In vitrofunctional studies of mononuclear cells in patients with CLL. Evidence for functionally normal T lymphocytes and monocytes and abnormal B lymphocytes

Cancer ◽  
1979 ◽  
Vol 43 (1) ◽  
pp. 109-117 ◽  
Author(s):  
Tin Han ◽  
Barbara Dadey
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Mononuclear Cells

scholarly journals Defective lymphocyte glycosidases in the macrophage activation cascade of juvenile osteopetrosis

Blood ◽  
1996 ◽  
Vol 88 (4) ◽  
pp. 1473-1478 ◽  
Author(s):  
N Yamamoto ◽  
VR Naraparaju ◽  
PJ Orchard
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Serum Vitamin ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Beta Galactosidase

Generation of macrophage-activating factor requires a precursor protein, Gc protein (serum vitamin D3-binding protein), as well as participation of beta-galactosidase of inflammation-primed B lymphocytes and sialidase of T lymphocytes. The treatment of human peripheral blood mononuclear cells with an inflammatory lysophospholipid induced beta-galactosidase and sialidase activity of lymphocytes, leading to the generation of macrophage-activating factor and activation of monocytes/macrophages. However, lysophospholipid treatment of peripheral blood mononuclear cells from three infantile patients with osteopetrosis resulted in no significant activation of monocytes/macrophages. The lysophospholipid-inducible beta- galactosidase activity of B lymphocytes as well as that of the sialidase of T lymphocytes was found to be defective in these patients.

A Morphologic and Immunohistochemical Study of the Bronchus-associated Lymphoid Tissue of Pigs Naturally Infected with Mycoplasma hyopneumoniae

2003 ◽  
Vol 40 (4) ◽  
pp. 395-404 ◽  
Author(s):  
J. Sarradell ◽  
M. Andrada ◽  
A. S. Ramírez ◽  
A. Fernández ◽  
J. C. Gómez-Villamandos ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Lamina Propria ◽  
Lymphoid Tissue ◽  
Mononuclear Cells ◽  
Plasma Cells ◽  
Immunohistochemical Study ◽  
Mycoplasma Hyopneumoniae ◽  
High Morbidity ◽  
Alveolar Septa

Porcine enzootic pneumonia (PEN), caused by Mycoplasma hyopneumoniae (Mh), has been described in pigs in all geographic areas. The disease is characterized by high morbidity and low mortality rates in intensive swine production systems. A morphologic and immunohistochemical study was done to determine the cellular populations present in lung parenchyma of infected pigs, with special attention to the bronchus-associated lymphoid tissue (BALT). Polyclonal and monoclonal antibodies were used for the detection of antigens of Mh, T lymphocytes (CD3+, CD4+, and CD8+), IgG+ or IgA+ lymphocytes, and cells containing lysozyme, S-100 protein, major histocompatibility complex class II antigen or myeloid-histiocyte antigen. Findings in lung tissues associated with Mh infection were catarrhal bronchointerstitial pneumonia, with infiltration of inflammatory cells in the lamina propria of bronchi and bronchioles and alveolar septa. Hyperplasia of mononuclear cells in the BALT areas was the most significant histologic change. The BALT showed a high morphologic and cellular organization. Macrophages and B lymphocytes were the main cellular components of germinal centers. T lymphocytes were primarily located in perifollicular areas of the BALT, lamina propria and within the airway epithelium, and plasma cells containing IgG or IgA at the periphery of the BALT, in the lamina propria of bronchi and bronchioles, in alveolar septa, and around bronchial submucosal glands. The hyperplastic BALT in PEN cases consisted of macrophages, dendritic cells, T and B lymphocytes, and IgG+ and IgA+ plasma cells. CD4+ cells predominated over CD8+ cells. Local humoral immunity appears to play an important role in the infection.

scholarly journals Stimulation of HIV-1 Replication in Immature Dendritic Cells in Contact with Primary CD4 T or B Lymphocytes

2010 ◽  
Vol 84 (9) ◽  
pp. 4172-4182 ◽  
Author(s):  
Vincent Holl ◽  
Ke Xu ◽  
Maryse Peressin ◽  
Alexandre Lederle ◽  
Marina Elizabeth Biedma ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Lymphocytes ◽  
B Lymphocytes ◽  
Neutralizing Antibodies ◽  
Mononuclear Cells ◽  
Cell Contact ◽  
Specific Marker ◽  
Experimental Conditions ◽  
Hiv 1 ◽  
Stimulation Of

ABSTRACT Sexual transmission is the major route of HIV-1 infection worldwide. Dendritic cells (DCs) from the mucosal layers are considered to be the initial targets of HIV-1 and probably play a crucial role in HIV-1 transmission. We investigated the role of cell-to-cell contact between HIV-1-exposed immature DCs and various lymphocyte subsets in the stimulation of HIV-1 replication. We found that HIV-1 replication and production in DCs were substantially enhanced by the coculture of DCs with primary CD4 T or nonpermissive B lymphocytes but not with primary activated CD8 T lymphocytes or human transformed CD4 T lymphocytes. Most of the new virions released by cocultures of HIV-1-exposed immature DCs and primary B lymphocytes expressed the DC-specific marker CD1a and were infectious for both immature DCs and peripheral blood mononuclear cells (PBMCs). Cocultured DCs thus produced large numbers of infectious viral particles under these experimental conditions. The soluble factors present in the supernatants of the cocultures were not sufficient to enhance HIV-1 replication in DCs, for which cell-to-cell contact was required. The neutralizing monoclonal antibody IgG1b12 and polyclonal anti-HIV-1 sera efficiently blocked HIV-1 transfer to CD4 T lymphocytes but did not prevent the increase in viral replication in DCs. Neutralizing antibodies thus proved to be more efficient at blocking HIV-1 transfer than previously thought. Our findings show that HIV-1 exploits DC-lymphocyte cross talk to upregulate replication within the DC reservoir. We provide evidence for a novel mechanism that may facilitate HIV-1 replication and transmission. This mechanism may favor HIV-1 pathogenesis, immune evasion, and persistence.

Adenoviral Vector-Mediated Transfer of the Indian Hedgehog Gene Modulates Lymphomyelopoiesis In Vivo.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2205-2205
Author(s):  
Masayoshi Kobune ◽  
Yutaka Kawano ◽  
Katsunori Sasaki ◽  
Rishu Takimoto ◽  
Junji Kato ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Adenoviral Vector ◽  
Mononuclear Cells ◽  
Indian Hedgehog ◽  
Cd8 Cells ◽  
Proliferation And Differentiation ◽  
Mock Control ◽  
Single Positive

Abstract Indian hedgehog (Ihh) plays an essential role in angiogenesis, hematogenesis and epiphysis formation during embryogenesis. In the present study, we injected an adenoviral vector (Adv) carrying the mock-control (adv-control) or Ihh gene (Adv-Ihh) into SCID or BALB/c mice to evaluate the effects of lhh on the regulation of postnatal hematopoiesis in vivo. After the intravenous injection of Adv-Ihh, the expression of vector-derived Ihh mRNA was detected in the liver. Four weeks after administration of Adv-Ihh to SCID mice, we observed an increase in the number of c-Kit+ cells and clonogenic cells/105 mononuclear cells in the bone marrow as compared with adv-control administrated mice. Moreover, after administration of Adv-Ihh to BALB/c mice, the number of splenic B220+IgMlowCD23intCD21int B lymphocytes (Figure 1) and CD4+ T lymphocytes (Figure 2) was strongly increased. Furthermore, the number of thymic double negative (DN)2, DN3, CD8+ immature single positive and CD4+/CD8− cells was significantly elevated relative to the number in mice that received the control Adv vector. Our results suggest that enhanced signaling by Ihh can modulate the proliferation and differentiation of splenic B lymphocytes and thymic T lymphocytes during BM hematopoiesis in vivo. Thus, modulation of the Hh signaling pathway may provide a therapeutic strategy to stimulate lymphomyelopoiesis in vivo. Figure Figure Figure Figure

scholarly journals Multiple Quinine-Dependent Antibodies in a Patient With Episodic Thrombocytopenia, Neutropenia, Lymphocytopenia, and Granulomatous Hepatitis

Blood ◽  
1997 ◽  
Vol 90 (12) ◽  
pp. 4806-4811
Author(s):  
Ming Hou ◽  
Eva Horney ◽  
Dick Stockelberg ◽  
Stefan Jacobsson ◽  
Jack Kutti ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Mononuclear Cells ◽  
Cell Lineage ◽  
Laboratory Evaluation ◽  
Granulomatous Hepatitis ◽  
Color Flow ◽  
Flow Cytometric ◽  
Electrophoretic Mobilities ◽  
Elevated Liver Enzymes

A 58-year-old man experienced episodes of fever, vomiting, and diarrhea over a 2-year period. The laboratory evaluation during these attacks consistently disclosed thrombocytopenia, leukopenia, and elevated liver enzymes. A liver biopsy performed at one of these attacks showed a typical picture of granulomatous hepatitis. In retrospect, all episodes seemed to be associated with the ingestion of quinine. Indeed, such a correlation was established by a challenge with quinine. By using flow cytometry, quinine-dependent IgG antibodies to platelets were detected in the patient serum. By a two-color flow cytometric assay, the patient serum was also found to hold quinine-dependent antibodies specific for neutrophils, T lymphocytes, and B lymphocytes. Moreover, serum absorbed with neutrophils in the presence of quinine continued to react with platelets, T lymphocytes, and B lymphocytes; serum that was absorbed with mononuclear cells continued to react with neutrophils and platelets. These experiments indicated that the antigen targets were different on platelets, neutrophils, and lymphocytes. Further, the patient serum in the presence of quinine immunoprecipitated surface-labeled platelet proteins with electrophoretic mobilities closely resembling those of glycoprotein (GP) Ib/IX and GPIIb/IIIa. By a modified monoclonal antibody–specific immobilization of platelet antigens assay, the patient serum in the presence of quinine reacted with platelet GPIb/IX and GPIIb/IIIa. Also, the patient serum in the presence of quinine immunoprecipitated an uncharacterized 15-kD double-band from surface-labeled granulocyte proteins. We conclude that our patient's thrombocytopenia, neutropenia, and lymphocytopenia were caused by quinine-dependent antibodies and that these antibodies recognized cell lineage-specific epitopes.

scholarly journals Multiple Quinine-Dependent Antibodies in a Patient With Episodic Thrombocytopenia, Neutropenia, Lymphocytopenia, and Granulomatous Hepatitis

Blood ◽  
1997 ◽  
Vol 90 (12) ◽  
pp. 4806-4811 ◽  
Author(s):  
Ming Hou ◽  
Eva Horney ◽  
Dick Stockelberg ◽  
Stefan Jacobsson ◽  
Jack Kutti ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Mononuclear Cells ◽  
Cell Lineage ◽  
Laboratory Evaluation ◽  
Granulomatous Hepatitis ◽  
Color Flow ◽  
Flow Cytometric ◽  
Electrophoretic Mobilities ◽  
Elevated Liver Enzymes

Abstract A 58-year-old man experienced episodes of fever, vomiting, and diarrhea over a 2-year period. The laboratory evaluation during these attacks consistently disclosed thrombocytopenia, leukopenia, and elevated liver enzymes. A liver biopsy performed at one of these attacks showed a typical picture of granulomatous hepatitis. In retrospect, all episodes seemed to be associated with the ingestion of quinine. Indeed, such a correlation was established by a challenge with quinine. By using flow cytometry, quinine-dependent IgG antibodies to platelets were detected in the patient serum. By a two-color flow cytometric assay, the patient serum was also found to hold quinine-dependent antibodies specific for neutrophils, T lymphocytes, and B lymphocytes. Moreover, serum absorbed with neutrophils in the presence of quinine continued to react with platelets, T lymphocytes, and B lymphocytes; serum that was absorbed with mononuclear cells continued to react with neutrophils and platelets. These experiments indicated that the antigen targets were different on platelets, neutrophils, and lymphocytes. Further, the patient serum in the presence of quinine immunoprecipitated surface-labeled platelet proteins with electrophoretic mobilities closely resembling those of glycoprotein (GP) Ib/IX and GPIIb/IIIa. By a modified monoclonal antibody–specific immobilization of platelet antigens assay, the patient serum in the presence of quinine reacted with platelet GPIb/IX and GPIIb/IIIa. Also, the patient serum in the presence of quinine immunoprecipitated an uncharacterized 15-kD double-band from surface-labeled granulocyte proteins. We conclude that our patient's thrombocytopenia, neutropenia, and lymphocytopenia were caused by quinine-dependent antibodies and that these antibodies recognized cell lineage-specific epitopes.

scholarly journals Immunohistochemical Study of Lymphocyte Populations Infiltrating the Gastric Mucosa of Beagle Dogs Experimentally Infected withHelicobacter pylori

2000 ◽  
Vol 68 (8) ◽  
pp. 4769-4772 ◽  
Author(s):  
Giacomo Rossi ◽  
Damiano Fortuna ◽  
Laura Pancotto ◽  
Giacomo Renzoni ◽  
Ennio Taccini ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
T Lymphocytes ◽  
Gastric Mucosa ◽  
B Lymphocytes ◽  
Experimental Infection ◽  
Mononuclear Cells ◽  
Immunohistochemical Study ◽  
Beagle Dogs ◽  
Lymphoid Follicles ◽  
Lymphocyte Populations

ABSTRACT Experimental infection of beagle dogs with Helicobacter pylori induces recruitment to the gastric mucosae of neutrophils at early stages and later of mononuclear cells that organize into lymphoid follicles. These structures become macroscopically evident and consist of peripheral CD4+ T lymphocytes and central CD21+ B lymphocytes. Furthermore, transient expression of interleukin-8 (IL-8) parallels the presence of neutrophils in the gastric mucosae, whereas expression of IL-6 tends to persist chronically.

T Lymphocyte Proliferative Responses Induced by Recombinant Factor VIII in Hemophilia A Patients with Inhibitors

1996 ◽  
Vol 76 (01) ◽  
pp. 017-022 ◽  
Author(s):  
Sylvia T Singer ◽  
Joseph E Addiego ◽  
Donald C Reason ◽  
Alexander H Lucas
Keyword(s):  
T Lymphocytes ◽  
Factor Viii ◽  
Cellular Proliferation ◽  
Mononuclear Cells ◽  
Hemophilia A ◽  
Normal Subjects ◽  
Normal Male ◽  
Cell Fractionation ◽  
Severe Hemophilia ◽  
Human Factor Viii

SummaryIn this study we sought to determine whether factor VUI-reactive T lymphocytes were present in hemophilia A patients with inhibitor antibodies. Peripheral blood mononuclear cells (MNC) were obtained from 12 severe hemophilia A patients having high titer inhibitors, 4 severe hemophilia A patients without inhibitors and 5 normal male subjects. B cell-depleted MNC were cultured in serum-free medium in the absence or presence of 2 µg of recombinant human factor VIII (rFVIII) per ml, and cellular proliferation was assessed after 5 days of culture by measuring 3H-thymidine incorporation. rFVIII induced marked cellular proliferation in cultures of 4 of 12 inhibitor-positive hemophilia patients: fold increase over background (stimulation index, SI) of 7.8 to 23.3. The remaining 8 inhibitor-positive patients, the 4 hemophilia patients without inhibitors and the 5 normal subjects, all had lower proliferative responses to rFVIII, SI range = 1.6 to 6.0. As a group, the inhibitor-positive subjects had significantly higher proliferative responses to rFVIII than did the inhibitor-negative and normal subjects (p < 0.05 by t-test). Cell fractionation experiments showed that T lymphocytes were the rFVIII-responsive cell type, and that monocytes were required for T cell proliferation. Thus, rFVIII-reactive T lymphocytes are present in the peripheral circulation of some inhibitor-positive hemophilia A patients. These T cells may recognize FVIII in an antigen-specific manner and play a central role in the regulation of inhibitor antibody production

scholarly journals High levels ofbcl-2 protein in circulating t lymphocytes, but not b lymphocytes, of patients with systemic lupus erythematosus

1994 ◽  
Vol 37 (10) ◽  
pp. 1423-1430 ◽  
Author(s):  
Martin Aringer ◽  
Winfried Wintersberger ◽  
Carl W. Steiner ◽  
Hans Kiener ◽  
Elisabeth Presterl ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Lymphocytes ◽  
B Lymphocytes ◽  
Lupus Erythematosus ◽  
Systemic Lupus

Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress

2005 ◽  
Vol 288 (3) ◽  
pp. R591-R599 ◽  
Author(s):  
Mitsuharu Okutsu ◽  
Kenji Ishii ◽  
Kai Jun Niu ◽  
Ryoichi Nagatomi
Keyword(s):  
T Lymphocytes ◽  
Mononuclear Cells ◽  
Cxcr4 Expression ◽  
Peripheral Blood Mononuclear ◽  
Cycling Exercise ◽  
Ru 486 ◽  
Before And After ◽  
Stromal Cell Derived Factor ◽  
Chemokine Receptor 4

The aim of this study was to elucidate the mechanism responsible for lymphopenia after exercise. Seven young healthy men volunteered for this study. Peripheral blood mononuclear cells (PBMC) were cultured with cortisol and analyzed for C-X-C motif chemokine receptor 4 (CXCR4) expression by flow cytometry. To determine the effects of exercise, subjects performed exhaustive cycling exercise. PBMC were cultured with plasma obtained before and after the cycling exercise. Alternatively, PBMC obtained before and after exercise were cultured without plasma or glucocorticoid to examine whether PBMC were primed in vivo for CXCR4 expression. We analyzed cortisol- or plasma-treated PBMC to determine their ability to migrate through membrane filters in response to stromal cell-derived factor 1α/CXCL12. Cortisol dose- and time-dependently augmented CXCR4 expression on T lymphocytes, with <6 h of treatment sufficient to augment CXCR4 on T lymphocytes. Postexercise plasma also augmented CXCR4 expression. Cortisol or postexercise plasma treatment markedly enhanced migration of T lymphocytes toward CXCL12. Augmentation of CXCR4 on T lymphocytes by cortisol or plasma was effectively blocked by the glucocorticoid receptor antagonist RU-486. Thus exercise-elicited endogenous cortisol effectively augments CXCR4 expression on T lymphocytes, which may account for lymphopenia after exercise.

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