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Biomedical subjects

R H Weisbart

Publications and source records attributed to R H Weisbart.

51 records · Page 3Linked to original sources
PubMed1980

Effect of immunoglobulin G on the responsiveness of human neutrophils to soluble staphylococcal protein A-induced neutrophil migration inhibition factor from T-lymphocytes.

Staphylococcal protein A is a bacterial cell wall product that binds human immunoglobulin G and thereby interferes with opsonization and phagocytosis of Staphylococcus aureus by neutrophils. Phagocytic cells are also responsive to various non-immunoglobulin lymphocyte mediators. We utilized the detection of a newly recognized mediator, a neutrophil migration inhibition factor from T-lymphocytes (NIF-T), to show that aggregates of staphylococcal protein A and immunoglobulins G could inhibit the responsiveness of neutrophils to NIF-T. That such aggregates may alter the responsiveness of neutrophils to lymphocyte mediators that amplify or modulate phagocytic functions may have important pathogenetic implications in staphylococcal infection.

Cells, Cultured↗
PubMed1980

Requirement for B-lymphocyte alloantigen in the production of neutrophil migration inhibition factor from T lymphocytes (NIF-T).

Neutrophil migration inhibition factor from T lymphocytes (NIF-T) is produced in response to mitogens as the result of cellular interactions between T and B lymphocytes. The requirement for B-cell alloantigen in this interaction process was indicated by (1) collaboration between peripheral blood T cells with various B lymphoblast cell lines but not with non-B lymphoblast cells for NIF-T production, (2) inhibition of NIF-T production by treating collaborating B lymphoblasts with B-cell specific antiserum, and (3) inhibition of NIF-T production by peripheral blood lypmphocytes in the presence of anti-B-cell antiserum and F(ab')2 with anti-B-cell specificity.

Antibody Specificity↗
PubMed1980

Impaired cellular interactions involving lymphocytes from patients with chronic lymphocytic leukemia and ataxia-telangiectasia.

Abnormal cellular interactions between T and B lymphocytes were identified in patients with CLL and AT. The system employed utilized the detection of a newly recognized lymphokine, NIF-T. This mediator is produced by T lymphocytes as a result of the interaction between T and B cells. Our studies demonstrated impaired T cell function but normal B cell activity in patients with AT with respect to mitogenic stimulation and MLC reactivity. In contrast, patients with B cell CLL had normal T cell function. The leukemic B cells from these patients, however, failed to collaborate with normal T cells in response to mitogens, and they did not participate in MLC reactions. In contrast, lymphocytes from patients with HCL functioned normally with respect to NIF-T production.

Adult↗
PubMed1979

Neutrophil migration-inhibition activity produced by a unique T lymphoblast cell line.

Fifteen lymphoblast cell lines, including B cell, T cell, Null cell, and myeloblast cells, were examined for the production of human neutrophil migration-inhibition activity. Only one T lymphoblast cell line established from a patient with hairy cell leukemia produced a neutrophil migration-inhibition factor spontaneously and after stimulation with Con A and PHA.

B-Lymphocytes↗
PubMed1978

Cellular collaboration in the production of human leucocyte migration inhibition factor.

The participation of cell subpopulations in the expression of leucocyte migration inhibition factor (LMIF) in response to Concanavalin A and Protein A was evaluated for cells isolated from the peripheral blood of five healthy subjects. LMIF activity could not be attributed to the function of T cells, B enriched cells, or monocytes acting alone, or to a combination of B enriched cells and monocytes. The LMIF response was the result of a collaborative event that occurred between T cells and B enriched cells, or between T cells and monocytes.

B-Lymphocytes↗
PubMed1977

A microassay for leukocyte migration: analysis of its reproducibility.

A reliable microassay for human leukocyte migration is described by which 50 to 100 assays can be performed each day in quadruplicate with the number of indicator cells obtainable from 10 to 20 ml of peripheral blood. The reproducibility of this method is demonstrated with respect to the variability among replicate test wells (including reading), the variability among different test readers, the variability among replicate cultures, and the variability of using indicator cells from different subjects. A microculture system is described that requires only 75,000 mononuclear cells to consistently produce detectable polymorphonuclear leukocyte migration inhibition factor in response to PPD. The reproducibility of this culture system is demonstrated with respect to the variability of lymphocyte responsiveness on repetitive testing in the same individuals.

Antigens↗
PubMed1976

Lymphocyte response to IgG in patients with ankylosing spondylitis and their families.

Lymphocyte responsiveness to IgG was measured by an agarose method in nine patients with ankylosing spondylitis (AS), one patient with Reiter's Syndrome (RS), and thirty-six of their family members. Similar studies were also performed in five patients with rheumatoid arthritis (RA) and twenty-nine of their first degree relatives as well as in seven control families (twenty-seven subjects). Lymphocytes from the ten spondylitic patients and twenty-four of thirty-six family members responded in vitro to autologous IgG. Although most of these subjects had the histocompatibility antigen, B27, there was no association between B27 and response to IgG. Four of the five patients with RA and twenty of their twenty-nine first degree relatives responded in vitro to IgG, whereas only six of twenty-seven control family members gave a positive reaction. There was no difference in the incidence of antiglobulins (detected by agglutination tests) in the family members of patients with AS and RA or in control family members. These data indicate that lymphocyte responsiveness to IgG is the only aberrant immune response thus far described which is shared by patients with AS and RA and their family members.

Adolescent↗
PubMed1975

Cellular immunity to intrinsic factor in pernicious anemia.

Cellular immunity to hog intrinsic factor was detected by a modified agarose-leukocyte migration test in 18 patients with pernicious amemia. Lymphocytes from 17 out of 18 patients with pernicious anemia gave positive responses to a concentrate of hog intrinsic factor; the intrinsic factor present in 1 mg. of this concentrate bound 128 ng. of vatamin B12. Six patients with atrophic gastritis, 7 with regional enteritis, and 9 out of 10 healthy adults did not respond to this preparation. No correlation existed between the presence of serum autoantibodies to intrinsic factor and in vitro lymphocyte responsiveness to intrinsic factor. The results demonstrate that cellular immunity to intrinsic factor concentrates is present in the majority of patients with pernicious anemia.

Adult↗
PubMed1975

Human polymorphonuclear leucocyte migration inhibitory factor. Evidence for antigen dependency.

Sudies were performed on human polymorphonuclear leucocyte migration inhibitory factor (PMN-MIF) to determine its antigen dependence. PMN-MIF produced by lymphocytes in response to purified protein derivative or coccidiodin was measured in an agarose gel system with buffy coat leucocytes as indicator cells. PMN-MIF activity contained in the lymphocyte supernatants uniformly disappeared when the supernatants were diluted 1:50 with medium; the inhibitory activity was only restored when the diluted supernatants were reconstituted with specific antigen. PMN-MIF isolated by polyacrylamide gel electrophoresis showed the same properties as PMN-MIF present in whole supernatants. This factor consistently migrated in the albumin region on gel electrophoresis. These data indicate that human PMN-MIF is antigen-dependent.

Antigens↗
PubMed1974

Migration enhancement factor: a new lymphokine.

Production of human migration inhibitory factor by lymphocytes exposed to antigen was studied at intervals over a 7-day period. Migration inhibitory factor was measured by an agarose gel method, with buffycoat leukocytes as indicator cells. Lymphocyte supernatants from 7-day cultures consistently showed migration inhibitory factor activity; by contrast, enhancement of migration was frequently noted when effector cells were exposed to supernatants from 2- to 5-day cultures. Enhancement activity was manifested either by enhanced migration or by a sequential reduction in inhibitory activity consistent with a factor opposing the action of migration inhibitory factor. When supernatants were subjected to polyacrylamide gel electrophoresis, enhancement activity was regularly found in the beta-globulin region and migration inhibitory factor in the albumin fraction of the gel. The enhancement activity was heat-stable and nondialyzable. These findings characterize a hitherto unreported lymphokine, migration enhancement factor.

Cell Migration Inhibition↗
PubMedDate not supplied

Human granulocyte-macrophage colony-stimulating factor is a neutrophil activator.

The polymorphonuclear leukocyte (PMN), or neutrophil, is the major host defence cell protecting the body against invasion by bacteria and fungi. Products of oxidative metabolism mediate PMN microbicidal and tumoricidal activity but the mechanisms by which these pathways become activated are not well understood. We have previously described a human granulocyte-macrophage colony-stimulating factor (GM-CSF) of relative molecular mass (Mr) 22,000 that also inhibits neutrophil motility (NIF-T activity). Because of its direct action on granulocytes, this lymphokine is a candidate for a neutrophil-activating factor. We have studied the effect of GM-CSF/NIF-T on superoxide anion generation in response to the bacterial chemo-attractant N-formylmethionyl-leucylphenylalanine (f-MLP), and report here that PMNs preincubated with either purified natural GM-CSF or biosynthetic (recombinant) GM-CSF showed increased (as much as fourfold) superoxide anion production in response to f-MLP. These results indicate that human GM-CSF is a neutrophil-activating factor.

Colony-Stimulating Factors↗