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Biomedical subjects

J F Miller

Publications and source records attributed to J F Miller.

At least 253 records · Page 14Linked to original sources
PubMed1983

Dual effect of glia maturation factor on astrocytes. Differentiation and release of interleukin-1 like factors.

C6 glioma cells, and primary cultures of mouse astrocytes, stimulated with lipopolysaccharide (LPS) release an interleukin-1 like factor (IL-1) which enhances lectin-induced T-lymphocyte proliferation and promotes the release of interleukin-2 (IL-2) by ConA-stimulated thymocytes. In the present study, the glia maturation factor (GMF) was found not only to induce differentiation of glioblasts, but also to elicit the secretion of IL-1 like factors by cultured mouse astrocytes and their precursor cells. GMF was also effective in triggering IL-1 release by macrophages. Contamination of the 23 000 MW GMF preparation with LPS was excluded by the Limulus lysate assay and by using C3H/HeJ LPS-nonresponder mice whose glia and macrophages responded to GMF but not to LPS, by IL-1 release. Through its ability to induce glial differentiation and IL-1 release, GMF may represent an important endogenous signal, triggering both reactive gliosis and the development of an immune response within the central nervous system.

Animals↗
PubMed1983

Delayed hypersensitivity induced by anti-T-cell-line antisera is enhanced by pertussigen and not restricted by histocompatibility genes.

Anti-T-cell-line antisera were raised by repeatedly injecting mice with syngeneic, antigen-specific, delayed hypersensitivity (DH) inducing cells grown as continuous T-cell lines in vitro. Many of these antisera could induce antigen-specific DH responses which, in some cases, were rather slight. For example, the DH reaction to azobenzenearsonate induced in A/J mice by an A/J antiserum produced against the syngeneic azobenzenearsonate-specific cell line AA3 was only a weak response. Administration of pertussigen, a protein purified from Bordetella pertussis, markedly enhanced this response and prolonged its duration. Histologically the reaction showed the classical mononuclear infiltration of DH. It could be transferred to naive mice by lymph node cells that were anti-Thy-1.2 sensitive, and the transfer was restricted by genes of the major histocompatibility complex (MHC). The induction of DH by antiserum, however, was not influenced by MHC or non-MHC gene products.

Animals↗
PubMed1983

Identification of the pifC gene and its role in negative control of F factor pif gene expression.

The pif region of the F factor includes two genes, pifA and pifB, that lead to abortive T7 infection. We have identified a new gene in this region, pifC, by constructing an in vitro fusion of pif DNA at 41.6 kilobases on the F factor physical map to the lacZ gene. A PifC-LacZ fusion protein of 149,000 daltons has been identified by immunoprecipitation and polyacrylamide gel electrophoresis. This allows us to assign the N terminus of pifC to 42.5 kilobases on the F map. Using fusions of pifC, pifA, and pifB to lacZ, we have studied the regulation of pif gene expression and have shown that the product of pifC negatively controls its own expression and that of pifA and pifB.

Bacterial Proteins↗
PubMed1983

Hapten-specific help mediated by an anti-ABA T cell line.

Long-term cultures of functional T cells were grown from mice injected with azobenzene arsonate (ABA) coupled spleen cells or mice painted with the diazonium salt of p-phenylarsonate. All cell lines produced delayed hypersensitivity to ABA. When tested for helper function in an antibody-forming cell assay only one line, AA3, helped plaque-forming cell formation. It was able to help anti-FLU response of FLU-HGG primed B cells to ABA-KLH-FLU. The help required linkage of the ABA and FLU determinants because cultures stimulated with a mixture of ABA-KLH and TNP-KLH-FLU did not show increased PFC. These experiments demonstrate hapten-specific help in a system which eliminates involvement of passively absorbed antibody in hapten recognition.

Animals↗
PubMed1983

Induction of suppressor T cells by monoclonal anti-idiotope antibody in strains of mice not expressing the idiotope in hyperimmune serum.

A monoclonal antibody, reactive with an idiotope present on some but not all A/J anti-azobenzenearsonate antibodies bearing the cross-reactive idiotype, was used to induce suppressor T cells. These cells suppressed the effector phase of the delayed hypersensitivity response to ABA but not to oxazolone. They could be enriched on dishes coated with ABA but not with trinitrophenylated human gamma-globulin, and the enrichment could be blocked by the anti-idiotope. Suppressor activity was also enhanced by first incubating T cells with the anti-idiotope and then collecting immunoglobulin-coated cells on dishes coated with anti-mouse immunoglobulin. The suppressor cells could be induced in A/J and CBA mice, even though hyperimmune CBA mice did not produce antibodies bearing this idiotope.

Animals↗
PubMed1982

A search for messenger RNA molecules bearing immunoglobulin VH nucleotide sequences in T cells.

Expression of VH-coded mRNA molecules in T cells, antigen-specific T cell lines, or T cell hybridomas was not detected using four different VH DNA probes under conditions that permitted cross-hybridization between distantly related VH genes. In contrast, VH gene expression was readily detected in two B cell lymphomas and in splenic B cells. Less than one molecule per cell of RNA, exactly complementary to the DNA probes used, would have been detected in these T cell populations. The results thus seriously question the proposition that T cells use the B cell VH repertoire to code for antigen receptors.

Animals↗
PubMed1982

Hapten-specific T cell lines mediating delayed hypersensitivity to contact-sensitizing agents.

Continuous cultures of T cells from the lymph nodes of mice sensitized to the contact sensitizers 4-ethoxymethylene-2-phenyl oxazolone or picryl chloride have been established. For continuous proliferation, the lines required specific antigen, syngeneic antigen-presenting cells, and growth factors from the supernatant of concanavalin-A-stimulated lymphoid cultures. Cells from the lines showed antigen specificity and major histocompatibility complex restriction in proliferation assays and in delayed hypersensitivity. They could mediate delayed hypersensitivity to the sensitizer presented as a reactive hapten or coupled to keyhold limpet hemocyanin.

Animals↗
PubMed1982

Antigen-specific production of immune interferon by T Cells lines.

Continuous cultures of T cells reactive to the hapten 4-ethoxymethylene-2-phenyloxazolone were tested for interferon production after antigenic stimulation in vitro. Induction of interferon was antigen-specific and also restricted by the I region of the major histocompatibility complex. Kinetics of antigen induced interferon production were different from those reported for mitogen induced synthesis.

Animals↗
PubMed1982

Anti-T-cell idiotype activity in serum of mice injected with syngeneic hapten-specific T-cell lines.

T cells able to mediate specific delayed type hypersensitivity (DH) in mice in response to the haptens azobenzenearsonate (ABA), oxazolone (OX), and picryl chloride have been grown in continuous cultures. They were tested for their ability to react with the hapten in vitro and to induce anti-idiotype antibody in syngeneic mice. Incubation in vitro with OX-glycine blocked the ability of an anti-OX cell line to produce DH in vivo but had no effect on an anti-ABA cell line. However, this was inhibited by ABA conjugated to bovine serum albumin (ABA-alb) but not by irrelevant haptens such as OX-glycine or trinitrophenyl-alb. Antisera prepared by immunizing syngeneic mice with the anti-OX line blocked the inhibitory effect of OX-glycine on that line but did not reverse the effect of ABA-alb on the anti-ABA line. Neither normal mouse serum nor inappropriate anti-line antisera could influence the effect of OX-glycine on the anti-OX line. When given alone to naive mice, a specific anti-line antiserum induced DH specific for the antigen to which the line was responsive. Thus, for example, antiserum directed to an anti-OX line produced OX-specific DH. The results suggest that anti-T-cell idiotype antibodies can be induced by immunizing mice with syngeneic antigen-specific T-cell lines and that these antibodies can block the specific in vitro interaction of antigen with the corresponding antigen-specific T cells and induce specific DH in vivo.

Animals↗
PubMed1982

Differentiation among T lymphocytes. The cloning approach.

The immune response comprises a complex series of cellular interactions between antigen-presenting cells (APC) of various types and a large number of subsets of lymphocytes which belong to two main categories: B cells or the precursors of antibody-secreting cells derived from the bone marrow and T cells which do not produce antibodies and are derived from the thymus. Experiments in the last decade have led to the identification of numerous subsets of T and B cells and to the realization that the cell interactions in immune responses are extremely complex, consisting essentially of circuits and feedback loops integrated into an intricate network. We have now reached a stage where it is difficult to distinguish between what is actually happening in a response and what is thought to be occurring to fit the investigator's preconceived notions. Clearly one of the ways out of this dilemma is to clone each individual cell type within a circuit in order to identify its characteristics unequivocally, and then to attempt to reconstruct the circuit with all the cloned cells artificially. We realize that this procedure may not be optimal, since the sum is always greater than the parts, but it must surely allow a more precise identification of some of the cell types and their effects.

Animals↗
PubMed1982

Early embryonic mortality in women.

Measurements of human chorionic gonadotropin (hCG) have been used to assess early embryo loss in women. Urine samples obtained from a control group of sterilized women with normal ovulatory menstrual cycles enabled a concentration limit of 56 IU/l to be determined so that any nontrophoblastic hCG or other cross-reacting compounds could be accounted for. One hundred ninety-eight ovulatory cycles were collected from a normal population attempting to conceive. Fecundability was 22% to 27% for this population. The risk of pregnancy in exposed ovulatory cycles was 59.6%; however, 61.9% of conceptuses will be lost prior to 12 weeks. Most of these losses (91.7%) occur subclinically, without the knowledge of the mother.

Adult↗
PubMed1981

Use of arginine compounds to examine the role of an essential arginine in the mechanism of glycogen phosphorylase.

The possible role of arginine in the mechanism of muscle glycogen phosphorylase qas studied by examining the effect of arginine compounds. Guanidino compounds with an aromatic group inhibit native phosphorylase b, reduced phosphorylase b, phosphorylase b', and phosphorylase a. The inhibition was found to be uncompetitive with respect to glucose 1-phosphate and noncompetitive toward glycogen for phosphorylase b. This is consistent with a kinetic mechanism where the inhibitor binds after the substrate, glucose 1-phosphate. In the presence of citrate and l-cysteine, N-alpha-tosylarginine methyl ester, a good inhibitor, promotes the removal of tightly bound pyridoxal phosphate. Potato phosphorylase has many similarities to the muscle enzyme, but it lacks the regulatory sites and does not have a polysaccharide storage site [Shimomura, S., & Fukui, T. (1980) Biochemistry 19, 2287]. N-alpha-Tosylarginine methyl ester inhibited the potato enzyme, was uncompetitive with glucose 1 -phosphate, and was competitive with starch; therefore, it seems likely that TAME is binding near the active site of both the potato and muscle enzyme. The different inhibitory patterns with respect of polysaccharide for potato and muscle phosphorylase can be explained by the absence of the polysaccharide storage site on the potato enzyme. Inhibition by arginine compounds is related to the pKa of the guanidino fuction, i.e., the lower pKa value, the greater the inhibition. On the basis of these studies and those of Dreyfus et al. [Dreyfus, M., Vandenbunder, B., & Buc, H. (1980) Biochemistry 19, 3834], who found that Arg-568 was essential for activity, we suggest that arginyl compounds inhibit when an unprotonated guanidino group competes for the "binding site" of Arg-568.

Animals↗
PubMed1981

Contact sensitivity to azobenzenearsonate and its inhibition after interaction of sensitized cells with antigen-conjugated cells.

Painting mice on the skin with the diazonium salt of p-arsanilic acid elicited two types of T cell activity. One was restricted by the I region of the major histocompatibility complex and was responsible for the transfer of azobenzenearsonate (ABA) sensitivity to naive mice. The other was H-2K restricted and could be demonstrated by its ability to interact specifically with ABA-coupled cells in vitro and to inhibit nonspecifically the transfer of sensitivity by cells sensitized either to ABA or to another antigen. Free antigen, or antibody directed against the cross-reactive idiotype on the anti-ABA antibodies of A/J mice, could inhibit the H-2K-restricted suppressive activity induced in the ABA immune A/J cells.

Animals↗