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B Merchant

Publications and source records attributed to B Merchant.

At least 37 records · Page 2Linked to original sources
PubMed1983

Nuclear antigen detected in hepatoma cell lines containing integrated hepatitis B virus DNA.

We identified, by anticomplement immunofluorescence, a nuclear antigen (hepatitis B virus-associated nuclear antigen [HBNA]) in two human hepatoma cell lines containing integrated hepatitis B virus DNA but not in three hepatoma cell lines lacking it. The antigen resembled neoantigens associated with the oncogenesis of certain papovaviruses, adenoviruses, and herpesviruses. Antibody to the antigen (anti-HBNA) was found in 7.3% of hepatitis B surface antigen-positive sera from patients with hepatocellular carcinoma but not in surface antigen-negative sera. The staining of HBNA was characterized by two patterns, reticular nuclear fluorescence and nucleolar fluorescence. The expression of HBNA did not parallel the production of extracellular hepatitis B surface antigen. Treatment of cells with proteinase K, RNase, DNase, or cycloheximide significantly diminished the staining of HBNA.

Animals↗
PubMed1982

Functional antigen binding by the defective B cells of CBA/N mice.

CBA/N mice have an X-linked B cell defect which prevents them from responding to nonmitogenic thymic independent (TI-2) antigens such as dinitrophenylated DNP-Ficoll (1,2). The F1 male progeny of CBA/N female mice express the same defect. Spleen cell suspensions from such defective mice (CBA/N X C3H/HeN F1 males) could not respond to DNP-Ficoll following in vitro immunization and subsequent transfer into irradiated, syngeneic, F1 male recipients as expected. In contrast, normal CBA/N X C3H/HeN F1 female spleen cells could respond and effect a "rescue"; they mounted strong plaque-forming cell responses 7 days after in vitro exposure to DNP-Ficoll and subsequent transfer into irradiated F1 male recipients. Defective F1 male spleen cells, however, could bind significant quantities of 125I-DNP-Ficoll after in vitro exposure. Extensive washing of these spleen cells could not reverse this binding. Such DNP-Ficoll-exposed and washed F1 male spleen cells could, after transfer, aid normal untreated F1 female cells in their rescue function. The defective F1 male spleen cells could convey immunogenic quantities of DNP-Ficoll to the "rescuing" F1 female cells. Mitomycin treatment of F1 male cells did not interfere with their conveyor function. Goat anti-mouse mu serum impeded the passive antigen conveyor function of defective F1 male cells as did prior exposure to high concentrations of free DNP hapten. Our data support the view that the B cell defect of CBA/N X C3H/HeN F1 male mice does not relate to antigen binding, but rather to an inability to be effectively triggered by certain cell-bound polymeric antigens.

Animals↗
PubMed1982

Murine in vivo carrier-specific IgG memory to DNP-Ficoll: variation among inbred strains.

BALB/cAnN and C3H/HeN mice were primed and challenged with DNP-Ficoll, a thymic independent (TI-2) antigen. They developed significant carrier-specific IgG memory responses: DNP-pneumococcal polysaccharide or DNP-hemocyanin challenge did not elicit memory responses. NZB/B1NJ mice failed to develop this memory response. Genetically controlled events apparently regulate the phenotypic expression of this effect.

Animals↗
PubMed1982

Characterization of immunogenic properties of haptenated liposomal model membranes in mice. VI. Response in B-cell-defective CBA/N mice.

This paper describes the immunogenicity of haptenated liposomes in a number of inbred mouse strains. The tripeptide-enlarged hapten, dinitrophenyl-beta-alanylglycylglycine (J) was conjugated to phosphatidyl-ethanolamine (PE) and incorporated into liposomal model membranes. The magnitude of the response to this thymus-independent (TI) antigen was measured by the appearance of direct plaque-forming cells in the spleen. The response to J-PE-liposomes in the different mouse strains varied sufficiently to suggest the existence of high, intermediate and low responders. On the basis of this preliminary survey no correlation was found between the immunogenicity of J-PE-liposomes and H-2 haplotype. The positive responses obtained in CBA/N mice appear to classify J-PE-liposomes as a TI-1 antigen. Further characterization of this response was carried out in CBA/N X C3H/HeN F1 male and female mice. The magnitude of the response was dependent on dose and epitope density of the hapten-PE derivative. The response could be blocked in F1 male mice by prior immunization with the TI-2 antigen J53-Ficoll. This suggests that J-PE-liposomes have no intrinsic mitogenic properties. Non-haptenated liposomes could not be used as an adjuvant to restore the response in F1 male mice to haptenated Ficoll (TI-2) preparations.

Animals↗
PubMed1982

Characterization of immunogenic properties of haptenated liposomal model membranes in mice. VII. Synergistic responses to haptenated liposomes and haptenated thymus-dependent antigens in CBA/N mice.

CBA/N mice have an X-linked B-cell defect which prevents them from responding to non-mitogenic thymus-independent (TI-2) antigens such as haptenated Ficoll. The CBA/N mice do, however, respond to another group of thymus-independent (TI-1) antigens among which are haptenated liposomes. The F1 male progeny of CBA/N female mice express the same characteristics. Hapten-specific plaque-forming cell (PFC) responses to haptenated proteins (thymus-dependent, TD, antigens) by CBA/N mice and CBA/N x C3H/HeN F1 male mice can be blocked by concomitant exposure to TI-2 antigens bearing the same hapten. Simultaneous exposure to haptenated liposomes (TI-1 antigen) and TD antigens, however, results in a synergistic response to the hapten if the antigens share common epitopes. The tripeptide-enlarged hapten dinitrophenyl-beta-alanylglycylglycine (J), conjugated to phosphatidyl-ethanolamine (PE) and incorporated into liposomal model membranes, was used throughout the experiments. In F1 male mice the moderate responses to TD antigens could be restored to values equivalent to those seen in F1 female mice. This adjuvant effect of haptenated liposomes is hapten-specific, time-dependent, and restricted to certain structural forms of the liposomes.

Animals↗
PubMed1981

An assay for virus-specific help for B cells.

Spleen cells from mice immunized with vaccinia or influenza viruses were mixed with spleen cells from mice immunized by dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH) and transferred into irradiated syngeneic recipient mice which were subsequently restimulated with trinitrophyenylates (TNP) or unmodified viruses. One week later, spleens were removed and assayed for indirect anti-DNP plaque-forming cells (PFC). When spleen cells from both influenza and vaccinia primed mice were restimulated with the haptenated form of the virus used for the initial immunization there was an enhanced PFC response compared to that seen with spleen cells from unprimed mice.

Animals↗
PubMed1981

Murine immune memory to a TI-2 antigen, DNP-Ficoll: carrier-specificity, genetic enhancement and phenotypic dominant inheritance.

C3H/HeN x NZB/BIN F1 mice were primed and challenged with DNP-Ficoll, a thymic independent (TI-2) antigen. They developed strong IgM and IgG carrier-specific memory responses: DNP-pneumococcal polysaccharide or DNP-haemocyanin challenge did not elicit memory responses. The IgG response component appeared to be inherited dominantly from the C3H/HeN parent. The IgM component resulted from genetic enhancement.

Animals↗
PubMed1981

Increased multiclonal antibody-forming cell activity in the peripheral blood of patients with SLE.

21 patients with criteria for systemic lupus erythematosus (SLE) and 12 normal controls were studied for their spontaneous circulating IgM and IgG plaque-forming cells (PFCs) reactive against sheep erythrocytes (SRBC) and against a panel of five haptens. Quantitatively defined active and mildly active SLE patients had significantly elevated IgM- and IgG-producing PFCs in their peripheral blood reactive with the panel of five chemically defined haptens. Those patients having inactive SLE also showed increased circulating IgM PFCs. Significant elevations in circulating hapten-reactive PFCs were found to correlate progressively with disease activity in the inactive, mildly active, and active SLE patient groups. Circulating IgM- and IgG-secreting PFC reactive against SRBC were both significantly elevated only in those patients with active SLE. The data support the concept that SLE patients have a generalized increase in B cell activity against a broad repertoire of determinants, even those ostensibly unrelated to natural tissue antigens.

Animals↗
PubMed1981

Lack of susceptibility of congenitally athymic nude mice to human non-A, non-B hepatitis.

Nude mice were inoculated intravenously with chimpanzee serum containing a human non-A, non-b hepatitis agent. Control groups of nude mice were inoculated with normal saline or normal chimpanzee serum. During 77 days of observation, evidence of non-A, non-B hepatitis was not detected. Serum alanine aminotransferase levels remained within normal limits, and normal liver histology was seen in serially killed mice.

Alanine Transaminase↗
PubMed1981

Immune memory to a nonmitogenic, thymic independent antigen in mice: variation among inbred strains and possible relationship to oncogenesis.

Immune memory to DNP-Ficoll, a nonmitogenic, thymic-independent (TI-2) antigen, was demonstrated in several inbred strains of mice. Direct and indirect splenic plaque-forming cell responses were measured in mice given a secondary challenge with DNP-Ficoll and in appropriate control mice. Strong IgM memory, but no IgG memory, was observed in SJL/J, AKR/J, and C58/J mice. C57L/J mice gave both a strong IgM memory response and a relatively strong IgG memory response to DNP-Ficoll. C57BL/6N, C57BR/cdJ, and A/HeJ mice were unable to mount significant IgM or IgG memory responses to this antigen under an identical immunization schedule. These results are indicative of marked genetic variation in mice in the capacity for B memory cell expression. They also identify a provocative but unexplained association between positive IgM memory responses to DNP-Ficoll in SJL/J, AKR/J, and C58/J mice and a propensity to develop lymphoreticular neoplasia. This association is observed when there is no clear evidence for IgG memory.

Animals↗
PubMed1980

Hapten-specific blockade of CBA/N x C3H/HeN F1 B cell responses in a cell transfer system.

CBA/N mice harbor an X-linked B cell defect which is transmitted by CBA/N female mice to their hybrid male progeny. Hapten-specific plaque-forming cell (PFC) responses to haptenated proteins by B cell-defective CBA/N mice and CBA/N X C3H/HeN F1 male mice can be blockaded by concomitant exposure to polysaccharide agents bearing the same hapten. Various experimental approaches were explored in an attempt to study this phenomenon in a syngeneic cell transfer system. Unprimed donor spleen cells were unable to mount adequate PFC responses to dinitrophenylated-hemocyanin (DNP-KLH) in irradiated, syngeneic recipients. DNP-KLH-primed donor spleen cells produced strong PFC responses after challenge in irradiated recipients, and these secondary responses were subject to hapten-specific blockade by DNP-derivatized polysaccharide agents. Both direct and indirect PFC responses could be blocked. DNP conjugated to bovine serum albumin also produced hapten-specific blockade in this cell transfer system. Under some cell transfer conditions normal CBA/N X C3H/HeN F1 female spleen cells were just as susceptible to hapten-specific blockade as defective F1 male spleen cells.

Animals↗
PubMed1980

The specificity of antibody formation in mice following immunization with hapten-carrier complexes mixed with the surfactant, dimethyl dioctadecyl ammonium bromide.

Mice were immunized i.c. with various enlarged haptens conjugated to bovine serum albumin and mixed with the cationic, surface active lipid, dimethyl dioctadecyl ammonium bromide (DDA). This immunization generated delayed-type hypersensitivity (DH) in these mice without detectable concomitant antibody formation. The DH was measured as footpad swelling. However, both direct and indirect hapten-specific PFC could be detected in peripheral lymph nodes and in spleens 4 days after a challenge injection. Although the adjuvant, DDA, promotes a strong cross-reactivity in DH between heterologous hapten-carrier complexes, the antibody-forming cells produced 4 days after challenge showed relatively high specificity for the immunizing hapten. This indicates only weak cross-reactivity at the antibody-forming cell level co-existent with high cross-reactivity in DH expression to the same hapten-carrier complexes. These results are consistent with the possibility that B-cell receptors may be capable of expressing a greater degree of hapten specificity than T-cell receptors. It is tentatively concluded that Thelper cells participating in antibody formation may represent a subset of the T cells involved in DH.

Animals↗
PubMed1980

Variable expression of delayed hypersensitivity in different mouse strains using dimethyl dioctadecyl ammonium bromide as an adjuvant.

Delayed-type hypersensitivity measured as footpad swelling was studied in large number of inbred mouse strains. A conjugate of bovine serum albumin (BSA) with the small 2,4-dinitrophenyl (DNP) hapten served to generate strong reactions, specific for the DNP group. Delayed hypersensitivity was produced with the DNP-BSA complex mixed with the cationic, surface active lipid, dimethyl dioctadecyl ammonium bromide (DDA). Great variation was observed in delayed hypersensitivity among different mouse strains. For convenience, the mice were classified into five groups, notably: non-, low, moderate, good and high responders. The highest responding animals were BALB/cJ mice, the lowest were P/JN and outbred nu/nu mice. No correlation was observed between H-2 type and the intensity of the elicited reactions.

Adjuvants, Immunologic↗
PubMed1979

Carrier-specific immune memory to a thymus-independent antigen in congenitally athymic mice.

Immune memory to the DNP epitope coupled to a nonmitogenic thymus-independent carrier, Ficoll, was demonstrated in congenitally athymic outbred Swiss mice. Strong IgM and modest IgG components of this memory were detected. Moreover, this memory was carrier specific since it was elicitable only when DNP-Ficoll primed mice were challenged with DNP-Ficoll and not when similarly primed mice were challenged with DNP coupled to pneumococcal polysaccharide or to keyhole limpet hemocyanin. Ficoll primed mice also demonstrated a memory response when challenged with DNP-Ficoll. These findings indicate that a non-T cell, presumably a B cell, is capable of recognizing the carrier epitopes of this thymus-independent hapten-carrier complex. Unlike their athymic counterparts, euthymic mice of the same genetic background failed to demonstrate the IgM component of this memory, but they did demonstrate modest carrier-specific IgG memory. These results strongly suggest that suppressor T cells are either directly or indirectly important in regulating the IgM memory response of these mice to DNP-Ficoll. Indirect regulation could possibly occur via an antibody-mediated specific immune suppression mechanism.

Animals↗
PubMed1978

Cellular and molecular requirements for X-linked, hapten-specific B-cell blockade in CBA/N mice.

CBA/N mice, a mutant CBA subline, harbor an X-linked B-cell defect which prevents them from mounting immune responses to certain thymic-independent antigens such as pneumococcal polysaccharides and haptenated-Ficoll derivatives. These mice and the hybrid male progeny of CBA/N females are also exquisitely sensitive to a hapten-specific blockade of their otherwise adequate immune responses to thymic-dependent antigens such as N-2,4-dinitrophenylated-hemocyanin (DNP-KLH). As little as 10 ng of a DNP-Ficoll conjugate given 2 h before immunization with a 5,000-fold greater dosage of DNP-KLH, virtually abolishes the 4th-day direct plaque-forming cell (PFC) response specific for DNP. Responding hybrid (CBA/N x C3H/HeN) female mice are resistant to such blockade even at DNP-Ficoll dosages increased by three orders of magnitude. The DNP hapten and Ficoll must be chemically joined for this blocking effect to occur, and increasing the hapten derivatization of Ficoll increases its blockade-invoking capacity. Significant blockade can be produced by administering DNP-Ficoll as early as 4 days before or as late as 4 h after immunization with DNP-KLH. All currently available data point to the defective B cell as the target of this hapten-polysaccharide-mediated blockade. Mice bearing B memory cells, however, are refractory to such blockade. In addition, DNP-Ficoll injections which cause virtually total blockade of 4th-day primary direct PFC responses to DNP-KLH have little or no effect on the development of DNP-reactive B-cell memory measured at either 8 or 30 days. These findings suggest very different blockade susceptibilities for B cells or their precursors at various stages of differentiative development. Our findings also lead to the formulation of testable hypotheses regarding the mechanism of this selective B-cell blockade phenomenon.

Animals↗