bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal antibodies against HLA‐DR antigens acting on stimulator cells prevent OKT8+ T lymphocytes from acquiring sensitivity to interleukin 2 and expressing suppressor function
Authors: Palacios Ronald , Guy Keith , Van Heyningen Veronica 
Published: February 2007

AbstractPurified OKT8+ but not OKT4+ T lymphocytes generated suppressor activity in autologous mixed lymphocyte reactions (AMLR) in the presence but not in the absence of interleukin 2 (IL 2) as determined in proliferative responses of peripheral blood mononuclear cells induced by Concanavalin A, the OKT3 monoclonal antibody and allogeneic cells (indicator systems for suppressor activity used in this study). Furthermore, treatment of AMLR‐activated T cells with the OKT8 antibody plus complement abolished suppressor cell activity whereas treatment of the cells with the OKT4 antibody plus complement did not.The three monoclonal anti‐HLA‐DR antibodies used in this study abrogated the induction, but not the effector phase, of suppressor cells in AMLR. The anti‐DR antibodies acted specifically on the stimulator non‐T cells and not on the responder T cells. The addition of IL2 to AMLR cultures performed in the presence of the anti‐DR antibodies did not restore or increase the suppressor activity whereas IL2 added to AMLR cultures exposed to control antibodies or medium alone increased the suppressor activity. Moreover, purified OKT8+ T cells cocultured with autologous non‐T cells and IL2, in the presence of the anti‐DR antibodies, neither responded to IL2 by proliferating nor expressed suppressor function. In contrast, OKT8+ T cells from similar cultures, but performed in the absence of the anti‐DR antibodies or exposed to control antibodies, proliferated to IL2 stimulation and exhibited suppressor activity. Unactivated OKT8+ T cells were unresponsive to IL2 and unable to express suppressor function. Finally, the addition of the OKT8 antibody (in the absence of complement) to AMLR cultures had no effect on the generation of suppressor cells.From these results, we conclude the following: (a) OKT8+ T lymphocytes become sensitive to IL2 by interacting with HLA‐DR antigens on the stimulator non‐T cells and, with the help of IL2, they express suppressor cell activity; (b) the OKT8 antigenic determinant on AMLR‐activated suppressor cells does not seem to participate in their process of activation; (c) results of previous studies showing that OKT4+ T lymphocytes become sensitive to IL1 and are capable of synthesizing IL2 after interaction with HLA‐DR on the stimulator cells, and the findings presented here, lead us to suggest that both OKT4+ and OKT8+ T lymphocytes possess receptors for self HLA‐DR antigens and that neither the OKT8 nor the OKT4 antigenic determinants on these cells are involved in the recognition of HLA‐DR antigens. The suppressor activity generated in AMLR may be one mechanism whereby effector self‐tolerance is maintained in the face of inductive self‐recognition.
A spleen‐thymus interaction is involved in the tolerization of thymocytes to xenogeneic erythrocytes
Authors: Bunce Judi V. , Mason Donald W. 
Published: February 2007

AbstractPrevious work has shown that thymocytes of rats receiving two i.v. injections, 4 days apart, of large numbers of xenogeneic erythrocytes become tolerant of the injected cells whereas peripheral T cells in the same recipients make a vigorous response to the injected antigen. Results are herein presented of experiments on the effect of splenectomy on the induction of thymocyte tolerance produced in this way. Splenectomy performed either immediately before the first injection of erythrocytes, or between the two injections, completely prevented tolerance induction and tolerance was still incomplete when splenectomy was performed as late as a few hours after the second injection of tolerogen. Sham splenectomy had no effect on the erythrocyte‐induced thymocyte tolerance. The results demonstrate an essential role for the spleen in the tolerization of thymocytes in this system. Possible mechanisms and the implications for self tolerance are discussed.
Defective induction of antigen‐reactive proliferating T cells in B cell‐deprived mice II. Anti‐μ treatment affects the initiation and recruitment of T cells
Authors: Ron Yacov , De Baetselier Patrick , Tzehoval Esther , Gordon Julius , Feldman Michael , Segal Shraga 
Published: February 2007

AbstractMice injected from day of birth onwards with rabbit anti‐mouse IgM (anti‐μ) antibodies were found to be B cell‐deficient and defective for the induction of antigen‐reactive proliferating T cells (TPRLF). This defective induction was not due to the absence of circulating antigen‐specific antibodies since the daily injections of such antibodies during exposure to antigen did not restore the ability of anti‐IgM treated animals to generate TPRLF. Analyzing the cellular events implicated in the induction of virgin antigen‐reactive T cells, anti‐μ‐treated mice manifested impairment of the three interacting cell types involved in the induction of TPRLF. Thus, peritoneal and splenic antigen‐presenting cells from such animals were impaired in their capacity to signal a primary antigen‐specific T cell reaction. Their splenic lymphocytes could not function as initiator cells in transferring immunogenic signals to recruit TPRLF in normal recipients. Potent antigen‐specific splenic initiator cells failed to induce the recruitment of specific TPRLF in anti‐μ‐treated mice. The defective induction of TPRLF in anti‐μ‐treated mice may be due to a functional impairment of cells expressing membranebound IgM molecules which seemingly play a central role in the transfer of immunogenic signals for the recruitment of antigen‐specific circulating T cells. We suggest that splenic B cells function as initiators in the transfer of antigen‐induced signals from peritoneal antigen‐presenting cells to T cells. These seems to be the primary targets of anti‐μ treatment.
A highly conserved determinant on human rheumatoid factor idiotypes defined by a mouse monoclonal antibody
Authors: Pasquali Jean‐Louis , Urlacher Arlette , Storck Daniel 
Published: February 2007

AbstractDifferent human IgM rheumatoid factor (IgM RF) idiotypes have been described defined by polyclonal rabbit anti‐idiotypic antibodies. These antisera do not allow clear genetic analysis of the idiotypic determinants, be they cross‐reactive or private. Therefore, we tried to obtain a set of monoclonal anti‐idiotypic antibodies directed against RF idiotypes. Purified IgM RF serum from a patient with classical rheumatoid arthritis was used to immunize BALB/c mice. The spleen cells were fused with Sp 2/0 Ag 14, a nonsecreting mouse myeloma cell line, and a hybrid producing monoclonal anti‐idiotypic antibody was selected. The mouse antibody, an IgG1 x, reacts with an identical or similar determinant located on (or close to) the binding site of all tested monoclonal or polyclonal IgM RF from totally unrelated patients with Waldenströms's macroglobulinemias or rheumatoid arthritis. The monoclonal antibody also reacts with 2 rheumatoid arthritis patients' IgG RF and with a low proportion of normal polyclonal IgM without detectable RF activity. An hypothesis is proposed to explain the existence of a such highly conserved determinant on RF idiotypes.
A human lymphocyte‐associated antigen involved in cell‐mediated lympholysis
Authors: Hildreth James E. K. , Gotch Frances M. , Hildreth Phyllis D. K. , McMichael Andrew J. 
Published: February 2007

AbstractHuman lymphocyte function antigen (HLFA) is a cell surface protein defined by two monoclonal antibodies MHM23 and MHM24. It is present on both B and T lymphocytes but in greater amounts on the latter. Both antibodies precipitated antigen, from radiolabeled HSB‐2 cells, which ran as two chains on sodium dodecyl sulfate polyacrylamide gel electrophoresis at 180 and 94 kDa. Neither antibody inhibited binding of the other, indicating that distinct epitopes were recognized. Both antibodies were shown to inhibit HLA‐restricted lysis of influenza virus‐infected and Epstein‐Barr virus‐transformed target cells by cytotoxic T lymphocytes. Blocking occurred at the level of the effector cells and in the presence of subsaturating concentrations of antibody. Both reagents also inhibited lysis of K562 cells, mediated by natural killer cells. These blocking effects differ from the inhibitory effects of monoclonal anti‐HLA ABC and anti‐suppressor cytotoxic T cell antibodies which inhibit only HLA‐restricted lysis when present in saturating amounts. It is concluded therefore that HLFA is likely to be involved in the nonspecific adherence or lytic functions of killer cells rather than specific antigen recognition.
Clonal anergy: Inhibition of antigen‐driven proliferation among single B lymphocytes from tolerant animals, and partial breakage of anergy by mitogens
Authors: Pike Beverley L. , Abrams Judith , Nossal G. J. V. 
Published: February 2007

AbstractMice were injected with fluoresceinated human gamma globulin (FLU‐HGG) either at 2–3 days of age or as pregnant females. At 2 weeks of age, the spleen cells of the injected suckling mice or offspring were fractionated on FLU‐gelatin dishes to yield FLU‐binding B cells. These B cells were then cloned in microcultures using one of two recently described systems in which single B cells grow in the absence of feeder or filler cells, namely following stimulation with FLU‐polymerized flagellin (FLU‐POL) and conditioned media containing B cell growth and differentiation factor(s); or mitogenic activation by a mixture of E. coli lipopolysaccharide (LPS) and dextran sulfate (DxS). As such cultures permit visualization of clonal proliferation as well as ultimate harvesting of cultures for assay of hemolytic plaque‐forming cells, it was possible to ask whether the lesion in the tolerant state affected the B cell's capacity to divide, to differentiate to antibody secretion, or both.The results indicated that, when stimulated with antigen, the anergic cells could neither divide nor differentiate. However, when the strong mitogen mixture was used, clonal anergy was partially broken. The cells proliferated, and a small proportion of them differentiated into anti‐FLU antibody‐forming cells. A marked variation in antigen‐binding avidity of the FLU‐binding cells made it difficult to quantitate the degree of uncoupling of proliferation and differentiation among tolerant, LPS plus DxS‐stimulated cells. Nevertheless, a partial reversibility of clonal anergy must affect views on mechanisms of self‐tolerance.
Production of human immune interferon (Hu IFN‐γ) studied at the single cell level. Origin, evidence for spontaneous secretion and effect of cyclosporin A
Authors: Palacios Ronald , Martinez‐Maza Otoniel , De Ley Marc 
Published: February 2007

AbstractA reverse hemolytic plaque assay has been developed which specifically detects secretion of human immune interferon (Hu IFN‐γ) at the single cell level. Unstimulated peripheral blood lymphocytes from healthy adult volunteeers spontaneously secreted IFN‐γ. Stimulation of these cells with concanavalin A, phytohemagglutinin, or the UCHT1 monoclonal anti‐human T cell antibody significantly increased the number of IFN‐γ‐secreting cells. The cell producing IFN‐γ, both spontaneously and after UCHT1 antibody stimulation, is an OKT3+, 4+,8−,HLA‐DR− T lymphocyte as determined at the single cell level. Finally, cyclosporin A, a potent and selective immunosuppressive drug for T cells, strongly inhibited the secretion of IFN‐γ as assayed at the cell level. This IFN‐γ reverse hemolytic plaque assay has great potential for the further study of IFN‐γ both in physiological and pathological conditions.
Detection of interspecies idiotypic cross‐reactions associated with antibodies to hepatitis B surface antigen
Authors: Kennedy Ronald C. , Ionescu‐Matiu Irina , Sanchez Yanuario , Dreesman Gordon R. 
Published: February 2007

AbstractA common idiotype was defined by a rabbit anti‐idiotypic antiserum generated against human antibodies to hepatitis B surface antigen (anti‐HBs). This idiotype was detected in anti‐HBs from eight different individuals who had been previously infected with hepatitis B virus and is referred to as the CHBs idiotype. The CHBs idiotype was also identified in sera from rabbits, mice, guinea pigs, swine, goats and chimpanzees that had been immunized with hepatitis B surface antigen (HBsAg). Expression of the CHBs idiotype in sera from other species was associated with anti‐HBs molecules. These results suggested that variable‐region genes responsible for the CHBs idiotype have been conserved through long periods of evolution. It was noteworthy that the CHBs idiotype was not detected in the sera of a nonmammalian species, chickens, that had been successfully immunized with HBsAg.
Modulation of B and T cell subsets in mice treated with fractionated total lymphoid irradiation. III. Spleen and thymus dependency of B cell maturation processes
Authors: Zan‐Bar Israel 
Published: February 2007

AbstractThe role of spleen and thymus in maturation processes of B cell subpopulations was examined using mice which underwent fractionated total lymphoid irradiation (TLI). (BALB/BL)F1 mice received 200 rds lymphoid irradiation daily for 8 days. Mice were spleen‐shielded or ‐unshielded, or thymus‐shielded or ‐unshielded during the irradiation. One day after termination of the irradiation, TLI‐treated unshielded mice were reconstituted with 10 × 106 spleen, thymus or bone marrow cells of normal untreated syngeneic mice. Two and a half months after termination of the treatment, the ability of the treated mice to produce in vivo anti‐trinitrophenyl (TNP)‐Ficoll antibodies, and the capability of spleen cells of those mice to respond in vitro to dextran sulfate and lipopolysaccharide was checked. In parallel, stained spleen cells were analyzed on the fluorescence‐activated cell sorter. The results indicate that B cell maturation occurs only in mice where the spleens were shielded during TLI‐treatment or in TLI‐treated mice reconstituted with spleen cells of normal untreated mice. In these mice, the light scatter and the fluorescence distribution profiles were the same as those obtained from spleen cells of control mice: the treated mice gave a high anti‐TNP‐Ficoll antibody response and the proliferative response of the cells was low to dextran sulfate and high to lipopolysaccharide.Thymus shielding during TLI treatment or reconstitution of TLI‐treated mice with thymus or bone marrow cells could not abolish the blockage of B cell maturation processes. These findings indicate that the spleen plays an obligatory role in B cell subset maturation pathways, whereas the thymus appears to play no essential role in these processes.
Quantitation of anti‐NP (4‐hydroxy‐3‐nitrophenyl)‐acetyl idiotype expression on spleen and thymus cells
Authors: Wall Katherine A. , Frackelton A. Raymond , Reilly Edward B. , Azuma Takachika , Chang Tse‐Wen , Eisen Herman N. 
Published: February 2007

AbstractDirect binding of 125I‐labeled rabbit anti‐NPb idiotype antibodies (RaId) was used to quantitate the expression by immune spleen and thymus cells of NPbId, the characteristic Id of the λ1‐containing antibodies made by C57BL/6 (B6) mice to the (4‐hydroxy‐3‐nitrophenyl)acetyl (NP) group. Direct binding of RaId by B and T cell preparations reached a maximum of 12 ng RaId per 108 cells at 7 days after immunization. Spleen T cell preparations maintained similar levels of binding after positive selection for Thy‐1.2+ cells and overnight culture. RaId binding was also demonstrated for immune B6 thymus cells and for spleen and thymus cells of immune SJL mice, which have the appropriate heavy chain allotype for NPbId expression but have only barely detectable serum Id. However, the NPbId of T and B cell preparations were indistinguishable by (a) the susceptibility of RaId binding by the cells to inhibition by hapten or by antibodies to the variable regions of λ light chains (anti‐Vλ) and by (b) the ability of anti‐Vλ and of monoclonal antibodies to the constant region of λ1 chains (anti‐Cλ1) to immunoprecipitate antigen (NP10‐bovine serum albumin)‐binding proteins from detergent extracts of isotopically labeled cells. The results strongly imply that virtually all of the NPbId of T cell preparations is due to conventional NPbId antibody that is tightly bound to T cells. The results do not, however, exclude the possibility that the T cell preparations contain a trace amount (≤ 1 ng/108 cells) of unusual NPbId‐like molecules that lack λ chains.
A monoclonal antibody against a new differentiation antigen of thymocytes
Authors: Sidman Charles L. , Forni Luciana , Köhler Georges , Langhorne Jean , Lindahl Kirsten Fischer 
Published: February 2007

AbstractB14−2−14 is a monoclonal cytotoxic IgM antibody which reacts with thymocytes of all mouse strains tested. The fraction of positive cells (by visual immunofluorescence) varies between strains from about 25–45% in A. CA to 65–85% in C57BL/6, and high levels are dominant in F1 hybrids. In the periphery, the antigen is found on a few percent of lymph node and not on splenic T cells, and it is absent in nude mice. Among thymocytes, the distribution of the B14 determinant largely overlaps with that of the TL antigen and of molecules binding peanut agglutinin. The B14 antibody reacts only minimally with hydrocortisone‐resistant thymus cells. Biochemical analysis shows that B14 antibody, anti‐TL antibody and peanut agglutinin bind to separate molecules. The target of the B14 antibody may be either an immature, thymic form of Thy‐1, or another molecule associated with it. Two polypeptides, of 40 and 35 kDa are precipitated by both B14 and anti‐Thy‐1 antibodies from biosynthetically labeled thymus cell lysates, and two others, of 27 and 17 kDa, from surface‐iodinated thymus cell preparations. B14‐2‐14 offers an additional method for identification and selection of thymocytes at different stages of differentiation, and should also be useful for studies of the Thy‐1 antigen.
Specific in vivo and nonspecific in vitro alloreactivities of adult frogs (Xenopus laevis) that were thymectomized during early larval life
Authors: Nagata Saburo , Cohen Nicholas 
Published: February 2007

AbstractThymectomy of very young Xenopus larvae abrogated in vitro proliferative responses to phytohemagglutinin (PHA) and allogeneic leukocytes. Thymectomized (Txd) frogs, however, still rejected first‐set skin allografts chronically and second‐set grafts (but not third‐party grafts) more rapidly. The specific second‐set rejection reaction by Txd frogs was transferable in vivo to secondary Txd hosts (with major histocompatibility complex identical to the cell donor) by the subcutaneous injection of a mixture of splenic and peripheral blood leukocytes. Spleen cells used in this adoptive transfer experiment (i.e., immune cells) were responsive to allogeneic cells from the original donor strain as well as from unrelated donors in mixed leukocyte culture in vitro but were still unreactive to PHA. The results are consistent with an extrathymic pathway of alloreactive cell differentiation in this species, although the physiological significance of such a pathway is not clear.
Characterization of the cytolytic activity of a cloned antigen‐specific T suppressor cell derived from a tolerant CBA/J mouse
Authors: Heuer Joachim , Opalka Bertram , Rassat Jürgen , Themann Hermann , Kölsch Eckehart 
Published: February 2007

AbstractThe antigen‐specific T suppressor cell clone HF1 isolated from a CBA/J mouse made tolerant by low doses of bovine serum albumin has suppressive and cytolytic activity. The analysis of the latter gave the following results. Natural killer (NK)‐sensitive YAC‐1 (H‐2a) and RBL‐5 (H‐2b) target cells are lysed whereas other NK targets, like EL4 (H‐2b) or the human K562 cell line are resistant. Cytolytic activity is not antibody mediated. Its inhibition by sugar phosphate or monoclonal antibodies against LFA‐1 antigens is such that HF1 can neither by typed as T killer nor as NK cells. It seems to represent a distinct T lymphocyte type.
Genetic control of the response of chicken T lymphocytes to concanavalin A: cellular localization of the low responder defect
Authors: Pink J. Richard , Vainio Olli 
Published: February 2007

AbstractGenetic variation in the response of chicken lymphocytes to the T cell mitogen concanavalin A (Con A) has previously been studied by assaying tritiated thymidine ([3H]dThd) uptake of cultured cells following mitogen stimulation. Our present results show, firstly, that low [3H]dThd uptake (e.g. in cultures of Con A‐stimulated cells from low responder CB, CC or G‐B1‐lo birds) is correlated with low proliferative activity and with reduced capacity to form Con A‐dependent T cell colonies in semisolid agar. Secondly, in cultures containing mixtures of cells from high and low responder birds, the cells from each partner respond independently to Con A (there is neither suppression of high responder, nor activation of low responder cell proliferation). Finally, Con A‐stimulated cultures of high responder cells respond better to T cell growth factors, as well as producing more growth factor activity, than cultures of low responder cells. These results suggest that the basis for the low responder phenotype is an intrinsic inability of low responder T lymphocytes to respond to Con A by differentiating into growth factor‐sensitive blast cells.
The role of accessory cells in polyclonal T cell activation II. Induction of interleukin 2 responsiveness requires cell‐cell contact
Authors: Hünig Thomas 
Published: February 2007

AbstractIt has previously been reported (Hünig, T. et al., Eur. J. Immunol. 1983. 13: 1) that highly purified peripheral T cells do not respond to concanavalin A (Con A) even in the presence of Con A‐induced spleen cell supernatant as a source of interleukin 2 (IL2). In the present report, the hypothesis was tested whether this unresponsiveness correlates with the observed inability of Con A to mediate cell‐cell contact between highly purified T cells. It was found that T cells, pretreated with neuraminidase to reduce their net negative charge, were both aggregated and rendered IL2‐reactive by Con A. In addition, leukoagglutinin (LA) was found to be able to both agglutinate untreated T cells and to make them IL2‐reactive. Neuraminidase treatment reduced the concentration of LA required to mediate both effects. Neuraminidase treatment did not alter the overall Con A‐binding capacity of T cells, nor did it induce reactivity to IL2 in the absence of lectin. Furthermore, irradiated, neuraminidase‐treated T cells served as accessory cells (AC) in the induction of responsiveness to IL2, but not for production of IL2, which depends on Ia+ AC. Finally, Lyt‐2− neuraminidasetreated peripheral T cells responded in the same fashion as whole T cell populations, indicating that at least some T cells of the helper phenotype need not interact with Ia+ AC for the induction of IL2 responsiveness.