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S M Friedman

Publications and source records attributed to S M Friedman.

At least 109 records · Page 6Linked to original sources
PubMed1987

PolyI.polyC12U-mediated inhibition of loss of alloantigen responsiveness viral replication in human CD4+ T cell clones exposed to human immunodeficiency virus in vitro.

Two alloreactive human CD4+ T cell clones, recognizing HLA-DR2 and HLA-DR1 determinants, lost their specific proliferative capacity after infection with HIV. This system was used to explore the effect of polyI.polyC12U on HIV replication and immune suppression. The mismatched double-stranded RNA blocked HIV-associated particulate reverse transcriptase activity and viral-mediated cytopathic effects. Also, polyI.polyC12U preserved the alloreactivity of T cell clones after exposure to HIV.PolyI.polyC12U appeared to act at a level subsequent to host cell infection and reverse transcription. It had no effect on the enhancement of gene expression by the HIV transcription unit tatIII. These findings indicate that early in the course of infection of CD4+ T lymphocytes, HIV can directly abrogate proliferation to specific allodeterminants, and that this function is preserved in the presence of polyI.polyC12U. They also provide insight into the mechanism of antiviral action of a class of agent with potential clinical utility in AIDS.

HIV↗
PubMed1987

Rubella in the workplace: the need for employee immunization.

From 1983 to 1985, the New York City Department of Health investigated five workplace outbreaks of rubella. Approximately 40 per cent of the 265 cases were detected among women of child-bearing age (15-44 years). Data are reviewed from the 1983 Financial District outbreak to illustrate the continued susceptibility of young adults, the missed opportunities for rubella immunization, and the danger of congenital infection. A comprehensive rubella immunization program is required to protect pregnant women and eliminate congenital rubella. As one important component of this effort, employee health physicians are urged to assess the immune status of women of child-bearing age and to vaccinate all susceptibles who are not pregnant.

Adolescent↗
PubMed1986

Direct T helper-B cell interactions induce an early B cell activation antigen.

We have explored the consequences for the B cell of cognate interaction with T cells. Early expression of the B cell-restricted cell surface activation antigen, BLAST-2, has been used as an assay system to measure direct T-B cell collaboration. BLAST-2 is preferentially expressed by allogenic B cells cultured with MHC class II antigen-restricted Th clone cells matched to the DR specificity of the target B cells. B cells cultured with DR-mismatched allospecific Th cells express minimal BLAST-2. Th cell-induced BLAST-2 expression appears to be accessory cell independent and occurs as early as 8 h after initiation of culture, with peak expression at 18 h. Direct T-B cell contact, rather than Th-derived lymphokines, provides the most efficient stimulus for BLAST-2 expression. Crosslinking of sIg on B cells is a poor stimulus for BLAST-2 expression. The BLAST-2 assay permits the evaluation of early events associated with B cell activation through cognate interactions, and may facilitate subsequent studies of the mechanism of B cell differentiation.

Antibodies, Anti-Idiotypic↗
PubMed1986

Antigen-specific, MHC nonrestricted T helper cell-induced B cell activation.

We used a cloned, TNP-specific, MHC-restricted, human Th cell line, E-11, and an assay of cognate Th-B cell interaction, BLAST-2 antigen expression on the B cell surface, to investigate the functional nature of the Th cell antigen receptor. We observed that E-11 induces BLAST-2 expression by resting B cells in a hapten-dependent, hapten-specific, but MHC nonrestricted manner. The implication of these results for the Th cell receptor are discussed.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1986

Human helper-T-cell function does not require T4 antigen expression.

The relationship between immunoregulatory T-cell function and the expression of T-cell subset-specific differentiation antigens was examined using a phenotypically anomalous human T-cell line (TCL), termed H-1. H-1 cells were found to express T11, extremely high levels of T3, but no T4 nor T8 antigen. Despite their lack of T4 antigen expression, H-1 cells could be activated by coculture with pokeweed mitogen (PWM), anti-T3 antibody, or autologous B cells to provide potent help for B-cell differentiation into plaque-forming cells (PFC). In contrast, H-1 cells did not suppress the PFC response triggered by PWM-activated T4+ cells. These results demonstrate that the expression of the T-cell subclass-specific differentiation antigen, T4, is not required for a T cell to become activated and to implement the program for helper function. In addition, enhanced expression of T3 on the T4-, T8-, H-1 cell surface may reflect a compensatory upregulation of the T3/Ti receptor complex on T cells which are deficient in these nonpolymorphic associative recognition structures.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1986

Inherited polymorphism of the human T-cell antigen receptor detected by a monoclonal antibody.

Three different murine monoclonal antibodies to the human clonotypic T-cell antigen receptor immunoprecipitate the alpha-beta chain heterodimer; induce comodulation of the clonotypic molecule with the T3 molecular complex; stain small populations of normal polyclonal T cells, suggesting that they react with variable or joining region determinants of the clonotypic receptor; and induce proliferation of resting T cells. While two of these antibodies detect the clonotypic receptor in all individuals studied, the third antibody (OT145), described herein, does not detect the T-cell antigen receptor on T cells of all individuals. By indirect immunofluorescence, three groups can be distinguished within a population of individuals (n = 138) by OT145. Individuals lacking T cells reactive with OT145 have a homozygous OT145-phenotype. T cells from such individuals fail to proliferate in the presence of OT145 in contrast to T cells from OT145+ individuals. Individuals with a relatively large percentage of OT145+ T cells, 4.5 +/- 1.54% (mean +/- 2 SEM) are homozygous OT145+, while those with an intermediate percentage, 2.04 +/- 0.9%, have a heterozygous phenotype. Family studies suggest autosomal codominant inheritance of the OT145 phenotype. The distribution of the three OT145-defined phenotypes varies considerably in populations of different ethnic background. Taken together these data suggest that the polymorphism detected by OT145 may represent a variable or joining region allotypic system of the human T-cell antigen receptor. In addition, our results indicate that allelic exclusion governs the expression of the clonotypic receptor by human T cells.

Alleles↗
PubMed1986

Prehypertensive changes in sodium transport induced by deoxycorticosterone acetate in incubated rat tail artery.

The transport and distribution of sodium, potassium, and water were examined in tail arteries of rats treated with deoxycorticosterone acetate (DOCA)-saline for 10 days, a time that marks the earliest onset of a rise of blood pressure in the strain (Wistar) used. The arteries were incubated for more than 20 hours to ensure that any change observed was sufficiently built in so that it could not readily be washed out. Three distinct changes were observed. First, the steady state transmembrane sodium gradient (operationally [Na]o/[Na]i) was increased. Second, the amount of sodium excluded from participation in the sodium gradient, and hence probably bound, was increased. Third, after prolonged potassium depletion, the ouabain-insensitive loss of cell water and sodium that follows the readmittance of potassium was increased. These results suggest that fundamental embedded changes in sodium transport occur well before the blood pressure rises in response to DOCA-saline.

Animals↗
PubMed1985

Transmission of hepatitis B virus to classroom contacts of mentally retarded carriers.

The risk of the spread of hepatitis B virus infection from deinstitutionalized, mentally retarded carriers to pupil and staff school contacts in the New York City public school system was measured serologically in a three-phase study from 1978 to 1982. In the third phase, undertaken in 1982, blood samples were drawn and questionnaires were completed on students and staff tested in either of the first two phases and on comparison groups with intermediate and no known school exposure to deinstitutionalized carriers. Univariate and logistic regression analyses revealed that staff and pupils with a history of classroom exposure to a hepatitis B virus carrier had significantly increased prevalences of hepatitis B virus infection (13.4%, odds ratio = 1.9; 9.3%, odds ratio = 2.5, respectively). Similarly, yearly seroconversion rates of 1.3% and 0.67% indicate that staff and, to a lesser extent, pupils are at increased risk of infection.

Adolescent↗
PubMed1985

Acquired immunodeficiency syndrome in New York City. Evaluation of an active surveillance system.

In January 1983, the New York City Department of Health initiated an active surveillance program for acquired immunodeficiency syndrome (AIDS) in 19 hospitals and a modified-active surveillance program in the remaining 69 hospitals. We reviewed hospital laboratory and autopsy records in 12 active surveillance hospitals and three modified-active surveillance hospitals six months later. Patients who had opportunistic diseases characteristic of AIDS diagnosed in 1982 (before active surveillance) and 1983 (after implementation of active surveillance) were matched against health department AIDS surveillance reports. For the 16 months we evaluated, 96% of patients identified with AIDS in the 12 active surveillance hospitals and 100% of those in the three modified-active surveillance hospitals had been reported to the health department. The delay between diagnosing a case and reporting it to the health department significantly decreased between 1981 and the first six months of 1983 in all hospitals. The proportion of cases reported within one month of diagnosis increased from 45% to 69% during this period. We conclude that the current surveillance program for AIDS in New York City is effective and that case reporting is sufficiently complete for accurate analysis of disease trends.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Botulism and botulism-like illness in chronic drug abusers.

From 1982 to 1983 we received reports of a neurologic illness characterized by a symmetric descending paralysis in six drug abusers from widely separated geographic areas. Botulism was confirmed in two patients; type B botulinal toxin was found and Clostridium botulinum was isolated from a small abscess in one, and type A botulinal toxin was found in the serum of the other. The clinical illness in the remaining four patients, although not laboratory confirmed, was also compatible with botulism. None of the patients had histories suggestive of foodborne botulism, and wound botulism was suspected as the cause of illness. There are several reports of tetanus associated with parenteral drug abuse; wound botulism is another toxin-mediated clostridial infection that may occur as a complication of chronic drug abuse.

Abscess↗
PubMed1985

Cloned allospecific human helper T cell lines induce an MHC-restricted proliferative response by resting B cells.

To analyze helper T (Th) cell-induced B cell proliferation in man, we have cloned allospecific Th cells, grown them as long-term IL 2-dependent T cell lines (TCL), and analyzed their phenotypic and functional properties. The two TCL described in this report, A-7 and A-57, are both composed exclusively of T3+, T4+, T8- T cells blasts. In proliferative assays, with a panel of x-irradiated allogeneic stimulator cells, A-7 was found to proliferate in response to DR3-bearing cells, whereas A-57 responds to DR2-positive stimulators. Both TCL are capable of providing MHC-restricted polyclonal help for allogeneic B cells, as measured in the reverse hemolytic plaque assay. Of greater interest, x-irradiated A-7 and A-57 cells are capable of inducing a proliferative response by allogeneic B cells that is absolutely MHC restricted at the inductive (Th-APC) level. Thus, x-irradiated A-7 cells only trigger proliferation by DR3+ B cells, whereas A-57 cells selectively activate DR2+ B cells. In contrast, after antigen-specific activation, x-irradiated A-7 and A-57 cells can recruit a significant proliferative response by allogeneic B cells bearing "irrelevant" DR antigens. The possibility that Th-induced B cell proliferation may be restricted at the effector (Th-B cell) level was addressed by fractionating B cell populations into "activated" and "resting" subsets by discontinuous Percoll density gradient centrifugation and further purification by employing a monoclonal antibody directed against an antigen expressed on activated B cells (4F2). These studies demonstrate that activated B cells are readily and nonspecifically recruited to proliferate by activated Th cells, whereas optimal proliferative responses by resting B cells require MHC restricted Th-B cell interaction.

Antibodies, Monoclonal↗
PubMed1985

The relation of sodium transport to blood pressure in the adrenalectomized rat.

The effects of treatment of the adrenalectomized rat with aldosterone or corticosterone were observed daily for 3 days. Blood pressure and plasma electrolytes were normalized within 24 h but cell Na and K remained essentially unchanged throughout. We conclude that blood pressure is associated with Na transport activity rather than with cell [Na].

Adrenalectomy↗
PubMed1984

Na transport and blood pressure in the adrenalectomized rat.

The transmembrane distribution of Na, K, and water in freshly excised rat tail artery was measured 7 days after adrenalectomy, 3 days after withdrawal of support with 1% NaCl as drinking water. Cell Na decreased from 35.8 +/- 0.9 to 31.6 +/- 0.7 mmol/kg dry wt, tissue water increased from 2.93 +/- 0.03 to 3.08 +/- 0.04 l/kg dry wt, and tissue K remained unchanged. As concentration, [Na]i decreased from 22.5 +/- 0.9 to 18.3 +/- 1.0 mM in parallel with [Na]o which fell from 140.6 +/- 0.3 to 133.6 +/- 1.0. Conversely, while [K]i fell from 140 +/- 2 to 128 +/- 3, [K]o rose from 2.15 +/- 0.12 to 5.40 +/- 0.33 so that EK dropped from -109 to -83 mV. Aldosterone (120 micrograms X 100 g-1 X 24 h-1 sc; 3 X 10(-7) M if immediately distributed in the extracellular fluid) partially restored blood pressure, plasma [Na] and [K], and tissue water within 24-26 h but did not increase cell Na. Similar effects were produced with corticosterone at 400 microgram X 100 g-1 X 24 h-1 (3 X 10(-6) M if immediately distributed in the extracellular fluid). We conclude that the restoration of blood pressure in the adrenalectomized rat is independent of [Na]i or [Na]o/[Na]i but is associated with enhanced Na transport activity.

Adrenalectomy↗
PubMed1983

A cloned major histocompatibility complex-restricted trinitrophenyl-reactive human helper T cell line that activates B cell subsets via two distinct pathways.

A cloned, trinitrophenyl (TNP)-specific helper T cell line (TCL), termed E-11, has been established in long-term, interleukin 2-dependent culture and used to study human T helper (Th)-B cell collaboration. Co-culture of E-11 with TNP-modified, but not unmodified or FITC-modified, autologous B cells results in a vigorous, polyclonally plaque-forming cell (PFC) response. E-11 helper activity is not constitutive, but requires antigen-specific, major histocompatibility complex-restricted activation of the TCL cells by interaction with TNP-modified autologous or DR 5+ allogeneic macrophages. Using B cell subsets isolated by discontinuous density gradient cengrifugation as responder populations, we determined that E-11 activates B cell subsets via two distinct mechanisms: (a) E-11 polyclonally activates large B cells in an unrestricted and nonspecific manner; and (b) E-11 preferentially induces a PFC response by TNP-modified small B cells. These results suggest that the large B cell subset is activated by helper signals generated during the Th-antigen-presenting cell interaction, while small B cells require an additional stimulus that is provided by antigen-specific Th-B cell contact.

B-Lymphocytes↗