bluuebunny/crossref_metadata_2025_split huggingface dataset:
The immune response to human type III and type V (AB2) collagen: antigenic determinants and genetic control in mice
Authors: Kemp John D. , Madri Joseph A. 
Published: February 2007

AbstractThe genetic influences on the specific IgG antibody response to helical antigenic determinants of native soluble type III and V (AB2) human collagen have been studied in mice. H‐2‐linked Ir genes have been detected for each of these collagens, as have background effects. The alleles controlling high antibody responses can be distinguished from those previously described for bovine collagen type I and type I propeptide. Apparent two‐gene complementation in the response to type V (AB2) may indicate that this antigen will be a useful probe in further studies of the complex nature of antigen presentation for T cell recognition. The present studies may facilitate the production of specific, high‐affinity monoclonal antibodies for the human collagens which, in turn, will facilitate the study of connective tissue biology and pathology.
Demonstration of T lymphocytotoxic human fetal antibody against maternal T and concanavalin A‐inducible adult T cells in cord IgM
Authors: Miyagawa Yukiaki , Komiyama Atsushi , Akabane Taro 
Published: February 2007

AbstractTo clarify reasons of the constant presence of IgM in human cord blood, some functions of this immunoglobulin class were analyzed. Cord IgM was collected from cord blood, and the cord IgM F(ab')2 fragment was obtained by trypsin cleavage. Maternal T and adult T cells were stained with fluorescein isothiocyanate (FITC)‐conjugated cord IgM and FITC‐cord F(ab')2μ. Cord IgM, unlike cord IgG, bound to about one‐third of maternal and one‐fourth of adult T cells and killed them, but it killed only a small proportion of the B cells. However, adult F(ab')2μ did not kill these cells. Cord T cells were not killed by cord IgM. Thus, it is apparent that cord IgM contains cytotoxic antibodies against maternal and adult T cells. T lymphocy‐totoxic fetal antibody (TLFA) may be largely responsible for the absence of maternal T cells in cord blood. The percentage of [3H]thymidine incorporation into concanavalin A‐induced adult mononuclear cells treated with cord IgM containing TLFA was 56.0 ± 17.9% (p<0.01) and that into pokeweed mitogen‐induced cells treated with the cord IgM preparation was 100.3 ± 17.8% (p>0.05) indicating the possibility that TLFA might kill a certain subset(s) of T cells.
Genetic control of T helper cell function in the clawed toad Xenopus laevis
Authors: Bernard Claude C. A. , Bordmann Gérard , Blomberg Bonnie , Pasquier Louis Du 
Published: February 2007

AbstractThe genetic control of the collaboration between Xenopus T and B cells has been analyzed in vitro using cells from five strains of major histocompatibility complex‐defined Xenopus.When carrier (fowl gamma‐globulin)‐primed T cells and hapten (dinitrophenylated keyhole limpet hemocyanin)‐primed B cells differed by minor histocompatiblity antigens or by only one haplotype of the major histocompatibility complex, the collaboration was efficient in the sense that large numbers of plaques, low‐molecular weight antibodies and high‐affinity IgM antibodies could be recorded in the cultures challenged with dinitrophenylated fowl gamma‐globulin. However, when T and B cells differed at both alleles of the major histocompatibility complex, lower numbers of plaques were obtained, no low‐molecular weight anti‐hapten antibodies could be detected, and the IgM antibodies that were sometimes synthesized were of low affinity. This suggests that the major histocompatibility complex, or a gene linked with it, affects the collaboration between Xenopus T and B cells in a way perhaps similar to that described in mammals.
Inhibition of secondary IgG responses by N‐acetyl‐D‐galactosamine
Authors: Tomaska Luba D. , Parish Christopher R. 
Published: February 2007

AbstractA range of monosaccharides were tested for their ability to inhibit a variety of in vitro immune responses. The most striking specific inhibition was produced by N‐acetyl‐D‐galactosamine (GalNAc). This sugar strongly inhibited the secondary IgG antibody response to two different hapten‐carrier systems, but had no effect on primary and secondary IgM responses, generation of cytotoxic T cells to alloantigens and mixed lymphocyte reactions. By exposing secondary antibody cultures to GalNAc for varying periods of time, it was observed that GalNAc only exerted its inhibitory effect on day 4 of the culture, the day when IgG plaque‐forming cells first appeared. Furthermore, GalNAc could override the action of T helper factor in T cell‐depleted cultures. Collectively, these data indicate that GalNAc inhibits the initiation of IgG synthesis probably by blocking the interaction of a helper factor for IgG synthesis with its target cell.
Histocompatibility requirements for T cell help in specific in vitro antibody responses to influenza virus by human blood lymphocytes
Authors: Callard Robin E. , Smith Caroline M. 
Published: February 2007

AbstractSpecific antibody responses to influenza virus were obtained in vitro from human blood mononuclear cells (PBM). The response was T cell‐dependent, as shown by separation of PBM into E rosette‐positive (E+) and ‐negative (E−) populations. The histocompatibility requirements for T‐B cell interactions in this response were analyzed by recombining E− and E+ fractions from donors with varying degrees of HLA compatibility. No antibody formation was obtained from any allogeneic combination except for the special case of HLA identical siblings. As these experiments included combinations with shared or identical HLA‐DR specificities, it was unlikely that genetic restriction alone could account for the failure of T‐B cell collaboration. Evidence that suppression was responsible for the lack of antibody formation was obtained from experiments in which allogeneic E+ cells profoundly depressed specific antibody responses of intact PBM. In contrast, no such suppression was seen in pokeweed mitogen‐driven polyclonal Ig synthesis for which there are no major histocompatibility complex requirements for T cell help. The suppressor activity of allogeneic E+ cells was found to be radiation‐sensitive. By irradiating E+ cells, it was, therefore, possible to test for T cell help across an HLA barrier without unwanted suppressor effects. Under these conditions, (irradiated) E+ cells were able to collaborate with allogeneic E− cells even with no HLA alleles in common. This was true even when autologous monocytes were depleted from the helper E+ population. Supernatants collected from antigen‐driven cultures of allogeneic E− and E+ cells were able to replace helper T cells in the specific antibody response to influenza virus. The apparent lack of genetic restriction in these responses might, therefore, be explained by the production of a nonrestricted helper factor.
Tolerogenic or immunogenic activity of hapten‐conjugated polysaccharides correlated with cellular localization
Authors: Humphrey John H. 
Published: February 2007

AbstractDinitrophenylated (DNP) conjugates of Ficoll, hydroxyethyl starch, levan, dextran, type 3 pneumococcal capsular polysaccharide SIII, pectin, alginic and hyaluronic acid at various epitope densities were tested for their capacity to inhibit secondary IgG anti‐DNP antibody responses using an in vivo transfer system. Some aminobenzylarsonate conjugates were examined similarly. Conjugates of the acidic polysaccharides were markedly more effective than those of uncharged polysaccharides. Conjugates with high epitope densities were particularly tolerogenic. DNP conjugates of Ficoll and hydroxyethyl starch elicited prolonged IgM responses over a wide dose range, and there are indications in the literature that conjugates of dextran do likewise. All the polysaccharide conjugates, labeled with radioiodine, persisted in the body for long periods (half‐lives 8.5–63 days), and all were cleared rapidly from, but remained detectable in the blood for many days. Gross tissue distributions varied markedly from one conjugate to another, and autoradiography revealed unexpected differences in cellular localization. Despite substantial retention in the liver, some uncharged polysaccharides were localized only in parenchymal and not in Kupffer cells. In the spleen, only the acidic polysaccharides were predominantly localized in red pulp macrophages, and the neutral polysaccharides were detectable exclusively, and in the case of Ficoll, hydroxyethyl starch and some dextrans very intensely in macrophages of the marginal zone of the white pulp. It is suggested that retention of thymus‐independent antigens in marginal‐zone macrophages favors, whereas trapping in red‐pulp macrophages diminishes immunogenicity, and that tolerogenic effectiveness depends upon a balance between tolerization of B cells by free antigen and stimulation by antigen presented by marginal‐zone macrophages. The distinction between functionally different macrophages in the spleen is elaborated in the following report.
Alteration of clonal profile II. Studies on the capacity of BALB/c splenic B cells to perpetuate responsiveness to phosphorylcholine and T15 idiotypic dominance
Authors: Quintáns José , Loken Michael R. , Quan Zoe S. , Dick Robert F. , Regueiro Benito 
Published: February 2007

Abstract(CBA/N × BALB/c)F1 hybrid male mice are unable to mount anti‐phosphorylcholine (PC) plaque‐forming cell (PFC) responses because they carry the CBA/N X‐linked immune defect of B lymphocyte differentiation. Transplantation of splenic B cells from BALB/c mice restores responsiveness to thymus‐dependent and thymus‐independent PC antigens up to 8 months after cell transfer. Cytotoxicity studies demonstrate the donor origin of PFC generated in reconstituted (CBA/N × BALB/c)F1 mice. Although responsiveness to PC is restored permanently, a shift in idiotype expression that leads to the loss of T 15 idiotypic dominance 3 months after cell transfer can be detected. This shift originates from Ig− cells because Ig+ splenic cells purified in a fluorescence‐activated cell sorter maintain T15 dominance. Therefore, the Ig+ cells have a remarkable capacity to maintain responsiveness to antigens and can perpetuate idiotypic dominance if the stem cell pool is removed.
Effect of anti‐Lyb3 antiserum on poly (L‐glutamic acid, L‐lysine)‐induced B cell tolerance
Authors: Sherr David H. , Huber Brigitte T. , Gershon Richard K. , Benacerraf Baruj , Dorf Martin E. 
Published: February 2007

AbstractThe effect of anti‐Lyb3 antiserum on antigen‐specific B cell tolerance was investigated. The intraperitoneal injection of the nonimmunogenic copolymer L‐glutamic acid60, L‐lysine40 (GL) specifically reduces the ability of murine B cells to form GL‐specific plaque‐forming cell responses following challenge with the immunogenic conjugate of GL coupled to fowl gamma‐globulin. It was found that this tolerance could be reversed or blocked by the intravenous injection of microliter quantities of anti‐Lyb3 antiserum. However, this dose of antiserum neither reversed T cell tolerance induced with protein‐coupled syngeneic erythrocytes nor induced tolerized B cells to secrete antibody. The results suggest that B lymphocytes can be rescued from GL‐induced tolerance soon after induction and that Lyb3 determinants may play a functional role in the activation of antigen‐specific B lymphocytes.
Allotype suppression in the chicken II. Suppression in homozygous chickens with antiallotype antibody and allotype‐disparate B cells
Authors: Ratcliffe Michael J. H. , Ivanyi Juraj 
Published: February 2007

AbstractInjection of heterozygous (M‐13/M‐1b, G‐1g/G‐1i) B 14‐line chickens with antisera directed against either IgM‐1a or IgM‐1b induced suppression of the relevant IgM‐1 and genetically linked IgG‐1 allotypes, whereas a mixture of anti‐M‐1a and anti‐M‐1b antibodies failed to produce allotype suppression. Injection of anti‐M‐1 antiserum into M‐1 homozygous chickens induced only a transient delay of a few days in the appearance and rise of serum IgM‐1 levels. However, suppression of host allotypes was induced by injecting M‐1, G‐1 homozygous neonatal or embryonal recipients with anti‐M‐1 antisera together with B locus‐histocompatible allotype‐disparate spleen, bone marrow or bursal cells. The active cell type were donor B cells, which established chimerism in the injected hosts, whereas peripheral blood T lymphocytes from agammaglobulinemic donors were ineffective. Allotype suppression was attributed to a homeostatic control mechanism which is exerted by normal B cells (but not T cells) over B cell recruitment in anti‐M‐1 antibody‐treated, immature hosts.
IgE‐induced histamine release from rat basophilic leukemia cell lines: isolation of releasing and nonreleasing clones
Authors: Barsumian Edward L. , Isersky Chaviva , Petrino Marianne G. , Siraganian Reuben P. 
Published: February 2007

AbstractThe rat basophilic leukemia (RBL) cell lines were cloned and the various sublines compared for their chromosome number, IgE‐mediated histamine release and for IgE surface receptors. It was found that cell lines started from tumors at different times vary in both their chromosome number and their ability to release histamine by an IgE‐mediated reaction. RBL‐I and III have ∼ 44 chromosomes and did not respond to an IgE‐mediated reaction, whereas RBL‐II and RBL‐IV have 68–73 chromosomes and showed moderate levels of histamine release (percent release x̄ = 5 ± 2 and 10 ± 4, respectively). The cloning of the RBL‐IV line resulted in some sublines which were excellent histamine releasers (range 39–100%) and some which were relatively refractory (< 10%) to IgE‐mediated histamine release. These clones did not differ significantly in chromosome number. Recloning the releasing lines gave rise to poor releasers, whereas the recloning of poor releasers did not produce good releasers indicating that the mutational drift in culture is toward loss of histamine‐releasing capacity. The number of IgE receptors and the rate of IgE association and dissociation were similar for the different cell lines. The study failed to disclose significant molecular weight differences in the IgE receptor from the various clones and sublines indicating that the failure to release probably does not reside in the receptor. The various cloned sublines are phenotypically stable, and the isolation of excellent histamine‐releasing sublines are useful for studies of the complex phenomenon of histamine release.
Inhibition of experimental allergic encephalomyelitis by carrier administered prior to challenge with encephalitogenic peptide‐carrier conjugate
Authors: Rauch Helene C. , Montgomery Ilene Nowicki , Swanborg Robert H. 
Published: February 2007

AbstractGuinea pigs can be rendered unresponsive to experimental allergic encephalomyelitis (EAE) challenge by prior injections of myelin basic protein (BP) or peptides derived from BP. The synthesized tryptophan‐containing peptide (TrpP, corresponding to residues 114–122) which is the primary encephalitogenic sequence in BP (for guinea pigs) has been conjugated to the non‐central nervous system protein bovine serum albumin (BSA) and used for EAE challenge. It has been shown in this study that prechallenge treatment with the BSA carrier alone can significantly inhibit the induction of EAE by TrpP‐BSA conjugate. That carrier treatment is immunologically specific was determined when prior treatment with cytochrome c did not protect animals from EAE challenge with TrpP conjugated to BSA. In addition, in disease control animals, prechallenge treatment with BP protected guinea pigs against EAE induced with BP or TrpP, and while TrpP did protect guinea pigs challenged with TrpP, it did not protect those challenged with BP. This last finding raises the possibility of a second encephalitogenic sequence in BP or an important role for the carrier in the TrpP conjugate.
Nature of macrophage‐T cell interaction in secondary helper cell generation in vitro Genetic restriction of macrophage‐T cell interaction, which determines T‐B genetic restriction
Authors: Vogt Peter , Erb Peter , Keller Beatrice , Feldmann Marc 
Published: February 2007

AbstractTo investigate the histocompatibility requirements for the macrophage‐T cell interaction in the secondary antibody response, splenic T cells from antigen (carrier)‐primed F1 hybrid mice were restimulated in vitro with carrier‐pulsed F1, parental or allogeneic macrophages. Surviving T cells were cocultured with hapten‐primed F1 or parental “B cells” and restimulated with the appropriate hapten‐carrier conjugate. The IgG antibody‐forming cell response was then measured using a plaque assay.Mapping of the genetic restriction was performed by use of different strain combinations. T helper cells could be restimulated in the presence of macrophages only provided they shared the I‐A subregion of the major histocompatibility complex with the F1 T cells. T cells from F1 hybrids restimulated with parental or I‐A‐identical macrophages were shown to only cooperate with parental B cells of the same I‐A haplotype as the macrophages used for restimulation. The defect was at the level of the macrophage, as addition of macrophages of the I‐A haplotype used for the restimulation culture reconstituted the ability of F1 helper cells to cooperate with the I‐A‐nonidentical B cells.
Specificity of antigen binding by T cells; competition between soluble and Ia‐associated antigen
Authors: Lonai Peter , Steinman Lawrence , Friedman Varda , Drizlikh George , Puri Joseph 
Published: February 2007

AbstractCompetitive antigen binding experiments were performed with purified T and B cells of C3H.SW (H‐2b) mice. As antigen, (T, G)‐A–L [poly‐L(Tyr, Glu)‐poly‐DL‐Ala–poly‐L Lys] was used, both in an Ia‐containing form, released by adherent cells (IAC, Puri and Lonai, Eur. J. Immunol. 1980.10: 273), and in regular solution. It was found that regular (T, G)‐A–L did not compete with the binding of 125I‐labeled‐IAC‐(T, G)‐A–L even at a 104‐fold excess, whereas IAC‐(T, G)‐A–L inhibited binding at 10‐fold excess. The specificity of (T, G)‐A–L binding to high‐responder T and B cells was compared by using related branched synthetic copolymers as competitors. B cells cross‐reacted with (T, G)‐A–L, (H, G)‐A–L, (Phe, G)‐A–L, (G)‐A–L and (T, G)‐Pro–L. In contrast, antigen‐binding C3H.SW T cells cross‐reacted only with (T, G)‐A–L and (Phe, G)‐A–L, to both of which they are Ir gene‐controlled high responders. Evidence for the Ir gene control of IAC‐binding T cells was obtained by showing that high × low‐responder F1 hybrid T cells preferentially bind IAC‐(T, G)‐A–L processed by processor cells deriving from the high‐responder parental strain. These data are interpreted to suggest that T cells have high affinity for antigen plus self Ia complexes, whereas they have a much lower, if any, affinity for free antigen. It also follows from the results that the structure of the complex ligand may have a role in defining the specificity, H‐2 restriction and Ir gene control of T cells.
Control of idiotope expression by monoclonal anti‐idiotope and idiotope‐bearing antibody
Authors: Kelsoe Garnett , Reth Michael , Rajewsky Klaus 
Published: February 2007

AbstractPreinjection of C57BL/6 mice with nano‐to microgram amounts of a monoclonal IgG1 antibody directed against a binding site‐related idiotope of the anti‐NP [(4‐hydroxy‐3‐nitro‐phenyl)acetyl] antibody B1‐8 results in enhancement or suppression of the corresponding and of another B1‐8 idiotope in a subsequent anti‐NP response, depending on the dose of the injected anti‐idiotope antibody. The enhancing and suppressive effects appear two weeks after anti‐idiotope administration and are maximal after 6–8 weeks. They are predominantly expressed at the level of IgG, not IgM, antibodies. Enhancement of idiotype expression, i.e. idiotypic memory, can also be induced by the injection of idiotypic antibody of the IgM class, namely antibody B1‐8. This effect might represent one of the general mechanisms by which immunological memory is established.
Enhancing the frequency of antigen‐specific hybridomas
Authors: Fox Philip C. , Berenstein Elsa H. , Siraganian Reuben P. 
Published: February 2007

AbstractTechniques were developed to enhance the frequency of antigen‐specific hybridomas by enriching for antibody precursor or ‐producing lymphocytes prior to cell fusion. Spleen cells of immunized animals were either (a) cultured in vitro for 3–4 days in the presence of the immunizing antigen or (b) adoptively transferred into X‐irradiated syngeneic recipients followed immediately by an in vivo antigen boost 4 days prior to use in cell fusion. There was a 10‐fold increase in the percentage of wells which develop antigen‐specific, antibody‐secreting hybridomas following these treatments. These techniques allow an increased yield of hybridomas with a greatly decreased technical effort.
Suppression of the primary IgM response by environmental teichoic acid
Authors: Oldfather John W. , Chorpenning Frank W. 
Published: February 2007

AbstractIt has been shown previously that ingestion of glycerol teichoic acid (GTA) in the conventional laboratory diet (8 mg/kg) is the stimulus for natural background responses to GTA in rats. Since injected GTA suppresses responses to sheep red blood cells (SRBC), it was suspected that dietary GTA also might be acting suppressively. A comparison of rats fed the conventional diet with rats fed a GTA‐free diet showed that ingested GTA markedly suppressed immune and background direct plaque‐forming cell (PFC) responses to SRBC. It appeared that a direct causal relationship existed between the degree of suppression and the amount of GTA exposure. When GTA‐deprived rats were force‐fed varying doses of GTA or when conventional animals were injected (i.p.) with GTA, increasing the total GTA dose resulted in decreased direct PFC responses to SRBC. Suppression was also observed when GTA‐deprived rats were force‐fed GTA‐containing Bacillus sp. ATCC 29726. The phenomenon of suppression by dietary GTA was not restricted to responses to SRBC, as similar results were obtained with chicken erythrocytes. When IgG PFC were measured, no difference between conventional and GTA‐deprived groups was observed. Thus, an IgM‐IgG shift does not seem to play a role in the mechanism of suppression by GTA.
Common neuroectodermal antigens on human melanoma, neuroblastoma, retinoblastoma, glioblastoma and fetal brain revealed by hybridoma antibodies raised against melanoma cells
Authors: Liao Shuen‐Kuei , Clarke Bryan J. , Kwong Pak C. , Brickenden Anne , Gallie Brenda L. , Dent Peter B. 
Published: February 2007

AbstractThe hybridoma system has been utilized to produce antibodies to characterize the cell surface antigens on human melanoma cells. On initial screening, two antibodies derived by the fusion of mouse myeloma cells (SP2/0‐Ag14) and splenocytes from a mouse immunized with a melanoma cell line (CaCL 78‐1) showed cross‐reactivity with 10 melanoma cell lines and did not react with any of 4 epithelial cancer lines, or 4 normal adult fibroblast lines. However, because of reactivity with 2 neuroblastoma cell lines, additional testing with other neuroectodermal derivatives was carried out and revealed a broad cross‐reactivity among melanomas, neuroblastomas, retinoblastomas and glioblastomas and against antigens shared by fetal but not adult brain. Thus, these results indicate the existence of common neuroectodermal antigens on melanoma cells. Before melanoma specificity can be claimed for, an antibody reactivity with nonmelanoma cells bearing these neuroectodermal antigen should be excluded.
Rabbits immunized against b6 allotype express similar anti‐b6 idiotopes
Authors: Roland Jaques , Cazenave Pierre‐André 
Published: February 2007

AbstractSimilar idiotopes are detected on anti‐allotypic antibodies synthesized by all rabbits immunized against the b6 allotype. The expression of similar idiotopes on anti‐b6 antibodies has been found in rabbits of all VHa allotypic types thus far studied. For their expression, these idiotopes require the interaction between VL and VH domains.