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At least 199 records · Page 11Linked to original sources
PubMed2002

Multifocal progressive leukoencephalopathy occurring after refractory anemia and multiple infectious disorders consecutive to severe lymphopenia.

Progressive multifocal leukoencephalopathy (PML) is related to central nervous system infection with JC virus (JCV). This leukoencephalopathy occurs in immunocompromised patients such as those with acquired immunodeficiency syndrome (AIDS) or lymphoid malignancies. We describe here a patient with myelodysplastic syndrome who developed several life-threatening infections including listeriosis, tuberculosis, and PML. Listeriosis and recurrence of tuberculosis preceded the occurrence of PML. Neurologic features associated with major ataxia, speech disorders, and PML were documented by cranial magnetic resonance imaging showing typical features in the cerebellum and proven by polymerase chain reaction (PCR) detection of JCV DNA in the cerebrospinal fluid. No specific treatment was decided because of progression toward acute myeloid leukemia. In this case, PML occurred with no susceptibility and without immunosuppressive treatment. Our case adds further support to the association between the impairment of T-cell immune responses and myelodysplastic disorders.

Anemia, Refractory↗
PubMed1998

Functional Fas-ligand expression on T cells from HIV-1-infected patients is unrelated to CD4+ lymphopenia.

Recent studies have demonstrated that the expression of Fas by peripheral T cells from HIV-1+ patients is deregulated and increases the susceptibility of these cells to undergo apoptosis. Here, we show that secretion of Fas-ligand (L), the complementary agonist of Fas, is abnormally upregulated in CD4+ cells from HIV-1-infected individuals, particularly during the non-lymphopenic stages of the disease. An increase of soluble Fas-L occurred in T cell cultures from 26 patients with a number of CD4+ cells higher than 400/microliter, whereas it was almost undetectable in cultures from 21 severely lymphopenic patients (CD4+ < 200/microliter). The MTT test, cytofluorimetric analysis of cellular DNA, cytotoxicity, and proliferative assays using the Fas-transfected WC8 mouse lymphoma confirmed the cytocidal capability of T cell supernatants from non-lymphopenic patients. Double-fluorescence analysis revealed that the majority of CD4+ cells (approximately 90%) in these cultures secreted Fas-L in the presence of high intracellular gamma-interferon and low Bcl-2. In contrast, the CD8+/Fas-L+ population was comparably decreased (approximately 55%). Molecular cloning of Fas-L revealed a substantial expression of Fas-L mRNA in cells from non-lymphopenic patients compared with patients with advanced disease and healthy controls. Since CD4+ cells of Th1 phenotype are impaired during HIV-1 infection and show high cellular expression of Fas-L, it is conceivable that excess Fas-L during the early or non-lymphopenic phase of the disease increases the extent of apoptosis in these cells by the Fas/Fas-L pathway. The defective expression of the ligand in severely lymphopenic stages could be explained by exhaustion of this mechanism as the disease progresses.

Apoptosis↗
PubMed2006

An IL-7 splicing-defect lymphopenia mouse model revealed by genome-wide mutagenesis.

Homeostasis of the hematopoietic system is tightly regulated by an array of cytokines that control proliferation, differentiation and apoptosis of various cell lineages. To identify genes that are essential for hematopoietic homeostasis, we screened C57BL/6 mice that had been genome-wide mutagenized by N-ethyl-N-nitrosourea (ENU) to produce altered blood cell composition. We identified a mutant mouse line with a drastic reduction in the number of T and B cell lineages in lymphatic tissues and peripheral blood, as well as severe atrophy of the thymus and lymph nodes. Genotyping with a genome-wide single nucleotide polymorphism (SNP) marker set mapped the mutant phenotype to chromosome 3A and subsequent direct DNA sequencing revealed a G-to-A point mutation in the splicing donor site of the third exon of the candidate gene for IL-7, a lymphocyte survival cytokine. Such mutation resulted in skipping of exon 3 and production of an internally truncated IL-7 (DeltaE3-IL7). Furthermore, using recombinant proteins produced in a baculoviral system, we demonstrated that DeltaE3-IL7 had no detectable anti-apoptotic activity even at a dose that was 30 times more than that required for a wild-type protein to manifest a full activity in a naïve T cell survival assay. Our data suggest that this mutant mouse line provides an alternative animal model for the study of severe combined immunodeficiency (SCID) syndrome in humans.

Amino Acid Sequence↗
PubMed1988

Early lymphopenia in burned children with and without the toxic shock syndrome.

The white cell count (WCC) response to thermal injury in children in week 1 postburn has been investigated in a prospective study of 33 patients. Two of these patients developed the toxic shock syndrome (TSS) and, together with seven previously diagnosed cases of the TSS, were studied as a separate group. The WCC response in the non-TSS (control) patients was compared with the response observed in the TSS group. In all patients there was an initial leucocytosis followed by a fall in WCC to a nadir between days 2 and 4. The nadir was significantly lower in the TSS group than that observed in the control group. A rise in the WCC was observed over the following 3-4 days in both groups. In the control group the changes in the WCC were mainly attributable to changes in the granulocyte count with little change in the lymphocyte count. There were similar changes in the granulocyte count in the TSS group but, in contrast to the control group, the lymphocyte count fell, to below the normal range, on day 3. The lowest lymphocyte count observed in the TSS group was significantly lower than that seen in the control group. The observation of a profound fall in the total WCC, granulocytes, and in particular the lymphocytes, between days 2 and 4 are additional factors that may help with the diagnosis of TSS.

Burns↗
PubMed2005

Lymphopenia and spontaneous autorosette formation in SOD1 mouse model of ALS.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by motoneuron degeneration. Increasing evidence suggests immune system involvement in ALS pathogenesis but information about peripheral blood characteristics has been lacking. We evaluated hematological and morphological parameters in peripheral blood of G93A SOD1 mice. A significant decrease in white blood cells was found at the end stage of disease. The lymphocyte reduction may suggest immunodeficiency in ALS. Spontaneously forming rosettes with autologous erythrocytes were noted in approximately 28% of lymphocytes in SOD1 mice. To our knowledge, this is the first study characterizing hematology and revealing autorosettes in the SOD1 mouse model of ALS at the terminal phase of disease.

Amyotrophic Lateral Sclerosis↗
PubMed1977

Lymphopenia and lymph node histology following repetitive extracorporeal irradiation of blood in normal and thymectomized calves.

Repetitive extracorporeal irradiation of the circulating blood (RECIB) in normal or thymectomized calves and RECIB plus Imuran were used for comparative studies on the depletion of blood and lymph node lymphocytes. Elimination of the easily mobilizable pool of lymphocytes was almost complete within approximately 6 days after commencing RECIB and was reflected by a reduction of approximately 50% in the numbers of paracortical lymphocytes. Blood lymphocyte counts were reduced to approximately 1/3 to 1/4 of the pre-irradiation values. Thymectomized calves had lower pre-irradiation blood lymphocyte counts than non-operated controls, however, the reduction in the number of blood lymphocytes was proportionally similar. Continuation of RECIB beyond one week did not result in a further depletion of blood lymphocytes. The lymphocyte counts in the follicular cortex and in the medulla of lymph nodes were not significantly changed by the various procedures. RECIB of 8-16 days duration did not alter the number of germinal centers in non-thymectomized calves, however, in thymectomized animals treated with Recib, the number of germinal centers was reduced.

Animals↗
PubMed2001

Short-term hyperglycemia induces lymphopenia and lymphocyte subset redistribution.

Alterations in lymphocytes are a common finding in both type I and type II diabetes. Autoimmune phenomena in type I diabetes, the stage of the diabetic disorder and metabolic effects of therapeutic interventions may also affect actual distribution of lymphocyte phenotypes. This study investigated immunological effects specific to standardized hyperglycemia in non-diabetic individuals to exclude immunological changes potentially related to diabetes stage and treatment. 37 subjects (mean age +/- SD 39 +/- 5 years) underwent a sequence-controlled crossover with oral administration of a solution containing either 75 g glucose or artificial sweetener (i.e. placebo). At rest and at two hours, counts of white blood cells (WBC), mixed lymphocytes, mature T-cells (CD3), T-helper cells (CD4), T-suppressor/ cytotoxic cells (CD8), B-cells (CD19), natural killer cells (CD16/CD56), and interleukin-2 receptor bearing peripheral blood mononuclear cells (CD25) were measured by flow cytometry. Subjects showed a significant decrease in WBC, lymphocytes, and all lymphocyte subsets with the OGTT compared with the placebo solution (p < .05 to p < .001). In non-diabetic individuals, short-term hyperglycemia induces immunological changes that may be relevant to explain similar findings in patients with diabetes mellitus. Future studies need to validate these findings and their potential clinical implications in a diabetic population.

Adult↗