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Biomedical subjects

B G Carter

Publications and source records attributed to B G Carter.

At least 37 records · Page 2Linked to original sources
PubMed1991

Nuclear magnetic resonance studies of the snake toxin echistatin. 1H resonance assignments and secondary structure.

The 1H-NMR spectrum of the snake toxin echistatin has been assigned using homonuclear two-dimensional methods. Consideration of the NOE patterns, coupling constants and putative hydrogen bonds enabled two regular features of secondary structure to be deduced: a beta-sheet/turn between residues 8 and 13 and a small anti-parallel beta-sheet and bulge linking residues 16-20 with residues 30-33. The recognition region of the protein containing the residues RGD lies in a loop joining the two strands of the beta-sheet. The beta-bulge and the loop containing the RGD sequence undergo pH-dependent conformational interconversion, modulated by the side chain of Asp29.

Amino Acid Sequence↗
PubMed1987

Induction of in vivo helper activity for murine antibody responses by macrophages pulsed with ovalbumin-monomethoxypolyethylene glycol (OA-mPEG) conjugates.

Conjugates of protein antigens with an optimal number of monomethoxypolyethylene glycol (mPEG) chains of an appropriate molecular weight had been shown to suppress murine IgE responses to the unmodified antigen. To investigate the possibility that the tolerogenic capacity of these mPEG conjugates is attributable to a defect in macrophage (M phi) presentation of their antigenic determinants, the activity of ovalbumin (OA)-mPEG conjugates when pulsed onto mouse peritoneal adherent cells (M phi) was compared in this study with their activity in solution. Surprisingly, in contrast to the suppressogenic capacity of mPEG conjugates in solution, the OA-mPEG pulsed M phi appeared to exert a helper effect when injected intraperitoneally (ip), i.e., after subsequent immunization with dinitrophenylated OA (DNP3-OA) in Al(OH)3, the mice showed accelerated IgE and IgG1 antibody responses to OA and DNP. However, when M phi were exposed to limiting concentrations of OA or OA-mPEG, markedly higher concentrations of OA-mPEG were required to yield pulsed M phi, exerting a significant helper effect. It was concluded that although M phi were capable of presenting the OA determinants of OA-mPEG conjugates to helper T (Th) cells, the preparations of modified antigen were presented less effectively than native OA.

Animals↗
PubMed1984

Studies on the mechanism of suppression of experimental allergic encephalomyelitis induced by myelin basic protein-cell conjugates.

The mechanism of suppression of experimental allergic encephalomyelitis (EAE) induced in Lewis rats by pretreatment with myelin basic protein (MBP) coupled to syngeneic spleen leukocytes (SL) was examined. Studies on the kinetics of the tolerance induction showed that pretreatment with MBP-SL suppressed EAE if given 7 but not 3 days before the disease-inducing injection of MBP in Freund's complete adjuvant. Treatment with cyclophosphamide 48 hr before administration of MBP-SL completely abolished the suppression of EAE. Transfer of lymph node and spleen cells from MBP-syngeneic erythrocyte conjugate (MBP-RBC) but not MBP-SL-pretreated rats resulted in suppression of disease in recipients subsequently given a disease-inducing injection of MBP. Administration of MBP coupled to SL from the histocompatible rat strain F344 resulted in suppression of the MBP-induced proliferative response of spleen cells from Lewis rats which had been given a disease-inducing injection of MBP. Taken together these results are consistent with the suppression of EAE induced by MBP-SL being mediated by suppressor T cells.

Animals↗
PubMed1984

Suppression of the anti-trimellityl (TM) IgE response in mice by conjugates of TM with polyvinyl alcohol.

The i.p. injection of 1 microgram of TM3-OA or TM9-OA with 1 mg of A1(OH)3 into B6D2F1 mice elicited the production of antibodies of the IgE and other classes to the trimellityl (TM) group and ovalbumin (OA). The induction of anti-TM antibodies belonging to the IgE and other immunoglobulin classes was specifically suppressed by the administration of tolerogenic conjugates prepared by coupling trimellitic anhydride (TMA) to the hydrophilic non-immunogenic polymer, polyvinyl alcohol (PVA), prior to immunization with TM-OA conjugates. More importantly, established anti-TM responses were also suppressed by these TM-PVA conjugates. By contrast, however, treatment with TM-PVA conjugates did not affect either the primary or the established anti-OA antibody response. The tolerogenic effects of the PVA conjugates were dose-dependent and appeared also to be dependent on the epitope density. Treatment with these conjugates also prevented immunized mice from showing any symptoms of systemic anaphylaxis on challenge with polyvalent TM-protein conjugates. These findings indicate that these conjugates may have the potential of useful therapeutic agents for the treatment of TMA-induced pulmonary hypersensitivity diseases.

Anaphylaxis↗
PubMed1983

The suppression of experimental allergic encephalomyelitis in Lewis rats by treatment with myelin basic protein-cell conjugates.

Pretreatment of Lewis rats with guinea pig (GP) myelin basic protein (MBP) coupled to syngeneic spleen leukocytes (SL) suppressed the subsequent induction of experimental allegic encephalomyelitis (EAE) with GP-MBP in Freund's complete adjuvant. The degree of suppression correlated positively with the amount of antigen coupled to the SL. GP-MBP coupled to syngeneic red blood cells (RBC) also resulted in suppression of EAE and the extent of the suppression was related to the dose of cells. These regimens of pretreatment also resulted in a decrease in the in vitro lymphocyte proliferative response to GP-MBP and in the extent of perivascular cuffing in the spinal cord. No decrease in the anti-MBP antibody response was detected in rats pretreated with either GP-MBP-SL or GP-MBP-RBC conjugates. Transfer of lymph node cells from rats pretreated with GP-MBP-RBC resulted in a decrease in disease severity in recipients. It is concluded that prior administration of MBP-cell conjugates is an effective way of suppressing the symptoms of EAE.

Animals↗
PubMed1981

Regulation of the IgE antibody response in mice. II. Radioresistance of established IgE antibody production.

The protracted IgE anti-ovalbumin (OA) response given by BDF1 mice was studied using an adoptive transfer model. Spleen cells taken from immunized BDF1 mice can produce IgE antibody in irradiated recipients without further overt antigenic challenge. Depletion of macrophages in active spleen cell suspensions did not diminish the capacity of the remaining cells to give an adoptive response. Evidently the cells subserving the adoptive response are not fully developed in donor mice until 4 weeks after immunization, since spleen cells removed at shorter intervals after immunization gave either no or weak adoptive responses. The production of IgE antibody in irradiated recipient mice is prevented if transferred B or T lymphocytes are treated in vitro with either gamma irradiation or mitomycin C, suggesting proliferation of both B and T lymphocytes is essential for the adoptive response to develop. However, the requirement for proliferation is only transient, since one IgE antibody production reached a steady state in the adoptive recipients, it manifested extreme resistance to high dose irradiation. Whole body irradiation of 800 and 1000 rad was without effect on sustained IgE production. This latter observation was valid for both intact mice which were irradiated 8 weeks after immunization and also for irradiated adoptively immunized mice. It is suggested that the IgE anti-OA antibody measured in serum of BDF1 mice several months after immunization with 1 microgram OA and 1 mg Al(OH)3 is the product of long-lived antibody secreting cells.

Animals↗
PubMed1980

The enumeration of mouse IgE-secreting cells using plaque-forming cell assays.

With the aid of a specific rabbit antibody preparation to purified monoclonal murine IgE, two plaque-forming cell (PFC) assays have been developed for the detection and enumeration of mouse IgE-secreting cells. The first assay, utilizing protein A-coated sheep red cells (protein A-SRC), detected antibody-secreting cells on the basis of the class of the secreted Ig irrespective of antigen specificity. With this assay, 30% of the class of the viable cells of two distinct IgE-secreting hybridoma cell lines were scored as PFC. Under these conditions, plaques were not obtained with IgG1 or IgG2a-secreting hybridoma cells. The second PFC assay, which utilized SRC coated with ovalbumin (OA-SRC), enumerated cells secreting anti-OA IgE antibodies. Similar kinetic patterns were observed for the cellular (IgE PFC/spleen) and humoral (IgE serum levels) responses of (C57BL/6 x DBA/2)F1 mice following immunization with 10 micrograms of OA adsorbed to 1 mg of A1(OH)3. Thus, it is concluded that the reverse plaque assay detecting all IgE-secreting cells, as well as the antigen-specific IgE PFC assay, can be used for the quantitation of IgE responses at the cellular level.

Animals↗
PubMed1980

Immunogenicity of ovalbumin-Ficoll conjugates with particular reference to IgE antibody production.

Conjugates of ovalbumin with Ficoll (OA-Ficoll) were injected into BDF1 mice to establish their immunogenicity and specifically to determine their effect on the IgE anti-OA response. Mice injected with OA-Ficoll responded by producing IgG anti-OA, but not IgE anti-OA. Furthermore, soluble OA-Ficoll injected subsequent to native OA in the form optimal to elicit IgE antibody in fact suppressed the production of IgE anti-OA. Spleen cells from OA-Ficoll-injected mice when injected into normal mice suppressed the subsequent IgE response to OA. OA-Ficoll reacted only weakly with antibody to native OA and had no effect on the IgE antibody response to the unrelated antigen alpha-amylase.

Animals↗
PubMed1979

The enumeration of rat IgE-secreting cells using a reverse plaque-forming cell assay.

A reverse hemolytic plaque assay utilizing protein A-coated sheep red cells and a specific rabbit anti-rat IgE preparation has been adapted for the enumeration of rat IgE-secreting cells derived from the IR-162 rat plasmacytoma and from rats infected with Nippostrongylus brasiliensis. Under optimal conditions, approximately 10-15% of the viable plasmacytoma cells were scored as plaque-forming cells. In rats infected with 5000 Nippostrongylus brasiliensis larvae, a maximum of 2 x 10(6) IgE-secreting cells were found in the mesenteric lymph nodes, and no IgE plaque-forming cells in their spleens. The kinetics of the mesenteric lymph node plaque-forming cell responses closely coincided with total serum IgE levels, with maximum responses occurring 15-16 days after infection. There was a high degree of correlation between the mesenteric lymph node IgE plaque-forming cell responses and total serum IgE levels of individuals rats. It was concluded that the IgE-secreting cells in the mesenteric lymph nodes contributed, in a large way, to the elevated levels of IgE found in the circulation of these rats.

Animals↗
PubMed1977

Mast cell numbers and passive cutaneous anaphylaxis in irradiated mice.

IgE antibody levels in irradiated mice immunized with primed spleen cells are significantly higher than those measured in actively immunized intact mice. The possible role of mast cells in this elevated IgE response was assessed by the enumeration of mast cells and by determining their capacity to give rise to passive cutaneous anaphylactic (PCA) reactions in the skin of irradiated mice. The number of mast cells was found to be not significantly depleted over a period of 11 days by the irradiation doses used. Furthermore, the capacity of these mast cells to give PCA reactions was unimpaired. Radiation effects on mast cells in adoptively immunized mice therefore do not contribute to the high IgE levels observed in such animals.

Animals↗
PubMed1977

Murine and rat IgE: relationships in terms of binding to cell receptors and to antibodies against rat epsilon chain.

The similarity between murine and rat IgE was examined in terms of their fixation to target cells and interaction with monospecific antibodies to rat epsilon-chain (anti-epsilon). Purified rat monoclonal IgE (IgEr) was found to block the fixation of murine reagin (IgEm) to mouse and rat skin and to rat basophilic leukemia (RBL) cells. The capacities of mouse reaginic serum (MRS), rat reaginic serum, and IgEr to inhibit the binding of radiolabeled 125I-IgEr to RBL cells were shown to be similar. These results suggest that the binding of IgE of either species occurs on the same or on adjacent receptor sites of mast cells and RBL cells. The antigenic cross-reactivity between IgEm and IgEr was established by depletion of the reaginic activity from MRS by treatment of MRS with anti-epsilon. The reaginic activity of MRS could be recovered by the addition of IgEr to anti-epsilon:IgEm complexes. From these findings it may be inferred that i) IgEm and IgEr share some antigenic determinants and ii) the regions of the immunoglobulins responsible for fixation to receptors on mast cells and RBL cells are identical or similar.

Animals↗
PubMed1976

Age-dependent changes in sensitivity to antigen: its relationship with the antigen processing system.

The relationship between the antigen processing or accessory cell system and the maturation, with age, of antibody-producing capability was investigated in the mouse. This was done by analyzing the antibody responses given by immunocompetent cells from neonatal and from adult male mice in an identical antigen-processing system environment. Specifically, 4 x 10(7) normal spleen cells from either 12-day-old or adult mice were challenged with varying numbers of SRC in adult irradiated syngeneic recipients. The subsequent IgM and IgG2a PFC responses for both age groups were analyzed in terms of antigen dose-antibody response curves. Analyses of these curves indicate: 1) the dose of antigen required to elicit the optimal antibody response is essentially identical for both age groups and (2) the bandwidths obtained using neonatal donors are significantly narrower than those obtained with adult donors. Whereas, intact neonatal and adult mice exhibit differences in antigen optimal doses, these differences are eliminated when the immunocompetent cells are stimulated in the presence of identical antigen-processing systems. It is concluded that maturation of the antigen-processing system results in an increased sensitivity to antigen. Examination of the bandwidths of the dose-response curves revealed that immunocompetent cells from the young mice, either in situ or in adult irradiated recipients exhibited narrower bandwidths than did their adult counter parts. Thus, the increase in bandwidth observed with age is attributed to changes in the population of immunocompetent cells--perhaps a reflection of increased diversity, and is not due to the antigen-processing system. Quantitation of the antigen-processing function using accessory cell-depleted and partially restored mice indicated that when IgG responses were compared a higher frequency of accessory cells was demonstrated in adultspleens as opposed to neonatal spleens.

Aging↗