BSF-1 action on resting B cells does not require elevation of inositol phospholipid metabolism or increased [Ca2+]i.

B cell stimulatory factor-1 (BSF-1) acts on resting B cells to increase expression of class II major histocompatibility complex (MHC) molecules and to prepare for more prompt entry into S phase in response to anti-IgM and lipopolysaccharide. It also acts as a costimulant, with low concentrations of anti-IgM, to cause resting B cells to synthesize DNA. Unlike anti-IgM, BSF-1 does not cause elevation in inositol phospholipid metabolism or in concentration of intracellular free calcium, nor does it enhance such biochemical responses to anti-IgM.

Interferon-gamma inhibits the action of B cell stimulatory factor (BSF)-1 on resting B cells.

B cell stimulatory factor-1 (BSF-1) stimulates resting B cells to increase in volume and prepares these cells to enter the S phase in response to anti-IgM and other B cell mitogens. Interferon-gamma (IFN-gamma) blocks both the volume enlargement and preparation for DNA synthesis caused by BSF-1, although it has little effect on B cells already stimulated by BSF-1. The capacity of IFN-gamma to inhibit the action of BSF-1 on resting B cells suggests a mutual regulatory interaction between these two T cell-derived products.

Enhancement of radiation-induced cell kill by platinum complexes (carboplatin and iproplatin) in V79 cells.

Two second generation platinum complexes currently undergoing clinical chemotherapeutic trials, carboplatin (CBDCA) and iproplatin (CHIP), were evaluated for their ability to alter the survival of cultured Chinese hamster V79 cells following irradiation. Two protocols were employed. In the first, the drug was added to preplated cells, some of which were subsequently made hypoxic with nitrogen gas.

B cell stimulatory factor 1 (BSF-1) prepares resting B cells to enter S phase in response to anti-IgM and lipopolysaccharide.

BSF-1 prepares resting BALB/c, DBA/2, and BDF1 B cells to enter S phase more promptly in response to subsequent culture with anti-IgM-based stimulants. It prepares DBA/2 and BDF1 B cells to respond to LPS, but its preparative effect for LPS responses of BALB/c B cells is both inconstant and meager. Preparation mediated by BSF-1 requires extended contact of B cells with the stimulant for full effect.

T-cell and mast cell lines respond to B-cell stimulatory factor 1.

The murine lymphokine B-cell stimulatory factor 1 (BSF-1) has been described previously in terms of its action on B lymphocytes. We now provide evidence that BSF-1 is also responsible for two additional biological activities. The first of these is the stimulation or maintenance of a state of activation in mouse T-cell lines.

Three distinct signals can induce class II gene expression in a murine pre-B-cell line.

Expression of class II genes of the major histocompatibility complex (MHC) has been studied in an Abelson-murine-leukemia-virus-transformed pre-B-cell line, R8, and its class II molecule (Ia)-negative variant, R8205. These variant cells contained barely detectable levels of RNA specific for all class II genes, including the nonpolymorphic invariant chain gene (Ii), and did not express cell surface Ia. Fusion of this murine Ia-negative cell line to the human Ia-positive Raji cell produced an interspecies hybridoma that expressed the murine Ia.

B cell stimulatory factor-1 enhances the IgE response of lipopolysaccharide-activated B cells.

Supernatants from some mouse helper T cell (TH) lines contain an activity that can enhance IgE production by lipopolysaccharide (LPS)-stimulated B cells by at least two orders of magnitude. During purification, this activity could not be resolved from B cell stimulatory factor-1 (BSF-1). Highly purified BSF-1 from a different source, the T lymphoma cell line EL-4, enhanced IgE production to the same extent as TH supernatants, which suggests that BSF-1 is responsible for this increase in IgE production.

Regulation of B-lymphocyte activation, proliferation, and immunoglobulin secretion.

Lymphocyte growth and differentiation are controlled by signals resulting from the interaction of antigen and cellular products, such as lymphokines, with specific cell membrane receptors. Resting B lymphocytes can be activated by low concentrations (1-5 micrograms/ml) of antibodies to membrane IgM, which is the B-lymphocyte receptor for antigen. The binding of anti-IgM to B cells causes a rapid increase in intracellular free calcium concentration ([Ca2+]i), in inositol phosphate concentration, and in protein kinase activity.

In vitro translation of B-cell stimulatory factor-1 in Xenopus laevis oocytes.

B-cell stimulatory factor-1 (BSF-1) can be translated in vitro in Xenopus laevis oocytes. This activity is blocked by an antibody to BSF-1. The RNA species coding for BSF-1 activity sediments of approximately 8-9S and is separable from RNA coding for interleukin-2 activity which sediments at approximately 11.

Serological, biochemical, and functional identity of B cell-stimulatory factor 1 and B cell differentiation factor for IgG1.

By three criteria, we have demonstrated that B cell stimulatory factor (BSF-1) and B cell differentiation factor (BCDF-gamma) are the same lymphokine. Highly purified preparations of high performance liquid chromatography-purified or affinity-purified BSF-1 had BCDF-gamma activity but not BCDF-mu activity. A monoclonal anti-BSF-1 antibody coupled to Sepharose depleted both BSF-1 and BCDF-gamma activity but not BCDF-mu activity from two different T cell supernatants.

Recombinant interferon-gamma inhibits the B cell proliferative response stimulated by soluble but not by Sepharose-bound anti-immunoglobulin antibody.

Recombinant-derived interferon-gamma (reIFN-gamma) was found to inhibit B cell proliferation that was stimulated by soluble goat anti-mouse IgD or goat anti-mouse IgM antibodies, but not that stimulated by Sepharose-bound anti-Ig antibodies. Recombinant IFN-gamma also inhibited the BSF-1-enhanced soluble anti-Ig B cell proliferation but did not block BSF-1 enhancement of Sepharose anti-Ig-stimulated B cell DNA synthesis. Recombinant IFN-gamma concentrations as low as 0.

Partial purification of murine B cell stimulatory factor (BSF)-1.

BSF-1 was partially purified from serum-free culture supernatants of cells of the EL-4 thymoma line, which had been induced 48 hr earlier with 4 beta-phorbol-12 beta-myristate-12 alpha-acetate (PMA). BSF-1 in 10-liter batches was adsorbed onto and eluted from trimethylsilyl-controlled pore glass beads (TMS-CpG) and then subjected to reverse-phase high-performance liquid chromatography (RP-HPLC). The recovery of BSF-1 activity by TMS-CpG and RP-HPLC ranged from 52 to 55% and 187 to 227%, respectively.

Carboplatin as a potentiator of radiation therapy.

A rationale for coordinating the administration of carboplatin with radiation to achieve enhancement of cancer therapy is developed. This approach is based upon a review of the reports of effects in a variety of systems, effects attributed to interactions between cisplatin or other platinum analogs and radiation. Two major effects include radiosensitization (RS) of hypoxic cells with platinum present during irradiation and potentiation of cell kill with platinum complexes administered after irradiation.

Production of a monoclonal antibody to and molecular characterization of B-cell stimulatory factor-1.

B-cell stimulatory factor-1 (BSF-1), formerly designated B-cell growth factor, is a T-cell-derived factor required for entry into the S phase of the cell cycle by B cells stimulated with low concentrations of anti-IgM antibodies. BSF-1 acts directly on resting B cells to prepare them to synthesize DNA more promptly on subsequent exposure to competent stimuli and to strikingly enhance their expression of class II molecules of the major histocompatibility complex. Previous studies have shown that murine BSF-1 can be separated physically from interleukin-2 (IL-2) and that the molecule has an apparent relative molecular mass (Mr) of approximately 15,000 and pI values of 6.

B-cell stimulatory factor 1 activates resting B cells.

B-cell stimulatory factor 1 (BSF-1) is a T-cell-derived lymphokine that acts together with low concentrations of anti-IgM antibodies to stimulate resting B cells to enter the G1 phase of the cell cycle and to synthesize DNA. We show here that supernatants from EL-4 cells, rich in BSF-1 activity, and BSF-1 purified by high-pressure liquid chromatography (HPLC-BSF-1) act on resting B cells, in the absence of anti-IgM antibodies, to prepare them to respond to anti-IgM and BSF-1. A 24-hour preculture with BSF-1 speeds the entry into S phase of B cells subsequently cultured with anti-IgM and BSF-1 by approximately equal to 12 hours and causes substantial increase in cell volume of all resting B cells.

Relapsing post-transfusion purpura. A preventable disease.

Post-transfusion purpura is an isoimmune disorder that can recur if unrecognized. A 56-year-old woman is described who had her third episode of post-transfusion purpura 17 years after her last exposure to the inciting antigen. Clinical and immunologic features are reviewed, and specific preventive measures are proposed.

Decreased procollagen production in cultured fibroblasts from patients with Lowe's syndrome.

The oculo-cerebro-renal syndrome described by Lowe is a catastrophic disease in children characterized by progressive eye, central nervous system and kidney degeneration. We determined procollagen production in cultured skin fibroblasts originating from patients with Lowe's syndrome as well as normal individuals after incubation of cells with [14C]proline for 1,4 and 20 h. Using [14C]hydroxyproline formation, in relation to cell protein or DNA, as an index of procollagen production, we found that cultured cells from patients synthesized collagenous protein at a substantially reduced level.

Randomized crossover trial of isosorbide mononitrate (Elantan 20) and slow-release glyceryl trinitrate in the treatment of angina pectoris.

An open, randomized, comparative crossover clinical trial was carried out to compare the clinical efficacy of 20 mg isosorbide mononitrate 3-times daily and 6.4 mg sustained-release glyceryl trinitrate 3-times daily in the treatment of angina pectoris. Fifty patients entered the trial and 48 patients completed.

Ig RNA expression in normal B cells stimulated with anti-IgM antibody and T cell-derived growth and differentiation factors.

An increase in mRNA encoding the secretory form of the mu heavy (H) chain (mus) and in the ratio of mus mRNA to the mRNA encoding the membrane form of the microH chain (micron) occurs in normal B cells stimulated with anti-IgM and BSF-p1 together with the two B cell differentiation factors B15-TRF and EL-TRF. Stimulation of cells with anti-IgM and BSF-p1 with either B15- or EL-TRF causes no change in mus levels or mus/micron ratios. The requirements for induction of high rate IgM synthesis in normal B cells stimulated with anti-IgM were precisely the same as those required for elevation of mus, mRNA levels and for increase in mus/micron mRNA ratios.

An analysis of various aspects of atomic bomb dose estimation at RERF using data on acute radiation symptoms.

The dose-response curves for acute radiation symptoms reported by atomic bomb survivors are compared by dose estimation method (the method used to calculate the transmission factor), shielding category, and city. Circular symmetry is also investigated. It is found that response rates for acute symptoms differ considerably by dose estimation method and shielding category even after controlling for both gamma and neutron exposure as well as for city, sex, and age at the time of the bomb.