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PubMed2006

Lymphopenia-driven CD8(+) T cells are resistant to antigen-induced tolerance in NOD.scid mice.

T cells undergoing lymphopenia-driven proliferation acquire effector and memory properties that can be pathogenic. Indeed, generalized lymphopenia is associated with a variety of autoimmune diseases such as type 1 diabetes. The current study was carried out to determine how CD8(+) T cells undergoing acute lymphopenic expansion respond to antigen under tolerizing conditions in vivo. Adoptive transfer of diabetes by TCR-transgenic CD8(+) T cells was enhanced following treatment of NOD. scid recipients with a high dose of soluble peptide. Furthermore, whereas TCR-transgenic CD8(+) T cells underwent clonal deletion and failed to differentiate into CTL in peptide-treated lymphoreplete recipient mice, TCR-transgenic CD8(+) T cells in a lymphopenic environment were resistant to clonal deletion, and CTL differentiation was enhanced by a high dose of soluble peptide. Moreover, peptide treatment had distinct effects on expression of the anti-apoptotic protein Bcl-X(L) in TCR-transgenic CD8(+) T cells under lymphopenic versus lymphoreplete conditions. These results demonstrate that CD8(+) T cells undergoing lymphopenia-driven expansion in NOD. scid recipients are resistant to antigen-induced tolerance, and readily differentiate into CTL upon stimulation with a high dose of soluble peptide.

Animals↗
PubMed1989

Mechanisms of tumor necrosis factor alpha-induced lymphopenia, neutropenia, and biphasic neutrophilia: a study of lymphocyte recirculation and hematologic interactions of TNF alpha with endogenous mediators of leukocyte trafficking.

Tumor necrosis factor alpha (TNF) induces lymphopenia, neutropenia, and biphasic neutrophilia after intravenous injection of 3,000 U TNF in Lewis rats. The mechanism of TNF-induced lymphopenia was investigated by means of thoracic duct cannulation. Hourly measurements of lymphocyte recirculation via the thoracic duct failed to reveal any significant decrease in lymphocyte recirculation in TNF-treated vs. control rats, suggesting that a decrease in lymphocyte recirculation through the thoracic duct is not the mechanism for TNF-induced lymphopenia. The mechanism of TNF-induced neutropenia was investigated by administering TNF to rats in whom a neutrophilia had been induced with interleukin-1 (IL-1). In rats with neutrophilia, TNF resulted in a sharp decrease in the circulating neutrophil pool, demonstrating that TNF induces neutropenia by causing neutrophils to leave the circulating pool rather than decreasing neutrophil release from the marrow. The mechanism of neutropenia was furthermore shown to be due to the transient intravascular margination of neutrophils by administering epinephrine concomitantly with TNF. Epinephrine, which causes neutrophilia solely by demargination, abrogated the TNF-induced neutropenia and actually resulted in a neutrophilia that was greater than the neutrophilia occurring in epinephrine alone-treated rats, demonstrating both that TNF had already caused release of marrow neutrophils at the time of peripheral neutropenia, and that the paradoxical neutropenia was due to the transient intravascular margination of neutrophils. The known property of epinephrine to cause neutrophilia exclusively by demargination was proved by examination of the bone marrow of epinephrine-treated rats in whom no decrease in marrow neutrophils was observed (in contrast to TNF- and IL-1-treated rats in whom neutrophilia is accompanied by a depletion of marrow neutrophils). The mechanism of TNF-induced neutrophilia was investigated by modulating the magnitude of both the first and second peaks of neutrophilia by priming of rats with daily injections of IFN gamma for 2 days prior to administration of TNF. The first peak of neutrophilia in IFN gamma-primed TNF-treated rats was decreased in comparison to TNF alone-treated rats because of the well-known neutropenic and myelosuppressive effect of IFN gamma, which resulted in a decrease in the number of neutrophils that could be recruited to cause neutrophilia.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1997

Phenotypic consequences after restoration of lymphopenia in the diabetes-prone BB/OK rat.

Besides other factors, lymphopenia (ll) is essential for development of insulin-dependent diabetes mellitus in the BB rat. It is unknown which phenotypic consequence may have a non-lymphopenia. Therefore, the region containing the lymphopenia gene of the BB/OK rat was replaced with that of the non-lymphopenic (LL) and hypertensive rat, SHR (11 cM, D4Mit6-LL-Npy-Spr). The resulting congenic strain, BB.LL, did not develop diabetes up to an age of 30 weeks and was non-T-lymphopenic. The SHR region did not influence the blood pressure of the BB.LL rat, but influenced obviously the motor activity, body weight, serum lipids, and the 24h urine excretion of urea, sodium, and potassium.

Animals↗
PubMed1979

Lymphopenia and lymphocyte transformation in alcoholics.

The basis of peripheral blood lymphopenia observed in patients with chronic alcoholism and liver disease was investigated by examining the effect of sera of these patients on in vitro transformation of normal human peripheral blood lymphocytes. A positive correlation was demonstrated between the serum inhibition of phytohaemagglutinin- and pokeweed mitogen-induced transformation and the degree of lymphopenia. Thus serum factors may contribute to the observed lymphopenia by inhibiting lymphocyte production in vivo.

Alcoholism↗
PubMed2003

B-cell lymphopenia and hypogammaglobulinemia in thymoma patients.

Thymic tumors represent a unique neoplastic disease associated with various immune-mediated syndromes. Immune impairment is generically recognized to be associated with thymoma. Hypogammaglobulinemia and recurrent pulmonary infections in thymoma patients define Good's syndrome. Apart from sporadic reports focusing on this topic, there is still a lack of knowledge on immune assessment and clinical sequelae in thymoma patients. The present study was performed to evaluate immunoglobulin levels, CD19(+) B lymphocytes, and CD3(+) T lymphocytes in a large series of thymoma patients from a single institution. The occurrence of recurrent severe infections was related to immunological findings to identify the possible correlation with the immunodeficiency status. Eighteen patients (eight males, ten females, mean age: 56 years, range: 19-75) with a pathological diagnosis of thymic tumor were studied. Six patients suffered from clinical recurrent pulmonary infections. Blood samples were collected to measure serum immunoglobulins and analyze immunophenotype. Low T lymphocyte number was found in 22% of the patients. T lymphocytosis was present in one patient. Panhypogammaglobulinemia was found in 4 of 18 patients (22%). Conversely B lymphopenia was a frequent finding in this series of thymoma patients (9 of 18, 50%). Five of six patients (83%) with recurrent infections had B lymphopenia, while only two (33%) had panhypogammaglobulinemia. B lymphopenia often occurred in this series of thymoma patients and was related to susceptibility to recurrent infections more than hypogammaglobulinemia. Therefore, immunophenotype has to be monitored in follow-up of thymoma patients because it may reveal significant abnormalities.

Adult↗
PubMed1988

Neutrophilia and lymphopenia in major mood disorders.

Alterations in peripheral blood leukocyte distribution in major depression, including lymphopenia, neutrophilia, eosinopenia, and monocytopenia, have been described. The present study was designed to replicate these results, but with methodological improvements, including age-, sex-, and race-matched control subjects; DSM-III and Research Diagnostic Criteria diagnoses based on the Schedule for Affective Disorders and Schizophrenia interview; objective and subjective severity of depression measured quantitatively; and consideration of psychosocial stressors (DSM-III, Axis IV). We found relative lymphopenia and absolute neutrophilia and leukocytosis in depression, but did not find decreased numbers of eosinophils or monocytes. The relative lymphopenia and absolute neutrophilia were present in the subgroup of only unipolar depressed patients, but not in the bipolar, currently depressed subgroup. However, these blood cell changes were not found in a subgroup of patients who had been medication free greater than or equal to 1 month but only in the subgroup of patients using medication at the time of phlebotomy. Groups formed on the basis of psychosocial stress levels were not found to have significant significant intergroup differences in white blood cell (WBC) counts. The clinical significance of these findings needs study. While leukocytosis and neutrophilia can be found in major depression, these changes are perhaps secondary to medication use.

Adult↗
PubMed2004

A causal link between lymphopenia and autoimmunity.

It is well recognized that the composition of the mature T cell population is subject to strict homeostatic control. The TCR repertoire and relative proportions of various T cell subsets are established in the thymus, and continue to be shaped and regulated in the periphery. As the thymic function declines, peripheral homeostatic mechanisms assume increasing importance. Indeed, loss of thymic function does not lead to progressive decline of T cell numbers because peripheral mechanisms ensure that the size of the T cell population is maintained due to proliferation of residual cells. However, our current understanding of the basic mechanisms of 'homeostatic' or lymphopenia-induced proliferation suggests that this drive to maintain population size may be accompanied by loss of TCR diversity and emergence of auto-reactive effector T cells. This prediction is supported by experimental and clinical evidence. This consideration is important because lymphopenia is seen commonly in clinical practice as a consequence of viral infections, or medical treatment of cancer, autoimmunity, and graft rejection. Lymphopenia may be a simple link between viral infections and autoimmunity, and may be one reason for common failure of very potent, but non-specific, immunosuppressive drugs in current clinical use.

Animals↗
PubMed2005

Role of vascular cell adhesion molecules and leukocyte apoptosis in the lymphopenia and thrombocytopenia of patients with severe acute respiratory syndrome (SARS).

The immunopathogenesis of leukopenia and thrombocytopenia in patients with severe acute respiratory syndrome (SARS) is unclear. In order to explore the leukopenia mechanism, we studied 15 SARS patients who were previously healthy, and 15 age-matched normal controls in a paired design. Soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble Fas ligand (sFasL) in plasma were measured by ELISA, and intracellular activated caspase-3 fragment in different leukocytes was determined by flow cytometry. Patients with SARS had significantly lower lymphocyte and platelet counts and significantly higher sVCAM-1 and sFasL levels compared to healthy controls. sVCAM-1 levels correlated negatively with total leukocytes and platelet counts, but positively with plasma sFasL levels. Intracellular cleaved caspase-3 expression was also significantly higher in lymphocytes from SARS patients in acute phase than in convalescent stage. Lymphopenia and thrombocytopenia in SARS patients may be caused, in part, by enhanced vascular sequestration associated with increased sVCAM-1 levels. However, lymphopenia may be due to enhanced cell death. Inhibition of cell adhesion and caspase-3 activation could, therefore, have prevented SARS patients from developing thrombocytopenia and lymphopenia.

Adult↗
PubMed1983

Passive transfer of insulitis and lymphopenia in the BB rat.

The BB rat spontaneously develops insulitis followed by impaired glucose tolerance (IGT) or an insulin-dependent diabetic (IDDM) syndrome. Passive transfer of insulitis from newly detected diabetic BB rats to nude mice has been achieved by intraperitoneal or intravenous injection(s) of blood and spleen lymphocytes. After a single injection of cells, 37% of the mice (n = 72) showed insulitis with a mean intensity of 1.9 +/- 0.3 (on a scale of 0 to 3). After three successive injections, 58% of the recipient mice (n = 12) showed insulitis with a mean intensity of 2.5 +/- 0.3. Only one of the control mice (n = 45) demonstrated mild insulitis. The small number of affected islets (13% after a single injection, 17% after three injections) probably explains the absence of random or post IP glucose hyperglycemia in the recipient mice. During this study the yield of lymphocytes in diabetic BB rats was found to be consistently lower than in control normal Wistar rats. This lymphopenia was found not only in the blood and the spleen but also in the thymus and the lymph nodes. Peripheral blood lymphopenia antedated glucoregulatory disturbances. All rats showing either insulitis alone or with IGT or IDDM were lymphopenic. None with normal lymphocyte counts developed any abnormality. Diabetics showed a marked decrease in the proportions of T+ lymphocytes in all tissues whereas the proportion of B(Ia+) lymphocytes was normal in blood, spleen, and thymus but increased in lymph nodes. However, in absolute terms both T+ and Ia+ lymphocytes were decreased. The subset decreased by the greatest proportion in all tissues, except in the thymus was the one that includes helper T lymphocytes. This lymphopenia could be related to the presence of circulating antilymphocyte antibodies. These results strongly support a role for altered immunity in the etiology of the syndrome. If the observed anomalies of lymphocyte numbers and subsets are responsible, then a novel mechanism different from most other "autoimmune" disorders must be implicated.

Animals↗
PubMed1980

Prevention of postoperative lymphopenia and granulocytosis by epidural analgesia.

Blood leucocyte-counts, cortisol, and glucose were measured in twelve healthy premenopausal women undergoing elective abdominal hysterectomy during either general anaesthesia (six women) or epidural analgesia (T4 to S5) (six women). Surgery during general anaesthesia caused significant lymphopenia 6 and 9 h after skin incision and significantly increased granulocyte-counts 6, 9, and 24 h after skin incision. Epidural analgesia prevented lymphopenia and reduced granulocytosis to about 40% of that seen in the group receiving general anaesthesia. The normal increase in plasma glucose and cortisol during and after surgery was abolished by epidural analgesia. These results indicate that neurogenic stimuli from the surgical area, probably through their influence on adrenal hormones (cortisol and adrenaline), are the main mediators of postoperative lymphopenia and are partly responsible for postoperative granulocytosis. Inhibition of the endocrine-metabolic response to surgery may prevent postoperative immunodepression.

Adult↗
PubMed2003

Association of lymphopenia with porcine circovirus type 2 induced postweaning multisystemic wasting syndrome (PMWS).

The composition of peripheral blood leukocyte populations was studied following experimental PCV2-infection in 3-week-old piglets. Four of 10 PCV2-infected piglets developed clinical and pathological symptoms consistent with postweaning multisystemic wasting syndrome (PMWS) between 14 and 21 days post-inoculation (p.i.), and were characterised as PMWS-affected. Only these four PMWS-affected piglets, but neither the non-symptomatic infected nor control animals, developed a clear leukopenia. Kinetic analysis demonstrated a clear loss of both CD21(+) B and CD3(+) T lymphocytes in the PMWS-affected piglets. By CD3/CD4/CD8 triple labelling, the influence of PCV2 infection on all T cell sub-populations was discernible. A loss of CD3(+)CD4(+)CD8(+) memory/activated Th lymphocytes was particularly notable. However, all T lymphocyte sub-populations-CD3(+)CD4(+)CD8(+) memory Th, CD3(+)CD4(+)CD8(-) nai;ve Th, CD3(+)CD4(-)CD8(+) Tc and CD3(+)CD4(-)CD8(-) gammadelta TCR(+) lymphocytes-were susceptible to PCV2 infection-induced lymphopenia. CD3(-)CD4(-)CD8(+) NK cells were also depleted in the PMWS-affected animals, but granulocytes and monocytes were less affected. In conclusion, PCV2 infection induces primarily a lymphopenia, but only in animals which subsequently develop PMWS. The lymphopenia can be identified early p.i., particularly with the B lymphocytes. Memory/activated Th lymphocytes might be affected more than the other T cell sub-populations, but as time progressed a collapse of both T and B cell populations was clear.

Animals↗
PubMedDate not supplied

[Lymphopenia in patients submitted to assisted ventilation due to aggravated chronic respiratory failure: a prospective study].

OBJECTIVES: Evaluate and characterize lymphopenia in patients admitted to the Intensive Care Unit (ICU) for mechanical ventilation due to aggravated chronic respiratory failure and its probable relation to severity. MATERIAL AND METHODS: Prospective study over a period of 6 months with another 6 months follow-up after ICU discharge. The study included 24 patients, 22 males, with mean APACHE II of 19,7, three of whom with capacity for outpatient follow-up. Lymphocyte subpopulations were determined on admission and every 7 days after mechanical ventilation. Patients with evidence of infection or previous immunossupression, with the exception of steroids, were excluded from the study. RESULTS: Lymphopenia was found in 79,2% of patients with depletion of all lymphocyte series, although with greater expression for B lymphocytes CD19+. This depletion showed no relation with serum steroid levels, and although related to greater clinical severity, no correlation was found with mortality. Lymphocyte values recovered progressively during admission. CONCLUSIONS: Lymphopenia is frequent among ventilated patients with chronic respiratory exacerbation. It's a non-selective depletion, more evident with CD19+ B lymphocytes. These patients present higher severity scores but no difference in mortality. Outpatient follow-up was difficult and inconclusive.

Aged↗
PubMed2004

Congenital chylothorax: lymphopenia and high risk of neonatal infections.

AIM: To describe the clinical course of patients with congenital chylothorax focusing on infectious complications. Congenital chylothorax is a common manifestation of non-immune hydrops fetalis (NIHF). The drainage of chyle leads to loss of cellular and plasmatic factors that influence the patient's immune response and increase the risk of infections. METHODS: In a retrospective analysis of 24 preterm infants with NIHF treated between 1998 and 2002, congenital chylothorax was diagnosed in 7 patients. RESULTS: All 7 patients were treated conservatively with pleural drainage over a median period of 22 d (range 10-36 d). Lymphopenia was found in all patients (median of minimal lymphocyte counts 285/microl, range 80-770). The nadir was on day 5 (2-6 d). Lymphopenia lasted for 12 d median (range 4-39 d) and was significantly correlated with the duration of lymph drainage (p = 0.001). Cell-surface analysis of peripheral blood lymphocytes was performed in two patients. Both patients had a decreased number of total T cells. Four out of seven (57%) patients developed nosocomial infections. This incidence of nosocomial infections in patients with congenital chylothorax is about three times higher than that in other neonatal patients. None of the children suffered from fungal or viral infection. Although there was a very high incidence of infections, no correlation between lymphopenia and the occurrence of infections could be shown. CONCLUSION: Drainage of congenital chylothorax results in the loss of lymphocytes and bears a high risk of infections.

Bacterial Infections↗
PubMed2000

B lymphopenia in uremia is related to an accelerated in vitro apoptosis and dysregulation of Bcl-2.

BACKGROUND: Lymphopenia has been described in patients with chronic renal failure (CRF). It is postulated that the decline in lymphocytes is due to accelerated apoptosis. We investigated whether dysregulation of programmed cell death plays a role in the immunodeficiency described in CRF. METHODS: Peripheral blood lymphocytes (PBL) from pre-dialysis uraemic patients (nHD) and haemodialysed patients (HD) were cultured with no stimulus for 96 h. Apoptosis of lymphocytes was measured by propidium iodide staining and flow cytometry. Expression of Fas and Bcl-2 was also analysed by flow cytometry. RESULTS: Peripheral blood B cells were significantly lower in pre-dialysis and haemodialysis uraemic patients compared to control. Lymphocytes from both groups of patients had a higher rate of apoptosis in vitro than those from healthy controls. This effect was more pronounced in B lymphocytes and a significant correlation between the B lymphopenia and the percentage of apoptotic B cells after 48 h of culture without stimulus was observed. The increased lymphocyte apoptosis in CRF was accompanied by a significantly lower in vitro Bcl-2 expression. However, Fas did not seem to play a role in spontaneous lymphocyte apoptosis in end-stage renal disease. CONCLUSIONS: Our data indicate that B lymphopenia in CRF may be partially attributed to an increased susceptibility to cell death by apoptosis that is associated with a decreased expression of Bcl-2.

Adolescent↗
PubMed1997

Evaluation of lymphopenia among workers with low-level benzene exposure and the utility of routine data collection.

Whether low-level benzene exposure produces health effects is controversial. We used routinely collected data from our medical/industrial hygiene system to study 387 workers with daily 8-hour time-weighted exposures averaging 0.55 ppm. The cross-sectional repeated survey design included 553 unexposed workers. Lymphopenia is considered to be the earliest and most sensitive indicator of benzene toxicity. We found no increase in the prevalence of lymphopenia among benzene-exposed workers (odds ratio, 0.6; 95% confidence interval, 0.2 to 1.8), taking into account smoking, age, and sex. There also was no increase in risk among workers exposed 5 or more years (odds ratio, 0.6; 95% confidence interval, 0.2 to 1.9). Examination of other measures of hematotoxicity, including mean corpuscular volume and counts of total white blood cells, red blood cells, hemoglobin, and platelets, produced similar results. We conclude that risk of lymphopenia and other early indicators of hematotoxicity are not increased among workers in this study who were exposed to low levels of benzene.

Adolescent↗
PubMed2002

Lymphopenia in the BB rat model of type 1 diabetes is due to a mutation in a novel immune-associated nucleotide (Ian)-related gene.

The BB (BioBreeding) rat is one of the best models of spontaneous autoimmune diabetes and is used to study non-MHC loci contributing to Type 1 diabetes. Type 1 diabetes in the diabetes-prone BB (BBDP) rat is polygenic, dependent upon mutations at several loci. Iddm1, on chromosome 4, is responsible for a lymphopenia (lyp) phenotype and is essential to diabetes. In this study, we report the positional cloning of the Iddm1/lyp locus. We show that lymphopenia is due to a frameshift deletion in a novel member (Ian5) of the Immune-Associated Nucleotide (IAN)-related gene family, resulting in truncation of a significant portion of the protein. This mutation was absent in 37 other inbred rat strains that are nonlymphopenic and nondiabetic. The IAN gene family, lying within a tight cluster on rat chromosome 4, mouse chromosome 6, and human chromosome 7, is poorly characterized. Some members of the family have been shown to be expressed in mature T cells and switched on during thymic T-cell development, suggesting that Ian5 may be a key factor in T-cell development. The lymphopenia mutation may thus be useful not only to elucidate Type 1 diabetes, but also in the function of the Ian gene family as a whole.

Amino Acid Sequence↗
PubMed1979

Prognostic significance of lymphopenia in sarcoidosis.

During 1959--67, sarcoidosis were diagnosed in a series of 140 patients. All were followed up and 22 developed chronic sarcoidosis. In 134 patients (20 with chronic course) the initial granulocyte, monocyte and lymphocyte counts were known. No differences in granulocyte values were seen between different groups of sarcoidosis patients. Patients with erythema nodosum had significantly increased monocyte levels. Lymphopenia below 1 000/microliter was seen in only 7.5% of the patients. Lymphocyte counts below 1 500 microliter were a common finding, especially in patients developing chronic sarcoidosis. Significantly decreased lymphocyte values were also seen in patients older than 40 years at the time of diagnosis, in patients negative to 10 TU of PPD and in those with a disease requiring treatment with corticosteroids. A correlation was found between initial lymphopenia and less favourable prognosis, 85% of the patients having a very good prognosis. Patients with initial lymphopenia must be carefully followed up. The initial presence of erythema nodosum does not always guarantee a good prognosis.

Adult↗
PubMed1996

Parathyroid hormone resistance and B cell lymphopenia in propionic acidemia.

The mechanisms of hypocalcemia, recurrent infections and hypogammaglobulinemia associated with metabolic decompensation of propionic acidemia due to propionyl-CoA carboxylase deficiency have not been defined. A 7-week-old infant with this disorder presented with severe hypocalcemia and B cell lymphopenia during an episode of metabolic acidosis and hyperammonemia. Hypocalcemia (1.1 mmol l-1) was associated with elevated serum intact parathyroid hormone (122 ng l-1), hyperphosphatemia, hypophosphaturia and hypercalcuria, indicating parathyroid hormone resistance. B cell lymphopenia (20 cells microliters-1) was associated with transient neutropenia, anemia and subsequent hypogamma-globulinemia (IgG < 294 mg dl-1, IgM < 8 mg dl-1, IgA < 8 mg dl-1), while T cells were normal. Parathyroid hormone resistance and B cell lymphopenia resolved following treatment with hemodialysis, diet and carnitine. These complications may be due to interference with parathyroid hormone renal tubular action and B cell maturation/proliferation by accumulated organic acids.

Amino Acid Metabolism, Inborn Errors↗