30 83

We analysed BALF cell findings in 9 patients (group A: 5 patients without lung disease after bone marrow transplantation (BMT), group B: 4 patients with lung disease after BMT) before and after BMT. Before BMT, BALF cell findings in group A were almost normal, whereas a relative increase of lymphocytes was seen in group B. Although total cell counts and cell composition in group A changed little after BMT, CD4/CD8 ratios in BALF lymphocytes decreased. In contrast, a relative increase of lymphocytes and neutrophils was seen in group B and there was variation of CD4/CD8 ratios in BALF lymphocytes after BMT. We there studied the BALF lymphocytes of 3 patients in group A and 4 patients in group B after BMT by means of 2-color analysis. Among CD4+ cell populations, CDw 29+ cells were decreased in both groups after BMT. A relative increase of BALF-CD4+ HLA-DR+ cells and CD8+ HLA-DR+ cells was seen in group A, but was not seen in group B. These findings suggest that there is abnormality of local immunity in the lung after BMT.
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PMID:[Analysis of bronchoalveolar lavage fluid in patients before and after bone marrow transplantation]. 162 96

We analysed the reconstitution of lymphocyte subset during the first 4 weeks after human allogeneic bone marrow transplantation (BMT) in relation to the recovery of hematopoiesis. Lymphocyte subset analysis was performed with flow cytometry. We performed allogeneic BMT from HLA matched sibling donor in 9 patients. We analysed the positive percentage of each surface antigen and analysed data prior to conditioning therapy and weekly during the first 4 weeks after BMT. Results were as follows: Two or 3 weeks after BMT, percentages of CD8+ (CD8+ CD11b+) lymphocyte and CD16+ (CD16+ CD57-) lymphocyte (NK cell) were increased, and those of CD3+ lymphocyte and CD4+ (CD4+ Leu8+) lymphocyte decreased. And the ratio of CD4+ lymphocytes to CD8+ lymphocytes decreased below 1.0 at 2 or 3 weeks after BMT and remained low. In relation to the recovery of hematopoiesis, CD16+ lymphocyte (especially CD16+ CD57- lymphocyte) percentages at the third weeks correlated significantly to the recovery of granulocyte, reticulocyte, and platelet. It seems that CD16+ lymphocytes may play a role in bone marrow cell engraftment and the recovery of hematopoiesis.
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PMID:[Lymphocyte subset reconstitution following human allogeneic bone marrow transplantation]. 183 74

Patients who undergo transplantation with genotypically non-identical T cell-depleted bone marrow are at high risk of graft failure. We have previously shown that graft failure in this setting is an active immunologic process in which CD3+ CD8+ host T cells specifically cytotoxic for donor hematopoietic cells mediate rejection of the graft. In order to reduce the incidence of graft rejection in these patients, we conducted a pilot trial of total lymphoid irradiation (TLI) as an adjunct to total body irradiation (TBI) in an attempt to suppress the activity of residual host derived alloreactive lymphocytes capable of mediating rejection. Ten adults (ages 17-42 years) with hematologic malignancies were treated with TLI prior to hospitalization for allogeneic bone marrow transplantation (BMT). The BMT preparative regimen consisted of cyclophosphamide (60 mg/kg x 2) followed by TBI. The majority of patients received 750 cGy TLI delivered to two complementary radiation ports in five equal 150 cGy fractions. Nine of 10 recipients of genotypically non-identical CD6-depleted marrow who were pre-treated with TLI experienced full hematologic engraftment compared with none of four similar patients previously transplanted without TLI (p = 0.001). TLI induced significant lymphopenia in patients prior to marrow infusion, but had no suppressive effects on the reconstitution of donor lymphocytes. TLI, in combination with T cell depletion of donor marrow, may decrease the rate of graft rejection in individuals who lack perfectly matched HLA-identical sibling donors.
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PMID:Total lymphoid irradiation to prevent graft rejection in recipients of HLA non-identical T cell-depleted allogeneic marrow. 204 74

Severe combined immunodeficiency disease (SCID) with adenosine deaminase (ADA) deficiency is a genetic autosomic recessive disorder with profound impairment of T-cell function, invariably complicated by fatal infections. The absence of ADA-enzyme and the accumulation of deoxy-ATP, with toxic effects on the T-lymphocytes is the common feature of this disease. As a consequence, lymphoid precursors failure to develop into mature T-cells, resulting in absolute lymphopenia and atrophy of the thymus. Bone marrow transplantation from an HLA-identical donor is considered the treatment of choice for this disease. We describe the case of a 1-month-old child with ADA deficiency SCID who underwent bone marrow transplantation (BMT) using paternal haploidentical, lectin-separated marrow, as a source of hemopoietic stem cells.
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PMID:Successful lectin-separated bone marrow transplantation in adenosine deaminase deficiency-related severe immunodeficiency. 209 97

HLA-A, -B, -C, -DR, and -DQ antigens were determined by serology and in cases of severe lymphopenia by RFLP-DNA typing in 51 Caucasians with a diagnosis of AIDS (32 with opportunistic infections and 19 with secondary cancers). In addition, 86 HIV-1 seropositive and 39 HIV-1 seronegative drug abusers and 148 healthy controls were also studied. No significant differences in HLA antigen frequencies were found in comparison of HIV-1 seropositive and HIV-1 seronegative drug abusers with controls, suggesting that HLA polymorphism does not represent a genetic risk for infection with HIV-1. In contrast, a significant increased frequency of B35 (p less than 0.01) and CW4 (p less than 0.01) was observed in both groups of AIDS patients as compared to controls. Moreover, DR2 was increased in frequency in patients with opportunistic infections (p less than 0.01) and DR3 was completely absent in patients with secondary cancers (p less than 0.05). In the latter group, the DR5 frequency was increased, although nonsignificantly. These findings provide strong evidence for the existence of HLA-linked factors of susceptibility and host resistance to AIDS.
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PMID:HLA antigens are risk factors for development of AIDS. 278 69

We composed a model from autoimmune serologic findings, HLA antigens, and clinical findings that explains, at least partially, the clinical heterogeneity of 40 patients with systemic lupus erythematosus (SLE). In these patients, anti-RO (SS-A) was related to the HLA-DQ1/DQ2 heterozygotes, anti-La (SS-B) was related to HLA-B8 and HLA-DR3, and anti-nuclear RNP (Sm) was related to HLA-DR4. Lymphopenia was associated with anti-Ro (SS-A) and, secondarily, with anti-single-stranded DNA. Renal disease in these SLE patients was inversely associated with anti-La (SS-B) and was positively associated with anti-double-stranded DNA. There were no associations between the HLA antigens and these clinical manifestations. The results support a model of disease expression in which individuals are nonspecifically potentiated for SLE. Their HLA antigen composition influences the production of particular autoantibodies that are related in complex ways to the different particular clinical findings of SLE manifested in individual patients.
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PMID:A model for disease heterogeneity in systemic lupus erythematosus. Relationships between histocompatibility antigens, autoantibodies, and lymphopenia or renal disease. 278 39

Nineteen children who presented with fever, hepato-splenomegaly, bone marrow and/or hepatic failure, and biopsy evidence of histiocytic proliferations were evaluated for lymphocyte dysfunction and evidence of prior viral infection. Seventeen of the children had erythrophagocytosis consistent with the previously described virus-associated hemophagocytosis syndrome (VAHS) or Familial erythrophagocytic lymphohistiocytosis (FEL). The other two had benign histiocytic proliferations in the central nervous system (CNS) with liver and bone marrow dysfunction. There were two sibling pairs and six patients with known disorders of immune deficiency. The remaining nine cases appeared to be sporadic and idiopathic. Epstein-Barr Virus (EBV) was identified in patients by serologic or DNA hybridization studies (15), EBV and cytomegalovirus (CMV) (1), adenovirus plus EBV and CMV (1), or adenovirus and EBV (1). Herpes zoster was associated with reactivation of symptoms in one patient. Immunologic impairment was evidenced by lymphopenia in 10 of 19 patients. More extensive evaluations could be done at diagnosis on only some of the children because the histiocytic proliferative syndrome was not recognized or because there were insufficient numbers of lymphocytes in samples obtained. For those who could be evaluated, the following immune deficiencies were found: decreased lymphocyte proliferation to mitogens (4 of 9), absent or markedly decreased natural killer function (5 of 5), and decreased cytotoxic lymphocyte reactivity to allogenic EBV-infected target cells (3 of 3). A new finding reported here is a higher than expected prevalence of HLA types A30, B8, and A1/B8 among the patients tested.
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PMID:Virus-associated histiocytic proliferations in children. Frequent association with Epstein-Barr virus and congenital or acquired immunodeficiencies. 284 31

Initial reports of blood T cell subsets in insulin-dependent (type I) diabetes mellitus (IDDM) are conflicting and, consequently, difficult to relate to animal models of the disease. To minimize technical artefacts, which may have contributed to previous results, we used direct immunofluorescence on whole blood and counted 3,000 lymphocytes by flow cytometer. Forty-two IDDM patients divided in three groups of 14 according to the disease duration and 12 age and sex matched controls were studied for T3, T4, T8 and HLA-DR expression. No statistically significant differences were found in their total blood lymphocyte counts or in the percentage of T3, T4 and T8 positive cells, although mild lymphopenia was found in the group of long-standing diabetics. The percentage of activated T cells, identified as T3+/DR+ cells, was significantly increased in the groups of patients studied more than a month after diagnosis and in four of 14 patients studied within a month from diagnosis. Seven new onset IDDM patients were studied for co-expression of T8 and Leu 15 antigens (putative suppressor cell phenotype), but no significant differences was found compared with controls. We conclude that T4/T8 ratio abnormalities previously reported in Ficoll separated cells are not reproduced when unseparated cells are analysed by flow cytometry, although the presence of HLA-DR+ T cells is confirmed.
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PMID:T-lymphocyte subpopulations in insulin-dependent (type I) diabetes mellitus. 293 83

Cytomegalovirus (CMV) and Epstein-Barr virus (EBV), frequently found in the acquired immune deficiency syndrome (AIDS), have been suspected of contributing to the latter immunodeficiency. The ability of normal HLA-identical sibling bone marrow to reconstitute an 8-month-old infant with severe combined immunodeficiency infected with these two viral agents is of interest. After presentation with severe mucocutaneous candidiasis, cavitary pulmonary disease, nodular cutaneous lesions, and hepatic abscesses containing acid-fast organisms, immunologic studies revealed lymphopenia, 1-3% T cells, and no lymphocyte responses to mitogens. Prior to transplantation, the infant's blood B lymphocytes grew spontaneously in culture, suggesting they were infected with EBV. Indeed, an appropriate antibody response to EBV was detected at 2 months post-transplantation. At 3 weeks postgrafting, neutropenia and cholestatic jaundice developed without other signs of graft versus host disease. Liver biopsy demonstrated CMV but no EBV by DNA hybridization. There was evidence of T- and B-cell function by 2 weeks postgrafting, including vigorous in vivo and in vitro responses to candida. Although the blood lymphocyte T4:T8 ratio was inverted at 2 weeks, it reverted to normal by 6 weeks post-transplantation. All clinical disease resolved by 8 months and karotyping revealed all T and B lymphocytes to be XX. Thus, despite infections with both CMV and EBV, complete immunologic reconstitution was achieved in this, the most severe of all genetically determined immunodeficiency conditions, arguing against these viruses having a major role in the failure of bone marrow transplantation in AIDS.
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PMID:Successful immune reconstitution in severe combined immunodeficiency despite Epstein-Barr virus and cytomegalovirus infections. 298 Nov 67


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