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J F Miller

Publications and source records attributed to J F Miller.

At least 361 records · Page 20Linked to original sources
PubMed1972

Cell-to-cell interaction in the immune response. IX. Regulation of hepten-specific antibody class by carrier priming.

Mice primed to horse erythrocytes (HRBC) produced greatly enhanced 3,5-dinitro,4-hydroxyphenylacetic (NNP)-specific indirect plaque-forming cell (7S PFC) responses when given NNP.HRBC but no difference in hapten-specific direct (19S PFC) responses in comparison to non-carrier-primed mice. The effect was carrier specific and could not be produced by simultaneous challenge of rabbit erythrocyte (RRBC)-primed mice with RRBC and NNP.HRBC. When spleen cells from HRBC-primed mice were transferred to irradiated recipients, there was again an enhanced 7S response to NNP.HRBC. The primed spleen cells could be replaced by giving activated thymus cells to HRBC together with normal spleen as a source of B cells. It is concluded that T cells influence not only the amount but also the class of antibody formed by hapten-sensitive B cells.

Animals↗
PubMed1972

A receptor for antibody on B lymphocytes. I. Method of detection and functional significance.

Evidence is presented for the existence on all B lymphocytes, but not on T lymphocytes, of a membrane-associated receptor for antibody. The receptor was detected by a radioautographic technique in which lymphoid cells were incubated with antibody followed by the corresponding radioiodinated antigen. The ease with which antibody eluted during washing indicated that the bond between antibody and cell was weak. The formation of an antibody-antigen complex on the cell surface, however, stabilized the bond and permitted accurate quantitation of cells with adherent antibody. The ability of several combinations of antibody and antigen to adhere to the cells demonstrated the nonspecificity of the phenomenon and emphasized the need for care in interpretation of antigen-binding studies particularly when immune cells are being used. The identity of antibody-binding lymphocytes was established by two different approaches. In the first, mouse lymphocyte populations greatly enriched for either T cells or B cells were examined. Their T cell content was assessed by means of well-established markers such as the theta C3H isoantigen. When this was compared with the number of antibody-binding cells, an inverse relationship was obtained in each instance; thus almost all thoracic duct cells from athymic mice labeled with an immune complex although none were theta positive. The striking reduction in antibody-binding cells observed in bursectomized chickens provided a second and independent line of evidence suggesting that B cells, not T cells, bind antibody. The ability of B cells from primed animals to bind antibody in vivo made it important to test whether this phenomenon was related to the carriage of immunological memory. No correlation was, however, found between membrane-bound antibody and memory. It was proposed that the existence of a receptor of this kind may provide a rational explanation for antibody-dependent killing of target cells and may prove of importance in antigen concentration particularly during the secondary response.

Animals↗
PubMed1972

Regulation of lambda rex expression after infection of Escherichia coli K by lambda bacteriophage.

The ability of Escherichia coli K to support bacteriophage T4rII replication starts to decline at 3 to 6 min after infection by lambda. This inhibition appears to depend on expression of the lambdarex(+) gene, since little inhibition was observed following infection by a lambdarex mutant or by a hybrid bacteriophage lambdai(434) which lacks a functional rex gene. For promotion of the synthesis of rex product, cII(+) and N(+) genes are required and can act trans, whereas cY(+), also required, must be cis to a rex(+) gene. These genes presumably play a role in the transcription of the cI-rex operon because they are also known to be required for repressor (cI product) synthesis. Functional cIII, O, P genes are not necessary for ample rex product synthesis. We also observed full rex expression after infection by lambdasuscI mutants, suggesting that rex and repressor are separate gene products and that repressor is not required for inhibition of T4rII replication. We also report experiments with a rex mutant that is not leaky when in a lysogen but is sufficiently leaky shortly after infection to cause inhibition of T4rII replication.

Chromosome Mapping↗
PubMed1971

Cell-to-cell interaction in the immune response. VII. Requirement for differentiation of thymus-derived cells.

Experiments were designed to test the possibility that thymus-derived (T) cells cooperate with nonthymus derived (B) cells in antibody responses by acting as passive carriers of antigen. Thoracic duct lymphocytes (TDL) from fowl gammaG-tolerant mice were incubated in vitro with fowl anti-mouse lymphocyte globulin (FALG), which was shown not to be immunosuppressive in mice. On transfer into adult thymectomized, irradiated, and marrow protected (TxBM) hosts together with a control antigen, horse RBC, a response to horse RBC but not to fowl gammaG was obtained. By contrast, TxBM recipients of nontolerant, FALG-coated TDL responded to both antigens and the antibody-forming cells were shown to be derived from the host, not from the injected TDL. These findings suggested that, under the conditions of the experiment, triggering of unprimed B cells in the spleens of TxBM hosts was not achieved with antigen-coated tolerant lymphocytes. Another model utilized the ability of B cells to bind antibody-antigen complexes. Spleen cells from TxBM mice, incubated in vitro with anti-fowl gammaG-fowl gammaG.NIP, were injected with or without normal TDL (a source of T cells) into irradiated hosts. Only mice given both cell types could produce an anti-NIP antibody response. In a further experiment, spleen cells from HGG.NIP-primed mice were injected together with NIP-coated B cells (prepared as above) into irradiated hosts. A substantial anti-NIP antibody response occurred. If, however, the T cells in the spleens of HGG.NIP-primed mice were eliminated by treatment with anti-theta serum and complement, the NIP response was abolished. It was concluded that antigen-coated B cells could not substitute for T cells either in the primary or secondary response. Treatment of T cells from unprimed or primed mice with mitomycin C impaired their capacity to collaborate with B cells on transfer into irradiated hosts. Taken together these findings suggest that before collaboration can take place T cells must be activated by antigen to differentiate and in so doing may produce some factor essential for triggering of B cells.

Animals↗
PubMed1971

Cell-to-cell interaction in the immune response. VI. Contribution of thymus-derived cells and antibody-forming cell precursors to immunological memory.

Collaboration between thymus-derived lymphocytes and nonthymus-derived antibody-forming cell precursors occurs in the primary antibody response of mice to heterologous erythrocytes and serum proteins. The purpose of the experiments reported here was to determine whether collaboration took place in an adoptive secondary antibody response. A chimeric population of lymphocytes was produced by reconstituting neonatally thymectomized CBA mice soon after birth with (CBA x C57BL)F(1) thymus lymphocytes. These mice could be effectively primed to fowl immunoglobulin G (FgammaG) and their thoracic duct lymphocytes adoptively transferred memory responses to irradiated mice. The activity of these cells was impaired markedly by preincubation with CBA anti-C57BL serum and to a lesser extent by anti-theta-serum. Reversal of this deficiency was obtained by adding T cells in the form of thoracic duct cells from normal CBA mice. Cells from FgammaG-primed mice were at least 10 times as effective as cells from normal mice or from CBA mice primed to horse erythrocytes. These results were considered to support the concept that memory resides in the T cell population and that collaboration between T and B cells is necessary for an optimal secondary antibody response. Poor antibody responses were obtained in irradiated mice given mixtures of thoracic duct cells from primed mice and of B cells from unprimed mice (in the form of spleen or thoracic duct cells from thymectomized donors). In contrast to the situation with T cells, the deficiency in the B cell population could not be reversed by adding B cells from unprimed mice. It was considered that memory resides in B cells as well as in T cells and that priming probably entails a change in the B cell population which is fundamentally different from that produced in the T cell population.

Animals↗