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N L Abdou

Publications and source records attributed to N L Abdou.

15 recordsLinked to original sources
PubMed1981

Immunoregulatory T-cell dysfunction in polyclonal gammopathy.

The mechanisms responsible for the increased serum immunoglobulines in polyclonal gammopathy states are unknown. We have studied the regulation of peripheral blood B-cell immunoglobulin synthesis and secretion, by T cells of either blood or bone marrow compartments, in 20 patients with polyclonal gammopathy and 27 controls with normal serum immunoglobulin levels. When compared to B-T-cell cocultures of normals, cocultures of polyclonal gammopathy patients had significantly higher levels of immunoglobulin secretion (P less than 0.01). Normal T cells but not T cells from patients with polyclonal gammopathy suppressed B-cell immunoglobulin secretion (P less than 0.01) and not the number of cytoplasmic immunoglobulin-positive cells of the polyclonal gammopathy patients. T cells from patients with polyclonal gammopathy enhanced normal B-cell immunoglobulin secretion (P less than 0.05) but not the number of cytoplasmic immunoglobulin-positive cells. Controls' bone marrow T cells were more efficient than blood T cells in suppressing polyclonal gammopathy B cells (P less than 0.02). T cells in polyclonal gammopathy are predominantly helper cells and could play a role in the enhanced immunoglobulin secretion of B cells. Bone marrow T cells are more efficient than blood T cells in regulating B cells. It seems that T cells predominantly regulate B-cell immunoglobulin secretion and not the number of B cells with cytoplasmic Ig.

B-Lymphocytes↗
PubMed1981

Heterogeneity of pathogenetic mechanisms in aplastic anemia. Efficacy of therapy based on in-vitro results.

The mechanisms responsible for the bone marrow failure in 21 aplastic anemia patients were studied by the colony-forming units in culture assay (CFU-C). Twelve patients had no detectable in-vitro defect that could be responsible for the low CFU-C numbers. Three patients had suppressor T cells that inhibited CFU-C (p less than 0.001); one of two patients responded to antithymocyte globulin therapy and the third recovered spontaneously. Three patients had serum inhibitory immunoglobulins directed against their marrow CFU-C; plasmapheresis resulted in recovery of bone marrow function. Three patients had abnormalities at the colony-stimulating factor level: Two had inhibitors of colony-stimulating factor, corrected in vitro and in vivo by indomethacin and cholinergic agonists (p less than 0.01); and the third had colony-stimulating factor generation defect, corrected in vitro and in vivo by lithium. Testing for cellular or humoral suppressor factors directed against precursor cells or for abnormalities at the colony-stimulating factor level gives helpful guidelines to therapy in aplastic anemia.

Adolescent↗
PubMed1980

Suppressor T cells in tolerance to deaggregated horse anti-human thymocyte globulin in man.

To understand the mechanism by which deaggregated horse anti-human thymocyte globulin (dATG) fails to induce untoward immunological reactions in man, three patients who received ATG and two patients who received dATG were studied for evidence of sensitization or tolerance to the foreign globulin. The ATG but not the dATG recipients developed allergic or serum sickness reactions; antihorse serum antibody could be detected in their serum and their blood cells proliferated in vitro in the presence of horse serum and secreted antihorse serum antibodies (P less than 0.001). Tolerance of the dATG recipients was shown to be mediated by specific T suppressor cells that carry receptors for horse serum and could be detected in the blood of one patient, whom we have studied serially, 13 weeks after therapy. Deaggregated ATG does not induce allergic or serum sickness reactions. It induces tolerance to the foreign protein via the generation of specific short-lived suppressor cells.

Agglutination↗
PubMed1978

Aplastic anemia associated with bone marrow suppressor T-cell hyperactivity: successful treatment with antithymocyte globulin.

In five patients with idiopathic aplastic anemia, the colony-forming unit (CFU-c) assay was used to quantitate stem cells and test the possible presence of suppressor cells inhibiting bone marrow differentiation. All five marrows failed to form CFU-c. In one out of the five cases tested, coculture of the patient's marrow with normal marrow suppressed the latter to form CFU-c. Removal of T-cells from the patient's bone marrow freed the aplastic marrow to produce more colonies and, in the coculture study, abrogated its inhibitory activity on the normal bone marrow. Treatment of the patient with horse antihuman thymocyte globulin (ATG), improved the peripheral blood count and myelopoiesis. Furthermore, the aplastic marrow increased its colony forming capacity from less than 1% pre-ATG to 46% post-ATG of the normal control, and its inhibitory activity on the normal marrow was ablated. In selected cases of aplastic anemia, with evidence of T-suppressor cell hyperactivity, treatment with ATG may offer an alternative approach to bone-marrow transplantation.

Anemia, Aplastic↗
PubMed1978

Suppressor cell-mediated neutropenia in Felty's syndrome.

The mechanism of neutropenia in Felty's Syndrome (FS) was tested. The suppressor capacity of mononuclear cells from patients with FS on normal bone marrow granulopoiesis was tested by the in vitro colony forming unit in culture assay. Peripheral blood, bone marrow, and spleen cells from FS patients with marked neutropenia (less than 1,000 neutrophils/mm3) suppressed the colony forming unit in culture of normal bone marrow. Cells from rheumatoid arthritis patients without neutropenia, cells from patients with drug-induced neutropenia without rheumatoid arthritis, or plasma from FS patients failed to suppress the colony forming unit in culture. Though suppressor cells were predominantly thymus-derived (T) cells, monocytes were also effective in suppression. The suppressor efficiency of cells from the various compartments were spleen greater than bone marrow greater than peripheral blood. Splenectomy in FS transiently corrected the neutropenia and eliminated suppressor cell activity. Hyperactive suppressor cells may be responsible for the neutropenia in some patients with FS. Correction of neutropenia in these patients should be directed at modulating the suppressor cell subpopulation.

Adult↗
PubMed1978

Behçet's disease: possible role of secretory component deficiency, synovial inclusions, and fibrinolytic abnormality in the various manifestations of the disease.

Detailed study of four patients with BD, four controls with recurrent aphthous stomatitis, and 12 healthy controls has demonstrated markedly decreased levels of salivary SC in both its free and bound forms, and normal total protein concentration in BD salivas. In two BD patients, SC deficiency was also found in jejunal fluids. Depressed in vitro response of blood T cells to mitogens was also noted in BD. Levels of IgA in serum were normal, as well as total numbers of T cells and IgA-carrying B cells in blood. A fluid phase abnormality of the fibrinolytic system as tested by the clot lysis assay was demonstrated in the blood from BD patients. Studies of BD SF and synovial membrane by light and electron microscopy showed inclusions composed of degenerated neutrophils inside monocytes. Abnormalities of host defense mechanisms at the mucous membrane level due to SC deficiency, together with a systemic T cell functional defect and fibrinolytic abnormality, could be important mechanisms in the pathogenesis of recurrent mucosal ulcers and thrombosis in BD.

Behcet Syndrome↗
PubMed1976

Human bone marrow lymphocytes: B and T cell precursors and subpopulations.

Characterization of the different lymphocyte populations in normal human bone marrow (BM) was attempted and compared to that in the peripheral blood (PB). B cells comprised 34% +/- 11% of lymphocytes in BM and 23% +/- 9% in PB. The majority of B cells carried IgM in BM and IgG in the PB. In the BM, cells carrying complement or Fc receptors were fewer than cells carrying Ig, but in the PB they were equal. T cells comprised 6% +/- 4% of lymphocytes in the BM and 62% +/- 7% in the PB. The majority of BM lymphocytes did not have B or T cell markers; these probably included B and T cell precursors. BM lymphocytes carrying surface Ig increased in a 7-day culture, whereas those of the PB decreased. Pokeweed mitogen induced Ig synthesis in B cells of PB but not those of BM. BM-T cells were more efficient than PB-T cells in inhibiting Ig synthesis of PB-B cells. These results indicate that the BM compartment contains immature B cells that are capable of partial differentiation and maturation in vitro. BM-B lymphocytes are probably not involved in the effector phase of the immune response since they are unable to synthesize Ig and because they carry few receptors for complement of Fc, BM-T lymphocytes are very few and have suppressor capability and therefore may play an essential role in regulation of Ig synthesis by B cells.

Adult↗
PubMed1975

The monoclonal nature of lymphocytes in multiple myeloma. Effects of therapy.

Despite the increased amounts of serum immumoglobulins (Ig) in multiple myeloma, the percentage of bone marrow-dependent (B) cells carrying surface Ig in the peripheral blood compartment were decreased, when compared with that in control patients with polyclonal gammopathy or with that in normals (5 plus or minus 2% in patients with multiple myeloma and 19 plus or minus 5% or 22 plus or minus 7% in controls). Most circulating B cells in patients with multiple myeloma were shown to carry individually specific idiotypic Ig. The monoclonal idiotypic nature of the surface Ig was shown by using antiserums raised against the monoclonal Ig. The idiotypic antiserum was capable of actively binding to and stimulating the idiotypic lymphocytes to divide in vitro. Commercial anti-Ig antiserums raised against normal Ig did not bind to the myeloma lymphocytes. After chemotherapy, lymphocytes carrying the idiotypic Ig decreased in numbers, and this correlated with other variables of clinical improvements. Its role in the pathogenesis of myeloma and its importance for diagnosis and follow-up of patients with myeloma are discussed.

Animals↗
PubMed1973

Comparative study of bone marrow and blood B cells in infantile and acquired agammaglobulinemia. Possible role of circulating anti-IgM in pathogenesis.

The status of immunoglobulin (Ig) receptors of the bone marrow dependent (B) cells present in either the bone marrow (BM) or peripheral blood (PB) of three patients with infantile agammaglobulinemia (I-AGG), or seven patients with acquired agammaglobulinemia (A-AGG) is compared with those of 12 controls. Quantitative and qualitative changes of the different classes of Ig receptors on B cells were evaluated by their capacity to bind [(125)I]anti-Ig, to be stained with fluorescinated anti-Ig and their in vitro proliferative capacity upon incubation with the anti-Ig. Patients with I-AGG lacked B cells in both the BM and PB. Whereas BM cells of patients with A-AGG carried receptors similar to control cells, their blood B cells had fewer IgM, IgG, and IgA cells which failed to proliferate in vitro in the presence of the anti-Ig. An anti-IgM of the IgG class was detected in the sera of patients with A-AGG but not in sera of I-AGG. The isolated anti-IgM agglutinated human red cells coated with IgM. The anti-IgM partially blocked the binding of fluorescinated or radiolabeled anti-IgM to IgM peripheral blood lymphocytes of normal controls. The eluted anti-IgM in presence of complement was partially cytotoxic to normal cells. It is concluded that I-AGG-B cell defect is due to failure of B cell development in the bone marrow compartment whereas the peripheral exclusion of IgM cells by an anti-IgM with the subsequent failure of differentiation of both IgG and IgA cells could be an important mechanism in A-AGG-B cell defect.

Absorption↗
PubMed1972

Bone marrow: the bursa equivalent in man?

Human bone marrow lymphoid cells, particularly when enriched with plasma cells, as in multiple myeloma, respond to pokeweed mitogen and to antiserum to immunoglobulin but not to phytohemagglutinin. Cells of patients with X-linked agammaglobulinemia of the bursal deficient type failed to respond to either pokeweed or to the antiserum to immunoglobulin. Leukocytes of the agammaglobulinemia patients however responded in a normal fashion to phytohemagglutinin. Just as the in vitro response to phytohemagglutinin is taken as an index of the thymus-dependent system, the in vitro response to both antiserum to immunoglobulin and pokeweed may be considered an index for the bursaldependent system. Human bone marrow, therefore, contains bursal cells and probably very few or no thymus cells.

Agammaglobulinemia↗
PubMedDate not supplied

Platelet preservation by freezing. Use of dimethylsulfoxide as cryoprotective agent.

Variables important in the preservation of platelets by freezing with dimethylsulfoxide (DMSO) as cryoprotective agent were studied in normal volunteers and thrombocytopenic patients. Use of 5 per cent DMSO and a freezing rate of 1-3 degrees C/minute yielded optimal preservation of platelet viability. The addition of 5 per cent Dextrose did not improve results. In vivo yield using 5 per cent DMSO was superior to previous results in which glycerol was used as the cryoprotective agent. Viability after freezing was equivalent when platelets were frozen in small (10 ml) and large (60 ml) volumes of plasma. The larger volume had the advantage that a smaller percentage of the platelets was lost during transfer from one plastic container to another.

Blood Platelets↗