bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal IgM, IgA and IgG in the serum of a single individual: Immunofluorescence identification of cells producing the immunoglobulins
Authors: Krueger Robert G. , Fair Daryl S. , Kyle Robert A. 
Published: February 2007

AbstractMonoclonal IgM(ϰ) and IgA(ϰ) in the serum of patient CM were previously shown to share identical, individually specific (Ind) or idiotypic antigenic determinants. A component in the IgG fraction of CM's serum was shown by one of the assay systems to also share Ind determinants with the IgA and IgM. Recent experiments have indicated that the CM IgG monoclonal protein also shares identical Ind determinants with the other two CM immunoglobulins (Ig). These results suggested that the variable regions of the heavy and light chains of the three different classes of Ig were very similar. A direct immunofluorescence assay was used in this study on bone marrow smears of patient CM obtained at two different dates to identify the cells producing these Ig. The reaction of antisera specific for Ind determinants demonstrated that most plasma cells, whether containing IgM, IgA, or IgG, stained with the anti‐Ind antisera; this occurred irrespective of whether the anti‐Ind antisera were generated to the patient's IgM or IgA. The reaction with isotypic antisera revealed cell populations containing either IgM, IgA, or IgG and a significant cell population containing both IgM and IgA. The common occurrence of IgM and IgA‐containing cells which synthesize monoclonal Ig with shared Ind determinants provides evidence consistent with the IgM‐IgA pathway of differentiation of antibody‐producing cells. Further, the tendency toward decreasing numbers of IgM‐staining cells with concomitant increasing numbers of IgA and IgG‐containing cells suggests that the clones of cells producing these Ig were derived from a single precursor cell.
Nature and complexity of the FMR antigenic system
Authors: Bismuth Alain , Kremsdorf Dina , Debré Patrice , Levy Jean Paul 
Published: February 2007

AbstractThe FMR antigen is currently defined as a cell surface antigen shared by Moloney, Rauscher, Friend and Graffi virus‐induced leukemias. Different groups have reported contradictory results showing an association of FMR either with various internal or external virion components or with a nonvirion protein. A study of twelve supposed anti‐FMR antisera using complement‐dependent cytotoxicity assays, and quantitative absorption of their activity on different lymphoma cells show that there exists an “FMR system” rather than an FMR antigen. Several antigenic specificities can be defined which are either common to all the leukemia tested (FMRGi) or limited to the lymphomas induced by certain viruses. In the latter group, at least F, FR, and MRGi antigens can be distinguished. These “FMR antigens” are frequently associated at the lymphoma cell surface with non‐FMR specificities. The so‐called anti‐FMR antisera show a variable specificity pattern generally revealing some but not all of the FMR antigens. Many of them do not contain anti‐FMRGi antibodies. On the contrary, they can react against non‐FMR antigens. Cocapping experiments reveal a comigration of the common FMRGi antigen and the major viral glycoprotein, gp69/71. Absorption of anti‐FMRGi activity by both Rauscher or Moloney virions and by purified Rauscher gp69/71 confirm this result suggesting that FMRGi could be a subgroup specificity of the gp69/71 of exogenous type C viruses. The nature of the other FMR specificity was not studied here. The complexicity of the FMR system probably explains the contradictory results which have been published concerning the nature of FMR antigens. It is probable that several antigens have been studied by different groups under the same name. Very precise technical conditions must be used for the analysis of the FMR system if such confusion is to be avoided in the future.
Sequential study of C 1 q‐binding substances and of anti‐DNA antibodies in (NZB × NZW)F1 mice: Evidence for an acute phase of the lupus disease in 2‐month‐old mice
Authors: Fournié Gilbert J. , Minh Marline Gayral‐Ta , Haas Sylvie , Pourrat Jacques P. , Conte Jean J. 
Published: February 2007

AbstractLongitudinal studies of C1 q and DNA‐binding substances were performed in sera from 38 (NZB × NZW)F1 female mice between days 39 and 150 of life. Results suggest a two‐phase evolution of circulating immune complexes and anti‐DNA antibodies in young (NZB × NZW)F1 mice and show the existence of an acute phase of the disease during the second month of life of these mice.
Nonprecipitating pig anti‐dinitrophenyl antibody: Factors influencing the conversion into precipitating antibody
Authors: Franě Františ , Olšovská Zdeňa , Š Lubor 
Published: February 2007

AbstractA high affinity nonprecipitating anti‐2,4‐dinitrophenyl (DNP) IgG antibody constitutes a major fraction of circulating anti‐DNP antibodies at the decline of the anti‐ DNP antibody response in pigs. The purified nonprecipitating antibody forms exclusively soluble complexes with DNP‐PSA (pig serum albumin) or DNP‐PGG (pig IgG). The binding sites are accessible to large ligands; one antibody molecule can combine with two molecules of DNP‐PSA simultaneoulsy.The formation of complexes with DNP‐PSA was studied in various media. No precipitate was formed in saline, in 0.9 M or 0.05 M sodium chloride, in 0.5 M potassium thiocyanate and in several nonionic detergent solutions (0.5% and 1%). Normal pig or guinea pig sera were found to contain a factor, removable by an antigen‐antibody precipitate that caused a partial precipitation of the complexes. A mild alteration of the integrity of the antibody molecule by cleavage of interchain disulfide bonds did not affect the nonprecipitating character of the antibody. In media containing hydrophilic polymers, i.e. various dextrans, polyethylene glycols or a soluble polyamide (poly‐α,β5‐[N(2‐hydroxyethyl)‐DL‐aspartamide]), a functional conversion occurred; the antibody behaved like a precipitin. The precipitate with DNP‐PSA could not be resolubilized upon removal of the polymer by washing. The magnitude of the functional conversion depended on the concentration of the polymer and on its molecular weight, larger molecules being more effective. The effect of the hydrophilic polymers could be potentiated by replacing water in the solvent partly by deuterium oxide.The findings are compatible with a notion, that in polymer‐containing media the nonprecipitating antibody acquires a conformation functionally equivalent to the conformation of a precipitating antibody and that the altered conformation is stabilized by the lattice of the precipitate with DNP‐PSA.
Mechanisms of clonal abortion tolerogenesis III. Antigen abrogates functional maturation of surfaceimmunoglobulin‐negative adult bone marrowlymphocytes
Authors: Pike Beverley L. , Nossal G. J. V. 
Published: February 2007

AbstractThe fluorescence‐activated cell sorter (FACS) was used to fractionate adult CBAmouse bone marrow cells on the basis of their size and the amount of surfaceimmunoglobulin (sIg) expressed. It was noted that a population of viable, small sIg−cells could generate up to 28% slg+ cells within 24 h in tissue culture. The capacity of various cell fractions to respond to T‐independent stimulation by antibody productionwas studied. Fractionated cells were placed into microculture at limiting dilution inthe presence of thymus “filler” cells, stimulated with E. coli lipopolysaccharide (LPS)and after 3 to 5 days, assayed for the presence of antibody‐forming cell clones to thehapten (4‐hydroxy‐3‐iodo‐5‐nitrophenyl) acetyl (NIP). Through appropriate statistical means, the number of anti‐NIP precursors originally present was calculated. Whilethe sIg+ fraction contained approximately 70 cells in 106 capable of immediate development into anti‐NIP clones, the slg− fraction contained very few reactive cells. However, the cloning capacity of this fraction increased markedly following 24 h of maturation in tissue culture.When bone marrow cells were exposed to NIP‐coupled human gamma‐globulin (NIP‐HGG) acting as a B cell tolerogen, some tolerance was induced in vitro reflecting therelative immaturity of these cells. When the FACS‐sorted sIg− cells were similarlytreated, there was virtually complete abrogation of their functional maturation intoclonable anti‐NIP precursors. The effect of LPS on cells converting from the sIg− tosIg+ status was investigated. When LPS and NIP‐HGG were concomitantly present, about one‐third of the cells escaped tolerance induction. LPS thus “rescued” somecells from clonal abortion, but certainly did not totally abolish tolerance induction. The significance of these results for the clonal abortion theory of B lymphocytetolerance is briefly discussed. The conclusion is reached that cells converting from thesIg− to sIg+ status in the normal course of differentiation represent a prime target fortolerance induction.
Studies on the generation and expression of H‐2‐controlled T helper function in chimeric mice: Evidence for two levels of H‐2 restriction
Authors: Hiinig Thomas , Schimpl Anneliese 
Published: February 2007

AbstractF1 → parental, semisyngeneic/semiallogeneic and fully allogeneic bone marrow radiation chimeras were used as a source of helper T cells in the in vitro anamnestic response to dinitrophenylated keyhole limpet hemocyanin. In F1 → parental and in semisyngeneic/semiallogeneic chimeras, a small population of helper T cells restricted to the H‐2 haplotype present in the donor only was shown to co‐exist with T cells restricted to the shared haplotype. Only the population restricted to the donor H‐2 could be demonstrated in allochimeras, presumably due to a lack of antigen‐presenting cells of host origin during priming.Under assay conditions where, in addition to T cell/macrophage interactions, a direct T‐B cell contact was necessary (“linked” cooperation), the H‐2 restrictions observed were absolute. When direct T‐B cell contact was made unnecessary by a special experimental protocol (“unlinked” cooperation), H‐2 restriction between T and B cells was overcome. Thus, the cellular interactions during the anamnestic immune response to T‐dependent antigens seem to be H‐2‐restricted at two levels: T cell/ macrophage and T‐B cell interactions.
In vitro immunosuppressive effect of serum from orally immunized mice
Authors: Chalon Marie‐Paule , Milne Ross William , Vaerman Jean‐Pierre 
Published: February 2007

AbstractMice were orally immunized by 4 daily intragastric (IG) intubations of 4 × 109 sheep red blood cells (SRBC). The serum of such mice (OS), taken two weeks after the first intubation, was compared to normal mouse serum for its suppressive effect on in vitro primary responses of normal spleen cells to SRBC. OS regularly depressed the in vitro response to less than 10% of the normal response. The suppressive effect was dose‐ dependent, antigen‐specific and removable by absorption with SRBC. When cultures were stimulated with SRBC pre‐exposed to OS, the response was also depressed. The suppression was less when the addition of OS was delayed. OS from BALB/c mice efficiently depressed in vitro responses of spleen cells from other strains. Spleen cells, taken 2 weeks after IG immunization, responded normally to in vitro challenge with SRBC. The suppressive factor had the molecular size of an IgG and could be removed by anti‐Ig and anti‐IgG1 but not by anti‐α or anti‐μ immunosorbents. Purified IgG1 was more suppressive than IgG2a and IgG2b despite a similar anti‐SRBC antibody content.
Influenza virus infection of mouse lymphoblasts alters the binding affinity of anti‐H‐2 antibody: Requirement for viral neuraminidase
Authors: Liberti Paul A. , Hackett Charles J. , Askonas Brigitte A. 
Published: February 2007

AbstractThe requirement for histocompatibility in the T lymphocyte killing of virus‐infected cells has led us to investigate the effect of influenza virus infection on mouse cell surface histocompatibility (H‐2) antigens. Monoclonal anti‐H‐2 antibody made it possible to develop equilibrium binding conditions for the assay of H‐2 antigen‐antibody interactions on intact cells. Scatchard analysis of anti‐H‐2 binding with normal and virus‐infected cells yielded linear curves indicating homogeneity of the interaction at varied concentrations of antibody through saturating levels. The estimated number of 2 × 105 ‐ 5 × 105 H‐2 antigenic sites per mouse lymphoblast does not appear to change during the course of influenza virus infection.However, the Ka (binding affinity constant) of anti‐H‐2 binding is rapidly elevated by virus infection (“0” time), continues to increase for 3 h post infection, then decreases. Control cells, treated with normal egg allantoic fluid, show no change in Ka during similar incubation.This change in Ka requires the presence of active viral neuraminidase. Thermal denaturation of the neuraminidase of the virus particles abolishes their ability to induce Ka alteration, even though hemagglutinin activity is retained. Treatment of cells with neuraminidase of bacterial origin led to an elevation of Ka, but did not mimic the viral effect in time dependence and magnitude of peak responses. The time‐dependent lowering of Ka from peak values appeared to relate to virus replication, since UV light‐inactivated virus‐induced Ka elevation, but did not produce the typical Ka decline at 4‐5 h post infection.The changes in Ka of anti‐H‐2 binding during influenza infection reflects a virus‐ induced alteration of the H‐2 molecule or its environment in the host cell membrane. The molecular basis of this change and its relation to H‐2‐restricted recognition of influenza virus‐infected cells by cytotoxic T cells requires further study.
Cytotoxicity of human mononuclear cells against chicken and human red blood cells, induced by treatment of the effector cells with phospholipase C
Authors: Northoff Hinnak , Resch Klaus 
Published: February 2007

AbstractHuman mononuclear cells from peripheral blood which were treated with phospholipase C (PLC), became cytotoxic against human or chicken red blood cells. PLC‐ induced cellular cytotoxicity against human red blood cells was further analyzed and compared to anti‐D‐mediated, antibody‐dependent cellular cytotoxicity (ADCC), using the same target cells. ADCC, but not cytotoxicity of PLC‐treated effector cells, was inhibited by free IgG. In addition, iodoacetate strongly enhanced PLC‐induced cytotoxicity, but blocked ADCC completely. Addition of fetal calf serum or human AB serum impaired PLC‐induced cytotoxicity. A similar inhibition was found by adding lecithin liposomes suggesting that the inhibitory effect of sera was also due to their phospholipid content. The data show that cytotoxicity of PLC‐treated effector cells can be clearly distinguished from cellular cytotoxicity, occurring spontaneously or induced by target cell antibodies. We favor the notion that cytotoxicity of PLC‐ treated effector cells against human erythrocytes is due to the action of PLC, adsorbed to the effector cells.
Immunological activity of a T hybrid line I. Production of an H‐2‐related suppressor factor with specificity for sheep red blood cells
Authors: Taussig Michael J. , Corvalán José R. F. , Binns Richard M. , Roser Bruce , Holliman Andrew 
Published: February 2007

AbstractT lymphocyte hybrid lines have been produced by fusion of the thymoma BW 5147 with spleen cells of C57BL/10 mice primed to sheep red blood cells (SRBC). The supernatant (culture fluid) of a T hybrid designated A1 was able to suppress the primary (IgM) and secondary (IgM and IgG) antibody responses to SRBC in vitro. The suppressive activity of supernatants could be titrated to 50% end points at final dilutions of up to 1:270. The suppression affected only SRBC and haptens coupled to SRBC, except when used at high concentration when some nonspecific suppression was observed. Absorption of the A1 supernatant with SRBC removed all activity, while several other species of red cells failed to do so. The suppressor factor present in A1 supernatant was not removed by anti‐Ig adsorbents, but was removed by anti‐H‐2 antibodies reacting specifically with the haplotype of the spleen cells used in the fusion (H‐2b). The cellular target of action of the factor was apparently a B cell, based on absorption with different cell populations. No genetic restrictions in the activity of the factor were found. Al cells carried H‐2 and Thy‐1 alleles of both parental cells and formed rosettes with SRBC.
Frequencies of mitogen‐reactive B cells in the mouse. Lipopolysaccharide‐, lipoprotein‐ and Nocardia mitogen‐reactive B cells in CBA/N mice
Authors: Huber Brigitte , Melchers Fritz 
Published: February 2007

AbstractB cell‐defective (CBA/N × BALB/c)F1 male mice have 100 times less lipopolysaccharide‐reactive and 10‐100 times less lipoprotein‐ and Nocardia mitogen‐reactive B cell precursors than F1 female mice with normal B cells.
Allotype suppression in the chicken. I. Generation of chronic suppression in heterozygous but not in homozygous chickens
Authors: Ratcliffe Michael J. H. , Ivanyi Juraj 
Published: February 2007

AbstractThe injection of antibody directed against either the IgM‐1 a or IgM‐1 b allotype into heterozygous (M‐la/M‐lb, G‐lg/G‐li) B 14‐line chickens produced suppression of the relevant IgM‐1 and genetically linked IgG‐1 allotypes in their serum, as quantitated by single radial immunodiffusion. Suppression of the IgM‐1 and IgG‐1 allotypes was associated with a compensatory increase in the alternative IgM‐1 and IgG‐1 serum allotype levels. This suppression was induced (a) by passive injection of anti‐allotype antiserum into 13‐day‐old embryonal or neonatal recipients, or (b) by egg yolktransmitted antibody in chickens hatched from homozygous B 14 A (M‐la, G‐lg) hens immunized against the IgM‐l b of the homozygous B14C (M‐lb, G‐li) rooster. Heterozygous chickens injected embryonally with anti‐allotype antiserum were profoundly suppressed for at least 16 weeks after hatching, while neonatally injected chickens showed a gradual recovery of both IgM‐1 and IgG‐1 allotypes over the same period. Suppression of the IgM‐1 b allotype could be induced in heterozygotes which had inherited the M‐lb allele either maternally or paternally. However, no suppression of either IgM‐1 or IgG‐1 levels could be detected in homozygous chickens injected with the relevant anti‐allotype antiserum. Hence, allotype suppression only occurred in M‐1 heterozygous chickens which had an alternative source of B cells available. The involvement of a B cell surveillance mechanism in allotype suppression is postulated and the possible role of suppressor cells is discussed.
Cytotoxic T cell responses to haptenated cells II. On the role of H‐2 genes
Authors: Haas Werner , Pohlit Helmut , von Boehmer Harald 
Published: February 2007

AbstractCytotoxic T cell (CTL) responses to cells coupled with high or low doses of the hapten 3‐(p‐sulfophenyldiazo)‐4‐hydroxyphenyl acetic acid (SP) were studied. CTL responses to densely coupled cells were obtained with all mouse strains tested. Only mice carrying the Kk allele responded to sparsely coupled cells. Mice expressing I‐Akbut not Kk were nonresponders. (Responder × nonresponder) F1 hybrids responded in vitro to sparsely coupled cells from responder but not from nonresponder mice. However, responder mice could be cross‐primed in vivo with SP‐coupled cells from nonresponder mice. CTL responding to sparsely coupled cells were restricted to Kk. Cross‐reactive lysis of target cells not carrying the Kk allele was dependent on the hapten density and the H‐2 haplotype carried by the target cells.
Expression of b 4 and b 5 ϰ light chain allotypes by B and pre‐B cells in allotype‐suppressed and neutralized b4b5 rabbits
Authors: Simons Margaret A. , Hayward Anthony R. , Gathings William E. , Lawton Alexander R. , Young‐Cooper Glendowlyn O. , Cooper Max D. , Mage Rose G. 
Published: February 2007

AbstractIn previous studies, we described a primitive lymphoid cell found in fetal liver and in the bone marrow of older rabbits which contained cytoplasmic IgM but lacked surface IgM detectable by immunofluorescence. In heterozygous b4b5 rabbits, the pre‐B cells in which we could detect these kappa chain allotypes appeared to exhibit allelic exclusion. In the present study, we investigated the effects of allotype suppression and its neutralization on the expression of the b4 and b5 allotypes by B and pre‐B cells from the spleens and bone marrow of b4b5 rabbits. We found that in young allotype suppressed rabbits, pre‐B cells of the suppressed allotype persist in bone marrow when B cells of the suppressed allotype are absent or severely depleted. The persistence of pre‐B cells of the suppressed type supports the view that pre‐B cells differ in their responsiveness to external influences such as anti‐Ig compared to B lymphocytes. Injection of serum with b5 immunoglobulin into b4b5 animals suppressed 14‐23 days previously for b5 was followed by the appearance of increased proportions of b 5 B cells in spleen within 24 h. Surviving pre‐B cells are a likely source of these rapidly appearing B cells as well as of the B cells bearing surface immunoglobulin of the suppressed allotype which appear during the recovery phase of allotype suppression.
Specificity of H‐2‐linked Ir gene control in mice: Recognition of the core structure A–L in defined sequence analogues of (T,G)‐A–L
Authors: Stötter Hans , Imm Anita , Meyer‐Delius Margot , Rüde Erwin 
Published: February 2007

AbstractFor further characterization of the processes involved in Ir gene control, the specificity of antibodies and the cross‐reaction on the level of helper T cells was studied for a series of polypeptide antigens related to poly‐L(Tyr,Glu)‐poly‐DL‐Ala–poly‐LLys[(T,G)‐A–L] but carrying more defined side chains. Helper cell specificity was assayed in an in vitro secondary anti‐dinitrophenyl (DNP) response by cross‐stimulation of primed T cells with the various polypeptide carriers. It was established that these polypeptides, although showing the same response pattern, were recognized as distinct entities in the immune response by B and T cells. If this common pattern is due to the effect of the same Ir gene, the latter is unlikely to code directly for the binding site on helper T cells recognizing these antigens. The core structure A–L, although weakly immunogenic itself, is recognized in the response to these antigens concomitantly with the recognition of the tyrosine‐containing peptides. Furthermore, it is shown that the antibody response to DNP‐A–L is under genetic control and that in the antigen Tyr6‐A–L, which has the highest immunogenicity within this group of antigens, the poly‐m‐alanine side chain is important for the genetic control mechanism. Therefore, it is concluded that the effects of Ir genes are related to recognition of the core structure A–L. The relevance of these experimental findings is discussed.