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F Finkelman

Publications and source records attributed to F Finkelman.

33 records · Page 2Linked to original sources
PubMed1988

Exposure to crosslinked IgD induces receptors for IgD on T cells in vivo and in vitro.

IgD is a surface immunoglobulin, which is coexpressed with IgM on greater than 90% of mature B cells, but its levels in serum are extremely low compared to those of IgM. It role as a surface receptor has been reemphasized by our recent findings that IgD receptors are induced on helper T cells by exposure to IgD and that such cells have immunoaugmenting properties. The present study shows that crosslinking of soluble IgD or of monomeric cell surface IgD is required and sufficient for the induction of T cells bearing receptors for IgD, both in vivo and in vitro. Effective IgD crosslinking in this respect can be obtained with antigen or with heterologous and immunogenic as well as nonimmunogenic allotype-specific anti-IgD. These results reinforce the concept that the induction of T cells bearing receptors for IgD is an integral component of the normal immune response.

Animals↗
PubMed1988

Release of IgD-binding factor by T cells under the influence of interleukin 2, interleukin 4, or cross-linked IgD.

Helper T cells with receptors specific for IgD have immunoaugmenting properties. We have now detected soluble IgD-binding factor in cell supernatants immobilized on nitrocellulose paper by their ability to bind 125I-labeled IgD. IgD-binding factor is released by normal splenic T cells stimulated with recombinant interleukin 2, recombinant interleukin 4, or crosslinked IgD in amounts paralleling the induction of IgD receptors on the cells. IgD receptors are constitutively produced by antigen-specific helper T-cell hybridomas 2H10 and A3.4C6. Incubation of these hybridoma cells with recombinant interleukin 2 increases release of IgD-binding factor while reducing expression of IgD receptors. Specificity of the binding factor for IgD is established by (i) competitive inhibition; (ii) the ability of the binding factor to bind radiolabeled IgD and not monoclonal IgE, IgG2a, or polyclonal IgG; and (iii) the removal of the binding factor on passage through an IgD-Sepharose column and recovery in a subsequent acid eluate.

Animals↗
PubMed1984

Reevaluation of the effects of alcohol consumption on rat liver microtubules: effects of feeding status.

The ability of total, free and microtubule-derived tubulins to bind colchicine was studied (using 4 different methods) in the liver of 12 male rat littermates pair-fed liquid diets containing 36% of energy either as ethanol or as additional carbohydrate and kept in the fed state up to the time of sacrifice. In the alcohol fed rats, we found a reproducible decrease in microtubule-derived tubulin and in the percentage of total tubulin present in the polymerized form. This was due to an alteration of the microtubular protein rather than to inhibitory factors of the liver supernatants. An equal group of pair-fed rats was tested after a 24-hour fast. Fasting decreased microtubule-derived tubulin and abolished the inhibitory effect of ethanol, probably by decreasing the rate of ethanol oxidation.

Animals↗
PubMed1983

A modified colchicine-binding assay for the measurement of total and microtubule-derived tubulin in rat liver.

The usual measurement of liver tubulin by the colchicine-binding assay does not take into account the accelerated decay of the colchicine-binding capacity of tubulin when liver supernatants, especially those containing microtubule-derived tubulin, are incubated at 37 degrees C. This results in marked underestimations. Our findings indicate that this alteration is due to an inhibitor of colchicine-tubulin binding in liver supernatants that is probably extracted from particulate fractions. The inhibitory activity is decreased by dilution of the supernatants and by increasing the concentration of colchicine. However, the former modification decreases the sensitivity of the assay and the latter increases the nonspecific binding of colchicine to liver proteins other than tubulin. Assessment of the decay and correction for it by calculating the initial binding capacity results in complete recovery of brain tubulin from liver supernatants and values for microtubule-derived tubulin that closely correspond to those expected from simultaneous morphometric assessment of liver microtubules by electron microscopy. The modified method also indicates that the fraction of liver tubulin assembled in microtubules is greater than previously reported.

Animals↗
PubMed1980

Acquisition of cell surface IgD after in vitro culture of neoplastic B cells from the murine tumor BCL1.

Murine BCL1 tumor cells bear large amounts of surface IgM and trace amounts of surface IgD. In the present studies we have shown that cultivation of these cells, in the absence of lipopolysaccharide, results in the acquisition of IgD by virtually all the cells. These results suggest that BCL1 cells can differentiate in vitro into more mature B cells and offer an attractive model for analyzing the factors controlling appearance of IgD on a monoclonal cell line.

Animals↗
PubMed1978

Reactivity of lupus erythematosus antibodies with leukemic helper T cells.

Immunoabsorbent columns, containing membrane fragments of either leukemic "helper" T cells or B cell lymphoblasts, were used to isolate and study antilymphocyte antibodies from plasmas of 2 patients with systemic lupus erythematosus (SLE). Both plasmas contained IgG which bound to and could be eluted from the "helper" T cell column. These antibodies significantly inhibited normal lymphocyte proliferative responses to microbial and histocompatibility antigens. The findings indicate that these SLE plasmas contain immunoglobulins of the IgG class which react with leukemic "helper" T cells and inhibit normal effector T cell function.

Antibodies↗
PubMedDate not supplied

8-Mercaptoguanosine-mediated enhancement of in vivo IgG1, IgG2 and IgG3 antibody responses to polysaccharide antigens in normal and xid mice.

We have examined the effects of the immune adjuvant 8-mercaptoguanosine (8sGuo) on the in vivo antibody response to the T-cell-independent type 2 antigen, TNP-Ficoll. While 8sGuo enhanced the IgG1, IgG2 and IgG3 antibody responses, it was without effect on the IgM antibody responses. Increasing the dose of injected 8sGuo from 30 to 300 mg or the frequency or its injection led to greater enhancement in the antibody response, which varied from 20 to 100 times that of control responses. The effect of 8sGuo was relatively early acting in that it no longer enhanced anti-TNP antibody responses when given 3 days after antigen injection. Its ability to mediate an adjuvant effect on antibody responses was demonstrable even under conditions where the injected antigen by itself stimulated either no or low-level antibody responses. Thus, it enhanced the antibody response to the very weak antigen, pneumococcal polysaccharide, and restored the antibody response of nonresponder immune defective xid mice to TNP-Ficoll. These results extend the earlier observations of Goodman and coworkers by demonstrating that in vivo IgG response to type 2 polysaccharide antigens can be enhanced in normal mice and restored in xid immune-deficient mice.

Adjuvants, Immunologic↗
PubMedDate not supplied

Exaggerated acetaldehyde response after ethanol administration during pregnancy and lactation in rats.

The exaggerated blood acetaldehyde response that has been reported after ethanol administration to pregnant rats was found to be the beginning of a much larger alteration occurring during lactation. Indeed, at the end of pregnancy, we confirmed a 4-fold increase in the acetaldehyde values above nonpregnant values after an intragastric dose of 3 g/kg ethanol. During gestational days 1 to 17, the levels did not differ. After delivery, the exaggerated acetaldehyde response to ethanol was increased, producing acetaldehyde concentrations 15-fold greater than in nonlactating controls. This response returned to nonpregnant levels with weaning and could be abolished by removing the pups at birth. The intensified response was associated with both an enhanced rate of ethanol oxidation and a decreased low Km aldehyde dehydrogenase activity in liver mitochondria. At the end of pregnancy, measurable concentrations of acetaldehyde were found in umbilical venous blood and fetal blood. However, they amounted to only one-quarter of maternal values whereas ethanol levels were similar. Thus, during late pregnancy and lactation, there is a marked increase in maternal blood acetaldehyde after ethanol intake. In the presence of a normal placenta, however, an acetaldehyde concentration gradient exists between the mother and the fetus.

Acetaldehyde↗