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Biomedical subjects

J Faust

Publications and source records attributed to J Faust.

At least 73 records · Page 4Linked to original sources
PubMed1986

Ontogeny of neutrophil chemotaxis in fetal lambs.

Ontogeny of neutrophil chemotactic response using endotoxin activated adult sheep plasma as a source of complement derived chemotactic factor was examined in fetal lambs of gestational age 120-150 days. (Gestational period in sheep is approximately 150 days.) Neutrophils from fetal lambs of gestational age 120-130 days failed to respond to this chemotactic factor whereas neutrophils from fetal lambs above 131 days of gestational age responded at levels comparable to adult values. Examination of neutrophil chemotaxis in older fetuses using a different chemotactic factor derived from mitogen stimulated adult mononuclear cells revealed a selective failure of fetal neutrophils to respond to lymphocyte-derived chemotactic factor in the presence of a normal response to complement derived chemotactic factor. Among prematurely delivered twin fetuses alterations in comparison with the first twin or age-matched controls in peripheral neutrophil count (increase) and in chemotaxis (increase or decrease) were noted in second of twins delivered greater than or equal to 20 min after the first lamb, suggesting an extreme sensitivity of neutrophil functions to a variety of influences, similar to that seen in humans.

Animals↗
PubMed1985

Differentiation and activation phenotypes of lung T lymphocytes differ from those of circulating T lymphocytes.

We used dual laser two-color flow cytometry to compare the expression of surface markers associated with activation and with differentiation in lung and peripheral blood T lymphocytes from normal subjects. T cell subsets, defined based on their reactivity with monoclonal antibodies (MAb) OKT3, OKT4, and OKT8, were analyzed for expression of activation antigens as detected by MAbs to the interleukin-2 receptor, the transferrin receptor, and HLA-DR determinants. Whereas circulating T lymphocytes expressed the three activation antigens at low levels, and the total of T4+ and T8+ cells always approximated the number of T3+ cells, lung T lymphocytes of the T3+, T4+, and T8+ populations expressed the activation antigens at variable levels in combinations not seen in circulating lymphocytes, and the sum of T4+ and T8+ cells always exceeded the T3+ total. A proportion of T4+T8+ cells was detected in lung lymphocytes.

Adult↗
PubMed1985

Allogeneic leukocyte and germ cell-induced murine immunodeficiency.

Immune deficiency, as defined by significant decreases in lymphocyte Con A and allo-reactivity and in natural killer (NK) function, was induced in normal adult mice by i.p. injections of combinations of allogeneic testicular germ cells and splenic leukocytes over 3 wk. This immune deficiency was evident at 8 wk after initial injection, and profound by 12 wk. Neither leukocytes nor testicular cells, given alone, were able to induce similar immune deficiency. These findings suggest the possibility that allogeneic germ cells and leukocytes of semen, on repeated administration, may induce immune deficiency and may act as co-factors to viral agents in the development of clinical AIDS in humans.

Animals↗
PubMed1984

Ontogeny of the immune system: fetal lamb as a model.

We examined adult sheep lymphocytes for the following surface markers: Surface membrane immunoglobulin, antigen identified by anti-sheep thymocyte globulin and complement receptors. We quantitated sheep peripheral blood mononuclear leukocyte proliferative responses to mitogens and alloantigens, and demonstrated a neutrophil-directed chemotactic factor (N-LDCF) liberated by mitogen-stimulated sheep mononuclear cells. A comparison of adult and fetal sheep from 120-150 d of gestation demonstrated that 1) fetal sheep had adult proportions of surface membrane Ig+ and T+ lymphocytes but a significant decrease in FcIgG receptor+ lymphocytes, 2) proliferative responses of fetal sheep blood mononuclear cells to mitogens and alloantigens were comparable to adult responses, and 3) fetal mononuclear leukocytes failed to produce the lymphokine, N-LDCF, in response to mitogen stimulation.

Age Factors↗
PubMed1984

The Fc receptor for IgG on human natural killer cells: phenotypic, functional, and comparative studies with monoclonal antibodies.

We compare five monoclonal antibodies ( B73 .1, 3G8 , Leu- 11a , Leu- 11b , and VEP13 ) that react with natural killer (NK) cells and polymorphonuclear cells (PMN). We show that all of these antibodies are directed against and inhibit the functional properties of the receptor for the Fc portion of IgG (FcR). Modulation of the FcR on NK cells after reaction with immune complexes induces the disappearance of the antigen(s) recognized by each of the five antibodies. Conversely, the antibodies block binding of IgG-sensitized erythrocytes to the NK cells and PMN and inhibit their ability to mediate cytotoxicity against antibody-sensitized tumor target cells. By using two-color immunofluorescence techniques, we characterize directly the lymphocyte population recognized by these antibodies and show that it is a homogeneous subset that does not bear markers of either B or T cells, with the exception of the 33,000 dalton antigen characteristic of suppressor/cytotoxic T cells present in 20 to 50% of the cells, and the 45,000 dalton receptor for sheep erythrocytes present on 80 to 90% of the cells. The phenotype of the cells reacting with the monoclonal antibodies corresponds to that of NK cells. Cross-competition experiments indicate that these antibodies detect at least two distinct epitopes on FcR, one ( B73 .1) preferentially expressed on NK cells and one or more ( 3G8 /Leu- 11a /Leu- 11b / VEP13 ) preferentially expressed on PMN. The lack of reactivity of these antibodies with B cells suggests that human B cells bear a different FcR from that on NK cells and PMN.

Antibodies, Monoclonal↗
PubMed1984

Surface phenotype of clonogenic cells in acute myeloid leukemia defined by monoclonal antibodies.

Colony-forming cells in ten cases of acute myeloid leukemia (AML) were studied with six cytotoxic monoclonal antibodies that react with antigens expressed at discrete stages of differentiation of normal and leukemic hematopoietic cells. The reactivity of the whole leukemic population was measured by indirect immunofluorescence, and the reactivity of the colony-forming cells was established by complement-mediated cytotoxicity and by fluorescence activated cell sorting. Comparison of the immunofluorescent reactivity with cytotoxicity and cell sorting showed that colony-forming cells were found within a fraction of the leukemic subpopulations that expresses these antigens. This finding implies that immunofluorescence reactivity of the total leukemic population does not necessarily predict the phenotype of the clonogenic cells. When the surface phenotype of the clonogenic leukemic cells was compared to that previously established for normal marrow hemopoietic clonogenic cells, several patterns were seen: (1) in four of ten cases, the clonogenic cells expressed a phenotype like that of relatively mature normal granulocyte-macrophage colony-forming cells (late CFU-GM) or, (2) in two cases, a phenotype similar to the less mature colony-forming cells (early CFU-GM or CFU-GEMM), and (3) in four cases, a composite phenotype of early and late CFU-GM. Thus, the level of impairment of differentiation in AML may vary from case to case. In those cases phenotypically similar to the late CFU-GM, it may be possible to separate leukemic clonogenic cells from less mature normal clonogenic cells using monoclonal antibodies selectively cytotoxic for the late CFU-GM.

Antibodies, Monoclonal↗
PubMed1983

Human natural killer cells analyzed by B73.1, a monoclonal antibody blocking Fc receptor functions. II. Studies of B73.1 antibody-antigen interaction on the lymphocyte membrane.

In this paper, we characterize the antigen recognized by the monoclonal antibody B73.1 and the modification occurring at the membrane of the positive cells after interaction with the antibody. The B73.1-defined antigen is a protein of 50,000 to 72,000 daltons that is sensitive to pronase but not to trypsin treatment. B73.1 antibody, and its F(ab')2 fragment, directly block, at high concentrations, the binding of IgG antibody-sensitized erythrocytes to the Fc receptors (FcR) of a subpopulation of lymphocytes and neutrophils. B73.1 antibody dissociates rapidly from the positive cells, but concomitant modulation of both B73.1 antigen and FcR is induced when cells are incubated in the continuous presence of antibody or when B73.1 antibody is cross-linked at the cell membrane with an anti-mouse immunoglobulin antiserum. Reaction of lymphocytes with immune complexes also induces modulation of both FcR and B73.1 antigen, without affecting the expression of other antigens on the positive cells. The possibility that the antigen is internalized and digested by the cell after reaction with the antibody is discussed. B73.1 antibody inhibits antibody-dependent cytotoxicity mediated by lymphocytes (K cells) and neutrophils, whereas it does not affect spontaneous cytotoxicity of NK cells. These results suggest the B73.1-defined antigen might be the FcR or a structure closely related to it on K/NK cells.

Antibodies, Monoclonal↗
PubMed1983

Differentiation antigens of human hemopoietic cells: patterns of reactivity of two monoclonal antibodies.

Two mouse anti-human monoclonal antibodies (S3.13 and S5.7) raised against cells of acute myelogenous leukemia were found to react with antigens expressed on the surface of subsets of monocytes and lymphocytes. S3.13 precipitates a peptide of Mr 29,000, and S5.7 precipitates a peptide of Mr 20,000 present on the surface of all the cell types tested. These two surface antigens were distributed on discrete subpopulations of normal hemopoietic cells. The antibodies reacted with all (S5.7) or a subpopulation (S3.13) of peripheral blood T-lymphocytes, and with a subset of monocytes. Both antibodies reacted with bone marrow blast cell progenitors of the myelomonocytes and erythroid lineage. S5.7 also reacted with non-T-lymphocytes and with cells of the eosinophilic lineage. Both antigens disappeared from the cell surface during normal myeloid and erythroid differentiation. Thus, these monoclonal antibodies define the molecular characteristics and the cellular distribution of two differentiation antigens present on cells of the hemopoietic lineage.

Animals↗
PubMed1982

Isolation of ovine lymphocytes, granulocytes, and monocytes by counterflow centrifugation elutriation.

A simple, brief 1-step counterflow centrifugation elutriation technique is described for the recovery of highly purified populations of lymphocytes and granulocytes from adult and fetal ovine peripheral blood. Monocytes are obtained as an enriched population. Lymphocyte and granulocyte recoveries average 80%, higher than with routine gradient centrifugation procedures. In this described technique, inexpensive medium is used, and it is completed in about 90 minutes. The individual blood cellular populations, when tested appropriately, demonstrated normal functional responses.

Animals↗
PubMed1978

Cranial morphology in the 18p-syndrome.

Three of four recently described children with the 18p- syndrome were reinvestigated using cranial computerized tomography (CCT). More severe deformities were found in the cases with severe cerebral malformation, but there was no correlation with the degree of mental retardation.

Child↗
PubMed1978

Human fetal cells. I. Mitogenic responses.

Human fetal cells from 10 prematures and newborn infants (28--38 weeks of gestational age) and isolated or non-isolated fetal cells circulating in the blood of 9 primigravidae were studied in their ability to respond to phytohemagglutinin, pokeweed, dextran sulfate and lipopolysaccharide. An age-dependent responsiveness of fetal cells obtained from the prematures to all mitogens tested was detected as well as a clear graduation of mitogenic capacity with phytohemagglutinin to produce the highest stimulation. Though a moderate mitogenic response to lipopolysaccharide and dextran sulfate was noted in the blood cultures of the infants, LPS and in part DS transformation of fetal cells obtained from maternal blood appeared to be reduced or absent. A selective stimulation of fetal cells occurring in the circulation of primiparae sufficient for prenatal diagnosis could not be achieved with the mitogens tested. The findings suggest that fetal cells crossing to the mother are different from normal fetal lymphocytes. The present study was performed to elucidate in as quantitative a manner as possible the responses of human fetal cells to different T- and B-cell mitogens. Cells were obtained from various sources for comparing the mitogenic responses of isolated and non-isolated fetal cells. Our results demonstrate that mitogenic responses depend on the gestational age of the fetal cells, the source of the cells and on experimental conditions.

Cells, Cultured↗
PubMed1977

[The clinical data of infected umbilical sinus].

We report the case of a female baby, three months of age, with anemia of chronic infection, hematuria and umbilical sinus. The patient did survive a sepsis and the extirpation of the umbilical sinus and died in a septic shock. Diagnosis and therapy of the anomalies of the umbilicus are discussed and a possible explanation for the hematuria is presented.

Anemia↗
PubMed1976

The 18 p-syndrome. Report of four cases.

Four children, two girls and two boys, were found to have a short arm deletion of chromosome No. 18. Three of them exhibit a typical dysmorphy of the face showing retraction of the midface, broad-based, flat nose, hypertelorism, epicanthus, "carp mouth", big, protruding, and low set ears, as well as a variable number of Turner-like features, failure of growth, mental retardation, and muscular hypotonia. A newly born child, who died at 2 days of age exhibited severe brain defects of holoprosencephalic series. The clinical and cytogenetic findings are compared with the reviewed data of the 18 p deletion. The hypothesis of "gene-dosis compensation" is discussed in order to explain the variable phenotypical expression of 18 p-syndrome as there is obviously to correlation between the extent of the deficiency and the expression of malformations.

Abnormalities, Multiple↗