bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multiple B cell stimulation by individual antigen‐specific T lymphocytes
Authors: Pierce Susan K. , Klinman Norman R. 
Published: February 2007

AbstractRecently, an experimental system has been described which allows for the isolation and antigenic stimulation of individual antigen‐specific helper T lymphocytes in collaboration with a nonlimiting number of primary B lymphocytes. In the studies presented in this report, this system has been employed to determine whether an individual T lymphocyte has the potential to interact with more than a single B lymphocyte, when the B cells are of different antigenic specificities. The results of these studies indicate that an individual influenza virus PR 8‐specific T lymphocyte has the ability to promote antibody responses of both trinitrophenyl (TNP)‐ and PR 8‐specific B lymphocytes in response to the in vitro antigen TNP‐PR 8. Similar results were obtained when T cells specific for the hapten TNP were used in collaboration with TNP‐ and PR 8‐specific B cells. These results demonstrate that an individual T lymphocyte has the potential to collaborate with more than one B lymphocyte, and that these B cells may differ in their antibody receptor for antigen. These results do not rule out a role for idiotype or allotype‐specific T cells in antibody responses but, rather, strongly argue that antigen‐specific T cells are able to independently initiate primary B cell responses of B cells with distinct antibody receptors. In addition, under these conditions, hapten‐specific helper T cells can be readily demonstrated and may facilitate the response of B cells specific for the same or different determinants.
Immunodepression in trypanosome‐infected mice VI. Comparison of immune responses of different lymphoid organs
Authors: Kar Santosh K. , Roelants Georges E. , Mayor‐Withey Kathleen S. , Pearson Terry W. 
Published: February 2007

AbstractMitogen stimulation of cells from various lymphoid organs of C3H/He mice chronically infected with an isolate of Trypanosoma congolense was studied at different time intervals after infection, using concanavalin A (Con A) and lipopolysaccharide (LPS). At the same time, changes in the percentages of T, B and null lymphocytes in these organs were determined by immunofluorescence staining. The responses of T and B lymphocytes in the spleen were totally depressed, and the cellular composition was drastically altered by day 14 after infection. Unlike the spleen, the lymph nodes showed minor changes in their T and B lymphocyte responses and cell composition during the course of the infection, except the B cell response and composition which were altered late in the infection. The thymus and bone marrow did not show any appreciable changes in their mitogen responses and cell composition throughout the infection. The peripheral blood lymphocytes showed reduced B cell responses. Spleen cells from chronically infected mice suppressed lymphocyte stimulation induced in normal spleen and lymph node cell populations by Con A, LPS and allogeneic stimulator cells. Lymph node cells from the same group of mice did not exhibit any such suppressor activity.In the experimental system used here, the spleen is the primary site of immune depression, and other lymphoid organs such as the lymph nodes and thymus are very little affected.
Activation of the alternative complement pathway by normal and transformed cells in homologous and heterologous sera
Authors: McConnell Ian , Gorman Neil T. , Raniwalla Joher , Powell Patrick 
Published: February 2007

AbstractA variety of both normal and viral transformed or infected cells have been tested for their ability to activate the alternative pathway of complement in either homologous or heterologous sera. Normal cell lines fail to produce alternative pathway activation in homologous sera but readily activate the alternative pathway in heterologous sera. In contrast, human cells, persistently infected with measles virus or chicken cells transformed with oncogenic avian viruses, produce a marked activation in homologous sera. It is suggested that in certain circumstances, the alternative pathway of complement can discriminate between normal and abnormal “self” cells or foreign cell surfaces.
Syngeneic thyroglobulin is immunogenic in good responder mice
Authors: Elrehewy M. , Kong Yi‐chi M. , Giraldo Alvaro A. , Rose Noel R. 
Published: February 2007

AbstractMouse thyroglobulin (MTg) or thyroid extract (TE) was given repeatedly to good responder C3H/Anf (H‐2k) and poor responder BALB/c (H‐2d) mice in the absence of adjuvant. Anti‐MTg antibodies reached high levels in good responder mice given high doses of thyroid antigen. To eliminate stimulation by alloantigenic determinants and reduce the chance of denaturation, TE from syngeneic mice was prepared freshly each week and injected into good and poor responder strains. Again, significant antibody titers were observed in good responder mice. The antibody was specific for MTg since (a) it was not inhibited by extracts of other organs and (b) it reacted strongly with the closely related rat Tg and weakly with Tg from other species. Histology revealed mononuclear cell infiltration of the thyroid of good responder, but not of poor responder mice, regardless of the strain used to provide the thyroid antigen. The data demonstrate the presence of both T and B cell populations reactive with this self antigen and their stimulation by repeated high doses of antigen, without the aid of adjuvant, to override the regulatory controls that normally prevent autoimmune responses.
Cytotoxic T lymphocytes generated across an I‐Ab mutant difference are directed against a molecule bearing Ia antigens
Authors: de Waal Leo P. , Melief Cornelis J. M. , Melvold Roger W. 
Published: February 2007

AbstractThe recently discovered B6.C‐H‐2bm12 (bm12) histocompatibility mutant bears a mutation of the I‐A subregion of the H‐2b haplotype. We have studied cytotoxic T lymphocytes (CTL) generated in secondary mixed lymphocyte culture (MLC) between the bm12 mutant and the strain of origin C57BL/6 (B6). In both directions, strong CTL responses were generated against lipopolysaccharide‐stimulated, but not against concanavalin A‐stimulated target cells.Studies of the specificity of the bm12 anti‐B6 CTL response, using target cells from a panel of H‐2 recombinants, showed that the CTL were directed against specificities of the I‐Ab subregion.This conclusion was confirmed by the observation that the bm12 anti‐B6 CTL could be specifically blocked by anti‐Iab, but not by anti‐Kb antisera. EL4 tumor cells, which express Kb and Db but not Iab antigens, were not lysed by these CTL. The combined data confirm that bm12 is an I‐A subregion mutant and indicate that the I‐A subregion antigens, recognized by antibody and those recognized by CTL, are probably present on the same molecule.The CTL effector cells generated in secondary MLC across the I‐Ab mutant difference had the surface phenotype Lyt 1−2+.
Regulation of experimental allergic encephalomyelitis III. Demonstration of effector cells in tolerant rats
Authors: Holda James H. , Swanborg Robert H. 
Published: February 2007

AbstractEffector cells, which transfer experimental allergic encephalomyelitis (EAE), can be demonstrated in the spleens of Lewis rats which have been rendered tolerant to myelin basic protein (BP). Transfer of EAE was achieved following in vitro culture of tolerant donor spleen cells with antigen. The donor animals were, themselves, protected against EAE induced by active challenge with BP in complete Freund's adjuvant, although BP‐activated effector spleen cells could partially override this protection. The finding that effector cells are present in unresponsive animals supports the hypothesis that immunologic self tolerance is actively regulated by suppressor mechanisms.
Genetic control of the immune response to the L‐Glu60‐L‐Ala30‐L‐Tyr10 (GAT) terpolymer V. Three types of idiotypic specificities on BALB/c anti‐GAT antibodies
Authors: Sommé Gerard , Leclercq Lise , Petit Christine , Thèze Jacques 
Published: February 2007

AbstractThree types of idiotypic specificities compose the major idiotype of anti‐poly (L‐Glu60‐L‐Ala30‐L‐Tyr10) (GAT) antibodies from BALB/c mice (idiotype termed GAT‐715). Assays have been designed to analyze and study the distribution of these specificities. The highly conserved idiotypic specificity (h.c.GAT) has been assayed by the binding of serum 715‐7A4 to radiolabeled rat anti‐GAT antibodies. Guinea pig and mouse anti‐GAT antisera all express the same h.c.GAT specificity. The public specificity (p.GAT) has been shown to be present in an identical form in all anti‐GAT antisera from all strains of mice studied. The assay used for p.GAT was the binding of serum 715‐7A4 to C57BL/6 anti‐GAT antibodies that express only p.GAT. Finally, the strain‐restricted specificity s.r.GAT has also been investigated by radioimmunoassay; this specificity is expressed only by strains BALB/c, BALB/b, BUB/J, DBA/2, DBA/1 and ATL. This expression is independent of known allotypic markers. However, the expression of the s.r.GAT specificity of BALB/c mice follows the genetic distribution of VH genes of BALB/c origin indicating that s.r.GAT can be considered as a genetic marker of some VH gene(s) involved in the specific immune response to the GAT terpolymer.
Biochemical characterization of avian T lymphocytespecific antigens
Authors: Pink J. Richard L. , Fedecka‐Bruner B. , Coltey M. , Péault B. M. , Le Douarin N. M. 
Published: February 2007

AbstractSera from rabbits injected with quail thymocytes were absorbed on quail bursal and liver cells. The absorbed sera reacted with avian T but not B lymphocytes in an immunofluorescence assay. Material precipitated by the anti‐T antisera from lysates of radioiodinated chicken or quail thymocytes was analyzed by one‐ and two‐dimensional electrophoresis. Of two anti‐T cell antisera studied in detail, one reacted mainly with a protein of an apparent molecular weight of 45000–55000, and the other with a protein of an apparent molecular weight 65000–70000. These proteins may be homologues of previously described mammalian T lymphocyte‐specific antigens.
Thirteen hybridomas secreting hapten‐specific immunoglobulin E from mice with Iga or Igb heavy chain haplotype
Authors: Rudolph Andreas K. , Burrows Peter D. , Wabl Matthias R. 
Published: February 2007

AbstractThirteen hybridomas producing 2,4,6‐trinitrophenyl‐(TNP)‐specific mouse IgE of Iga or Igb haplotype are described. They are freely available. Monoclonal IgE, as well as polyclonal serum IgE, is shown to bind to concanavalin A.
Influence of IgG and IgM receptor triggering on human natural killer cell cytotoxicity measured on the level of the single effector cell
Authors: Merrill Jean E. , Ullberg Måns , Jondal Mikael 
Published: February 2007

AbstractBy using an agarose single cell cytotoxicity assay, in combination with rosetting with IgG‐ or IgM‐coated ox red blood cells for detection of Fc receptors for IgG (FcγR) or IgM (FcμR), it was found that 60% of natural killer (NK) cells are FcγR+ and 17% FcμR+. This system was further used to investigate the consequence of FcμR and FcγR triggering on NK killing as measured on the single effector cell level. It was found that stimulation of the FcγR, but not the FcμR, resulted in substantial NK inhibition. In order for NK cells to be inhibited by IgG‐coated ox red blood cells, they must first be exposed to the IgG‐containing complex prior to conjugation with the target. While exposure of the FcμR to immune complexes can block up to 57% of NK activity, the particulate immune complexes do not interfere with binding of effector cells to targets. Modulation of Fcγ R by capping at 37°C does not interfere with the NK inhibition for up to 3 h, though after 20 h, when FcγR+ cells are almost completely modulated, NK activity has fully returned. Although to a lesser extent, the soluble immune complex human transferrin‐anti‐transferrin also reduces NK cell activity when activating effector cell FcγR prior to target cell binding. Also, pretreatment of target cells with high concentrations of specific antibody toward membrane antigens can block NK activity while not inhibiting target cell binding as evidenced by anti‐IgM IgG binding to Daudi cells. The regulatory influence of the FcγR on the NK system is discussed in terms of other functions associated with this receptor and in terms of its possible biological significance.
The effect of second signals on the induction of B cell tolerance: failure of helper T cells to block tolerance induction
Authors: Cambier John C. , Corley Ronald B. 
Published: February 2007

AbstractThe effect of carrier‐primed helper T (Th) cells and T cell‐replacing factors on the induction of hapten‐specific tolerance in B cells from adult mice has been tested. The 2,4,6‐trinitrophenyl conjugate of human γ‐globulin (TNP17HGG) was used as tolerogen in an in vitro tolerance induction system. Tolerance was assessed by the subsequent induction of plaque‐forming cell responses using TNP‐Brucella abortus and trinitrophenylated sheep red blood cells (TNP‐SRBC) plus SRBC‐primed Th cells as T‐independent (TI) and T‐dependent (TD) forms of TNP, respectively. B cells that respond to the different forms of TNP appear to be distinct B cell subpopulations. TNP17HGG induced TNP‐specific tolerance in B cells responsive to TI and TD forms of the antigen, although more tolerogen was required to induce unresponsiveness in the TD antigen‐reactive B cells. The presence of antigen nonspecific T cell‐replacing factors during tolerance induction had no effect on the induction of unresponsiveness in either TI or TD antigen‐responsive B cells, although these factors were able to support primary anti‐TNP responses in T‐depleted B cell populations to subtolerogenic doses of TNP‐HGG. Populations of irradiated lymphocytes enriched for HGG‐specific Th cells also had no effect on tolerogenesis in TI or TD antigen‐responsive B cells, although priming of TD antigen‐responsive B cells occurred at subtolerogenic doses of tolerogen. The inability of these Th cells to modulate B cell unresponsiveness was not due to their inability to exert helper function at higher concentrations of HGG. Thus, in this system, tolerance susceptibility is an intrinsic property of B lymphocytes, i.e. immunogenicity vs. tolerogenicity of signals is not determined by a “second signal” provided by Th cells.
Concanavalin A‐induced resistance to Listeria monocytogenes and activation of macrophages: defect in mice treated with 89Sr
Authors: Masuda Aoi , Bennett Michael 
Published: February 2007

Abstract89Sr‐treated mice injected with concanavalin A (Con A) 24 h prior to infection with Listeria monocytogenes (LM) could not enhance the clearance of LM from the spleen. Adoptive transfer of normal syngeneic spleen cells together with Con A rendered these animals more resistant. Spleen cells of 89Sr‐treated or age‐matched control mice were stimulated with Con A for 24 h, and supernatant fluids were assessed for macrophage‐activating factor (MAF), i.e. the ability to activate resident peritoneal macrophages to kill LM intracellularly in vitro. A defective MAF production by spleen cells was observed in 89Sr‐treated, 2 week‐old, and athymic nude mice. Also, treatment of spleen cells with anti‐Thy‐1.2 antiserum plus complement inhibited MAF production. Synergism between spleen cells from 89Sr‐treated and nude mice did not occur. The cells required for MAF production were relatively resistant to gamma irradiation. Nylon wool filtration did not modify the ability of spleen cells to make MAF. 89Sr‐treated mice possess macrophages responsive to MAF derived from normal spleen cells. The data suggest that the failure of 89Sr‐treated mice to develop an anti‐LM response observed in this system could be due to a defective capacity to produce protective humoral factors and/or cells in response to Con A.
Two structurally distinct and independently regulated idiotypic families associated with the A/J response to azophenylarsonate
Authors: Marshak‐Rothstein Ann , Margolies Michael N. , Benedetto James D. , Gefter Malcolm L. 
Published: February 2007

AbstractAt least two distinct subpopulations of A/J anti‐azophenylarsonate (Ars) antibodies can be defined on the basis of serological cross‐reactivity and sequence homology of heavy and light chains. The most frequently occurring idiotype family, IdCR, was initially identified by a rabbit antiserum and is present only in A/J mice. Examination of several randomly selected hybridoma proteins which failed to express IdCR‐associated determinants revealed a second set of closely related molecules. The second idiotype family, Id36–60, is recognized by a rabbit antiserum prepared against the hybridoma protein 36–60. It is present in practically all A/J and BALB/c, but not B10.A Ars immune sera. On average, A/J immune sera contain approximately one‐fifth as much Id36–60 as IdCR.A/J mice can be suppressed for subsequent expression of either idiotype by neonatal injection of anti‐IdCR or anti‐Id36–60 antisera. Suppression of IdCR does not affect the production of Id36–60 and vice versa. Together, these idiotype systems provide two independent markers for monitoring network regulation of the anti‐Ars antibody response in A/J mice.
Genetic control of the expression of immunoglobulin isotypes in the responses of mice to sheep red blood cells
Authors: Haber Jerome , Winn Henry J. 
Published: February 2007

AbstractStudies have been carried out on the genetic control of the expression of individual Ig classes in the responses of A/J (A) and C57BL/6J (B6) mice to sheep red blood cells (SRBC). An isotopic anti‐immunoglobulin test employing Ig class‐specific reagents was used to measure levels of IgM, IgA, IgG1 IgG2a, IgG2b and IgG3 anti‐SRBC antibodies in sera of hyperimmunized mice. Compared with B6 mice, A mice are low IgM and IgA responders but high responders with respect to all IgG subclasses. In (B6 × A)F1 mice low responsiveness was dominant for all Ig classes indicating that IgM and IgA responses are controlled by genes different from those which control IgG subclass responses. Analysis of the responses of [(B6 × A)F1 × A] and [(B10. A × A)F1 × A] backcross mice indicates multigenic control of IgG subclass responses. Expression of IgG2a and IgG3 responses appear to be regulated largely by single genes whose action is modified by genes at other loci; control of IgG1 and IgG2b is, clearly, polygenic with no evidence for major control by any single gene. The magnitude of all IgG subclass responses appears to be regulated by a gene(s) associated with or linked to the IgCH locus. Analysis of the responses of H‐2‐congenic mice shows that major histocompatibility genes do not have a strong influence on the patterns of IgM and IgG responses in A or B6 mice. The overall results indicate that while there is some common control of all IgG classes, there is also separate polygenic control of individual Ig classes.
Non‐H‐2‐associated genetic regulation of cytotoxic responses to hapten‐modified syngeneic cells Effect on the magnitude of secondary response and helper T cell generation after in vivo priming
Authors: Fujiwara Hiromi , Shearer Gene M. 
Published: February 2007

AbstractThe present study investigates the role of non‐H‐2 genes in controlling generation of the H‐2‐restricted, T cell‐mediated cytotoxic response against trinitrophenyl (TNP)‐modified syngeneic cells (TNP‐self). Spleen cells from C3H/He (H‐2k) or B10.BR (H‐2k) normal mice or from mice primed to TNP in vivo by skin painting with trinitro‐chlorobenzene were used (a) for in vitro sensitization to TNP‐self and (b) as a source of radioresistant helper cells for augmenting the TNP‐self cytotoxic T lymphocyte (CTL) response generated by normal syngeneic spleen cells. Although spleen cells from unprimed mice from these two strains exhibited a comparable CTL response in a primary culture, a strong difference was observed in a secondary CTL response after in vivo priming. CTL activities generated in the secondary culture were much stronger in C3H/He than in B10.BR strains. This difference in the magnitude of secondary CTL responses was paralleled by generation of strong and weak helper cell activity in C3H/He and B10.BR, respectively. No detectable difference was observed between the two H‐2k strains in the lysability of target cells and ability of stimulating cells to activate the primed unirradiated cells and radioresistant helper cells. This genetic difference detected in the H‐2k haplotype was also demonstrated in the H‐2b haplotype, by using C3H.SW and C57BL/10 mice which bear non‐H‐2 background genes corresponding to C3H/He and B10.BR mice, respectively. These results indicate the existence of a control mechanism influenced by non‐H‐2 genes, in addition to the established H‐2‐linked gene control.
Role of β1H for the binding of C3b‐coated particles to human lymphoid and phagocytic cells
Authors: Schmitt Manfred , Mussel Hans‐Hermann , Hammann Klaus P. , Scheiner Otto , Dierich Manfred P. 
Published: February 2007

AbstractCoating of EAC14oxy23b with highly purified human serum β1H globulin (β1H) led to acceleration of rosette formation with human peripheral blood lymphocytes (PBL), tonsil lymphocytes, B lymphoblastoid (Raji) cells, granulocytes and monocytes. This reaction was discernible from C3bi‐dependent rosette formation. Enhancement of rosette formation of C3b cells by β1H was most effective at limiting amounts of C3 per EAC14oxy23b. The β1H effect was not due to trace contamination with C3b inactivator. β1H‐dependent rosette formation with the various lymphoid and phagocytic cells could be suppressed by the F(ab′)2 fragment of anti‐β1H suggesting β1H‐mediated binding of β1H‐coated particles to complement receptor‐positive (CR+) cells.In turn, binding of fluid‐phase β1H to lymphoid and phagocytic cells could be demonstrated by fluorescence and by 14C‐labeled β1H. In addition, the functional status of these cells with respect to their receptor reactivity was altered.Treatment of normal lymphocytes (PBL, tonsil lymphocytes) and of granulocytes with β1H improved their rosette formation with both EAC14oxy23b and EAC14oxy23b‐β1H. The reaction of monocytes was hardly affected. The β1H effect on Raji cells resulted in reduced rosette formation with EAC14oxy23b‐β1H, while binding of EAC14oxy23b remained unchanged.These results suggest the presence of sites on CR+ cells, to which soluble and particlebound β1H can bind, leading to alteration of the functional status of the cells. In all likelihood, EAC14oxy23bi can attach to the β1H‐binding sites on CR+ cells.
Decline, in aging mice, of the anti‐2, 4, 6‐trinitrophenyl (TNP) cytotoxic T cell response attributable to loss of Lyt‐2−, interleukin 2‐producing helper cell function
Authors: Miller Richard A. , Stutman Osias 
Published: February 2007

AbstractThe in vitro generation of cytotoxic T lymphocytes (CTL) specific for 2, 4, 6‐trinitrophenyl (TNP)‐modified syngeneic spleen cells is found to be almost invariably depressed in apparently healthy 18‐month‐old mice of the long‐lived (BALB/c × C57BL/6)F1 hybrid strain. Studies of CTL production from Lyt‐2+ thymus cells have suggested that pre‐killer cells may require, for maturation into effectors, the presence of a soluble helper factor, interleukin 2 (IL2), produced by Lyt‐2− cells which are themselves devoid of pre‐CTL activity. We have therefore developed a petri‐dish adherence technique for separating spleen cells into Lyt‐2+ and Lyt‐2− populations in order to test for helper and pre‐killer activity independently. Pre‐CTL function is measured by stimulating Lyt‐2+ cells in the presence of exogenous IL2. Helper cell activity is tested by adding Lyt‐2− cells to “indicator” populations of Lyt‐2+ pre‐CTL. Estimation of IL2 levels in medium conditioned by unfractionated, TNP‐self‐stimulated splenocytes provides a second measurement of helper cell function.Mice 18 months of age, when compared to 4 month‐old controls, are found to retain nearly all of their pre‐CTL activity, but to have lost sufficient helper cell activity to account for the decline in unseparated spleen cell cultures. Older mice also produce lower IL2 levels.