bluuebunny/crossref_metadata_2025_split huggingface dataset:
T helper cell‐dependent induction of resting B cell differentiation need not require cognate cell interactions
Authors: Julius Michael H. , Rammensee Hans‐Georg 
Published: March 2007

AbstractWe have analyzed the role of cognate interaction with helper T cells (Th) in support of resting B cell differentiation to plaque formation. Co‐culture of histoincompatible resting B cells and resting Th cells resulted in the induction of plaque‐forming cells when dimeric but not monomeric fragments of anti‐T cell receptor (TcR) antibody were added to culture. The efficiency of B cell activation was comparable to that supported by lipopolysaccharide and lectin‐mediated Th‐B cell conjugate formation. Further, if resting Th cells were preactivated with antigen and histocompatible antigen‐presenting cells, the requirement for addition of anti‐TcR to mixtures of histoincompatible Th and B cells was obviated. These results demonstrate that TcR‐mediated Th recognition of major histoincompatibility complex class II/antigen composites on the resting B cell membrane does not provide obligate signals for B cell differentiation to plaque formation. We are left with two possibilities. Either the entire process of Th cell‐dependent induction of resting B cell differentiation is mediated by soluble lymphokines or if Th‐B cell contact is mandatory, it is mediated through nonpolymorphic cell surface determinants.
Genetics and strain distribution of concanavalin A‐reactive Ly‐2‐, L3T4‐ peripheral precursors of autoreactive T cells
Authors: Morisset Jean , Trannoy Emanuelle , Talance Anne De , Spinella Sylviane , Debré Patrice , Godet Philippe , Seman Michel 
Published: March 2007

AbstractCytotoxic treatment of BALB/c cells from different peripheral lymphoid tissues by a cocktail of monoclonal antibodies against Thy‐1, Ly‐1, L3T4 and Ly‐2 differentiation markers (anti‐T cocktail) plus complement eliminates all mature T lymphocytes. Yet a population of dull Thy‐1+, Ly‐1‐, L3T4‐, Ly‐2‐, corresponding to about 1% of the initial population, can be detected by flow cytometry which proliferate under concanavalin A stimulation. These anti‐T killing‐resistant cells (TKR) were previously shown to be capable of differentiating in culture into class II‐restricted autoreactive T helper cells. We demonstrate here that such cells can be detected in mice of BALB/c and DBA/2 genetic background but are absent in C57BL/6 and B10 animals. The presence of TKR cells is dominant in (BALB/c X C57BL/6)F1 hybrids and genetically controlled by two genes which are neither H‐2 nor Igh linked. TKR cells are also detected in young NZB mice but disappear with the development of the systemic autoimmune disease in old animals. Thy‐1+, L3T4‐, Ly‐2‐ cells from MRL lpr/lpr mice also respond to concanavalin A but are removed by the anti‐T treatment. Altogether, arguments are presented suggesting that TKR cells represent a particular subset of double‐negative peripheral T cells which may correspond to autoreactive T cell precursors that would escape the thymic selection. We postulate that these cells are present in all mouse strains but their susceptibility to killing by anti‐Thy‐1 antibodies differs depending on background genes.
Analysis of CD3 and antigen receptor expression on T cell subpopulations of aged athymic mice
Authors: Lawetzky Alexandra , Hünig Thomas 
Published: March 2007

AbstractThe expression of the T cell antigen receptor on subpopulations of extrathymically generated T cells from athymic mice was investigated and compared to antigen receptor expression in normal mice. To this end, spleen and lymph node cells from 18 individual athymic BALB/c nu/nu mice between 6 and 12 months of age and from normal controls were enriched for T cells by nylon wool filtration. Expression of the following cell surface markers was analyzed by two‐color flow cytometry: Thy‐1, CD4, CD8, Vβ8 and CD3. The distribution of subpopulations as defined by these markers varied much more among athymic than among normal mice. Some recurrent patterns did, however, occur that may be characteristic of the extrathymic pathway of T cell differentiation in nu/nu mice.Among Thy‐1.2+ cells, CD8+ cells predominated over CD4+ cells. No CD4+8+ “double positive” cells were found, but CD4‐8‐ “double negative” cells constituted 16% on average. All nu/nu nylon wool‐nonadherent cells expressing Thy‐1 at a normal level also expressed CD3, whereas Thy‐1low and Thy‐1‐ cells were CD3‐. The fraction of Vβ8 T cells among the CD4+ and CD8+ subsets was near to normal in the majority of these animals. Most interestingly, the density of Vβ8 and CD3 expression was lower in athymic than in euthymic animals. This level of T cell antigen receptor expression was, however, higher than on immature CD4+8+ thymocytes.A fraction of the nude T cells presently characterized responded with proliferation to both anti‐T cell receptor Vβ8 monoclonal antibody and to concanavalin A. Despite their apparently normal phenotype (with the exception of reduced T cell receptor expression), this response was, however, 4 to 10 times smaller than that of normal control cells. The presently described Thy‐1+ T cell receptor intermediate cells may either be a(n) aberrant lineage(s) only generated extrathymically, or represent the accumulation of an immature intermediate stage of normal (i.e. thymic) T cell differentiation.
Growth‐dependent variation of major histocompatibility complex (MHC) restriction and expression of Ly‐2 and CD3/α/βT cell receptor in cloned cytotoxic T cells
Authors: Weltzien Hans Ulrich , Kempkes Bettina , Studer Roland , Melchers Inga , Eichmann Klaus 
Published: March 2007

AbstractThe specificity of major histocompatibility complex (MHC)‐restricted antigen recognition by cytotoxic T cells (CTL) has been clearly correlated to the α/β T cell receptor (TcR) complex on the T cell surface. Occasional changes in the specificity of in vitro cultivated CTL clones, therefore, have been suspected to result from alterations of the genes coding for the TcR α and/or β chain. Here we demonstrate that pronounced variations in the stringency of MHC restriction, previously reported to occur during long‐term culture of 2,4,6‐trinitrophenyl (TNP)‐specific CTL clones, may occur rapidly in a growth‐dependent, reversible manner, i.e. without structural TcR variation. Several H‐2b TNP‐specific CTL clones were shown to possess strong cross‐reactivity for H‐2b TNP target cells when seeded at low cell numbers, but exhibit reduced or undetectable cross‐reaction to H‐2k TNP in high‐density cultures. Another clone revealed “heteroclitic” properties with sinificantly stronger cytotoxic activity towards allogeneic (H‐2k) than syngeneic (H‐2b) TNP‐modified target cells. In this case dilute cultures appeared as exclusively allo‐MHC restricted, whereas dense cultures were allo/self cross‐restricted.In all instances these phenomena were accompanied by cell density‐dependent quantitative changes in the expression of Ly‐2 and T cell antigen receptor. CTL from dilute cultures had at least 2‐fold higher surface concentrations of Ly‐2 and CD3 antigens than cells from dense cultures while other surface markers such as Thy‐1 or LFA‐1 were completely identical. No such effects were observed for CTL clones exhibiting cell density‐independent specificity patterns. We conclude from these findings that (a) the stringency of MHC restriction specificity may be significantly affected by the amount of expressed TcR and/or Ly‐2 molecules, (b) CTL possess mechanisms to regulate Ly‐2 and TcR expression and, hence, their MHC‐restricted antigen recognition, and (c) the ability to regulate Ly‐2 and TcR expression may be altered during prolonged culture of a CTL clone.
Specific antigedantibody complexes induce the in vivo production of a parallel set of nonantigen‐binding idiotype‐positive antibodies
Authors: Caulfield Michael J. , Cerny Jan 
Published: March 2007

AbstractImmune complexes prepared with the polysaccharide antigen (PnC) extracted from Streptococcus pneumoniae R36a and two different PnC‐specific antibodies were found to differ in their regulatory properties depending on the isotype of the antibody. Thus, complexes formed in antibody excess with TEPC15 (IgA) were suppressive whereas complexes formed with 96‐G (IgG3) antibodies enhanced the IgM response to PnC. During the course of these studies, we found that little or no PnC‐specific IgG antibody was induced during the response to PnC coupled to sheep red blood cells (PnC‐SRBC). Interestingly, however, immunization with 96‐G/PnC complexes either alone or with PnC‐SRBC resulted in the induction of IgG3 antibodies that express the TI5 idiotype (Id) but which do not bind PnC. This unique IgG3 response occurred after injection of 96‐G/PnC complexes formed in antibody excess but not when complexes were formed in antigen excess. The Id+ nonspecific IgG3 response peaked on day 5 and could be activated with 96‐G/PnC complexes but not with free PnC antigen. The Id+ nonspecific response was not due to polyclonal activation of IgG3 production since there was no difference in IgG3 levels in mice injected with 96‐G/PnC complexes with those injected with PnC‐SRBC. Finally, mice that had been suppressed for expression of the T15 Id by neonatal injection of anti‐Id antibody were able to produce Id+‐unspecific IgG3 antibody after immunization with 96‐G/PnC complexes, further suggesting that Id+ IgG3 was produced by different clones than those that usually comprise the antibody response to PnC. The results suggest that the formation of IgG immune complexes during an immune response may result in stimulation of idiotypically related clones thus resulting in degeneracy of the immune response.
The major surface protein of leishmania promastigotes is a fibronectin‐like molecule
Authors: Rizvi Farrukh S. , Ouaissi Mohamed Ali , Marty Béatrice , Santoro Ferrucio , Capron André 
Published: March 2007

AbstractThe major surface glycoprotein of Leishmania chagasi promastigotes showed cross‐reactivity with fibronectin (Fn), a large glycoprotein that is a major constituent of the extracellular matrix of most mononuclear cells. Polyclonal and monoclonal antibodies against Fn precipitated two molecules of 63‐58 kDa from the lysates of both 125I and [35S]methionine‐labeled promastigotes. In addition, a monoclonal antibody against a 15‐kDa fragment of Fn containing the Arg‐Gly‐Asp‐Ser (RGDS) sequence and several polyclonal monospecific mouse antibodies against a synthetic RGDS peptide also recognized the above two molecules. The attachment of Leishmania promastigotes to mouse peritoneal macrophages in vitro was partially inhibited when promastigotes were treated with F(ab')2 fragment of an anti‐Fn IgG. Identical results were obtained by saturating the Fn receptors on macrophages using different peptides containing the RGDS sequence. Moreover, antigen preparations rich in glycoprotein 63 could efficiently promote the attachment and spreading of 3T3 mouse fibroblasts to surfaces coated with the antigen. These results clearly suggest that the gp63 of L. chagasi promastigotes is an Fn‐like molecule that shares certain biological and molecular characteristics with Fn.
A cd3− subset of cd4−8+ thymocytes: a rapidly cycling intermediate in the generation of cd4+8+ cells
Authors: MacDonald H. Robson , Budd Ralph C. , Howe Rawleigh C. 
Published: March 2007

AbstractT lymphocytes with the surface phenotype CD4+8− and CD4−8+ are considered to be representative of functionally mature cells. We show here that adult murine thymus contains a subpopulation of CD4‐8+ cells that differ from CD4−8+ cells found d the periphery in that they do not express the T cell receptor‐associated CD3 molecular complex. Such CD3−4−8+ thymocytes are cortisone sensitive and rapidly cycling in situ. Furthermore, in contrast to mature T cells, most CD3−4−8+ thymocytes express low levels of CD5 and high levels of the B2A2 antigen. CD3−4−8+ thymocytes fail to respond to a variety of mitogenic stimuli in vitro but do give rise upon short‐term culture to CD4+8+ cells. It is suggested that CD3−4−8+ thymocytes represent a transitional stage of thymus differentiation between the CD4−8− and CD4+8+ compartments.
T cell epitopes in experimental autoimmune myasthenia gravis of the rat: strain‐specific epitopes and cross‐reaction between two distinct segments of the α chain of the nicotinic acetylcholine receptor (torpedo californica)
Authors: Zhang Yiping , Barkas Tom , Juillerat Marcel , Schwendimann Bernhard , Wekerle Hartmut 
Published: March 2007

AbstractT cell epitopes on the nicotinic acetylcholine receptor (AChR) of Torpedo californica were analyzed using T cell lines isolated from Lewis, BN, and (Lewis x BN)F1 rats. All lines selected for reactivity against either native or denatured AChR or for 6 selected synthetic peptides of the AChR α chain expressed the CD4 membrane phenotype and recognized their antigen in the context of major histocompatibility complex class II determinants. They were tested in vitro for reactivity with each of these antigens. The results indicate that parental Lewis and BN rat T lymphocytes recognize distinct molecular epitopes on the AChR protein, whereas (Lewis X BN)F1 hybrids respond against both sets of epitopes.Two peptides (P10 and P11) which represent distinct amino acid sequences on the putatively extracellular part of the AChR α chain, and which share only 4 common amino acids, two of them contiguous, showed an unexpected cross‐reactivity in the Lewis rat. T cells selected for either peptide co‐recognize the other peptide in vitro. In addition, these cells are responsive against full length AChR. P11, in particular, appears to be a major epitope for Lewis rats immunized with AChR.
Inverse correlation between the utilization of an idiotype in specific immune responses and its representation in pre‐immune “natural” antibodies
Authors: Portnoi Denis , Lundkvist Inger , Coutinho AntÓNio 
Published: March 2007

AbstractPreviously we have characterized an idiotype (Id) that accounts for half of all specific anti‐dextran B512 (Dex) antibodies in C57BL/6 mice. BALB/c mice produce the same Id in normal, pre‐immune sera but fail to use it in antibody responses to Dex, although Id+ anti‐Dex antibodies can be induced in this strain by anti‐Id immunization. By limiting dilution analysis of B cellclonal precursors, we show here that the frequencies of Id+ B cells are comparable in both strains, but their state of activity is sharply distinct: while all Id+ B cells are small, resting lymphocytes in C57BL/6 mice, they are all large, naturally activated cells in BALB/6 mice. The suggestion that naturally activated cells are poorly engaged in specific responses was supported by the delayed and lower Id+ responses obtained in BALB/c mice when they are immunized, in parallel with C57BL/6 animals, with a conjugate of anti‐Id antibodies and lipopolysaccharide. Finally, C57BL/6 responder mice were found to closely reproduce the normal BALB/c situation, if analyzed 3 months after anti‐Id priming: they produce low levels of serum Id and all Id+ B cells are in the large lymphocyte compartment. Upon immunization these animals develop serum Id+ responses that are undistinguishable from low‐responder BALB/c mice. The relevance of these observations for the questions of physiologic self‐reactivity is discussed.
An adjunct trait of hel/i‐ab‐specific t helper cell is sensitivity to antigen‐specific immunosuppression
Authors: Araneo Barbara A. , Dowel1 Tad , Bertelsen Karin 
Published: March 2007

AbstractThe present study tests whether the specific inhibition of helper T (Th) cell (and T hybridomas) by suppressor T (Ts) cells is a phenotypic trait of Th cells correlating with their acquired specificity for antigedmajor histocompatibility complex or a genotypic trait not related to selection of the T cell repertoire for antigen. To do this we took advantage of the fact that H‐2d parental strains of mice commonly restrict recognition of chicken egg‐white lysozyme to the L3 peptide (a.a. 105‐129) and H‐2b parental mice to the L2 peptide (a.a. 13‐105). F1 hybrids of these strains display two subsets of lysozyme‐reactive T cells, one for each parental phenotype. Using (B10 x B10.D2)Fl mice reconstituted with B10.D2 bone marrow, we were able to develop genetic H‐2d T cell clones that could express an atypical specificity, that is L2/I‐Ab. Clones of this type, like genetic H‐2b, are also sensitive to the inhibiting effects of HEL‐activated T, cells. To overcome some of the drawbacks of using heterogeneous populations of T, B and accessory cells in our assays, we constructed T hybridomas from HEL‐immune, chimeric lymph node T cell blasts which respond to a unique antigedmajor histocompatibility complex with production of the lymphokine interleukin 2. Our results indicate that all HEL/I‐Ab‐specific T cells (helper and hybridomas) are inhibited by suppression regardless of the T cell's haplotype at the H‐2 locus: H‐2b (B10), H‐2d (D2) or H‐2b,d (BDF1). Furthermore, there is a strict correlation between the antigen and I‐A specificity: I‐Ab‐restricted T cells recognize non‐L3 determinants even though some are derived from H‐2d mice.
B cell growth and differentiation activity of interleukin‐hp1 and related murine plasmacytoma growth factors. synergy with interleukin 1
Authors: Vink Anne , Coulie Pierre G. , Wauters Pierre , Nordan Richard P. , Snick Jacques Van 
Published: March 2007

AbstractIt was recently shown that T cells, macrophages and fibroblasts produce growth factors for B cell hybridomas and plasmacytomas. These factors were subsequently identified as members of a new family of cytokines on the basis of NH2‐terminal amino acid sequence analyses. Using T cell‐derived interleukin‐HP1 (HP1), purified to homogeneity, as the prototype of this family, we examined the effects of these molecules in conventional polyclonal B cell activation assays with anti‐immunoglobulin antibodies or dextran sulfate as co‐stimulators.In the absence of other cytokines, the only significant effect of HP1 was to stimulate moderately the proliferation of anti‐immunoglobulin‐activated B cells. By contrast, in conjunction with interleukin 1, HP1 became a major growth and differentiation factor not only for B cells activated with anti‐immunoglobulin antibodies but also for dextran sulfate‐stimulated and even for unstimulated B cells. In fact, with respect to cell proliferation or IgM synthesis, the IL1‐HP1 combination proved to be equivalent to B cell stimulatory factors like IL4 or IL5.This B cell stimulatory activity was not due to the presence of a contaminant in the HP1 preparation because it was also observed with purified plasmacytoma growth factors derived from macrophages and fibroblasts, and could be inhibited by a monoclonal anti‐HP1 antibody.
Epitopes recognized by human t lymphocytes on malaria circumsporozoite protein
Authors: Sinigaglia Francesco , Guttinger Maria , Gillessen Dieter , Doran Daniel M. , Takacs BéLa , Matile Hugues , Trzeciak Arnold , Pink J. Richard 
Published: March 2007

AbstractThe circumsporozoite protein of the malaria parasite Plasmodium falciparum contains regions of nonrepetitive sequences which are predicted to be T cell recognition sites. We synthesized peptides corresponding to three of these regions, and tested their ability to stimulate proliferation of peripheral blood lymphocytes from donors living in a malaria‐endemic area, or from nonimmune donors. Cells from 15 out of 22 donors (including 4 of 6 nonimmune individuals) were stimulated by one or more of the peptides. T cell clones specific for one of the peptides were obtained and shown to recognize the native protein purified from sporozoites. These data help to identify T cell epitopes which could be incorporated into a malaria vaccine.
Functional evidence that intercellular adhesion molecule‐1 (icam‐1) is a ligand for lfa‐1d‐ependent adhesion in t cell‐mediated cytotoxicity
Authors: Makgoba M. William , Sanders Martin E. , Luce Gale E. Ginther , Gugel Ellen A. , Dustin Michael L. , Springer Timothy A. , Shaw Stephen 
Published: March 2007

AbstractAlthough intercellular adhesion molecule‐1 (ICAM‐1) has been implicated as a ligand in some LFA‐1‐dependent adhesion, its importance to T cell function has not been established. The present studies investigate the importance of ICAM‐1 for human cytotoxic T lymphocytes (CTL), both in their formation of antigen‐independent conjugates (AIC) and in their lysis of targets. Analysis of monoclonal antibody (mAb) inhibition of AIC formation indicate that ICAM‐1 mAb 1 blocks (a) AIC formation with some but not all targets; (b)the LFA‐1 pathway but not the CD2LFA‐3 pathway of adhesion; (c) by binding to the target cell, not the T cell. In studies of cell‐mediated lysis (CML) ICAM‐1 mAb inhibited lysis of some targets, such as U‐937, that use ICAM‐1 predominantly in AIC formation; CML on some other targets is not inhibited by ICAM‐1 mAb. These data indicate that ICAM‐1 is a ligand for AIC formation, antigen‐specific CTL recognition and cytolysis of particular target cells. The data also indicate that ICAM‐1 is not used in LFA‐1‐dependent CTL interactions with all kinds of target cells, suggesting the existence of alternative ligands for LFA‐1.
Synergistic activation of human t cells by interleukin 1 and interleukin 6
Authors: Houssiau FrédéRic A. , Coulie Pierre G. , Olive Daniel , Snick Jacques Van 
Published: March 2007

AbstractPurified human interleukin 6 (IL 6) was found to stimulate the proliferation of human tonsillar and peripheral rosetting T cells subliminally activated with phytohemagglutinin (PHA). This response seemed independent of IL2 but highly dependent on the presence of accessory cells. Indeed, when accessory cell‐depleted tonsillar T cells were activated with PHA and exposed to IL6, only minimal proliferations were observed. A similar result was obtained with IL1. However, a combination of these two cytokines induced strong proliferations, indicating that IL 1 and IL 6 play a synergistic role in the interactions between accessory cells and T lymphocytes.
The relative contributions of immune system and target organ to variation in susceptibility of rats to experimental allergic thyroiditis
Authors: Eishi Yoshinobu , Mccullagh Peter 
Published: March 2007

AbstractPrevious investigations of the cellular basis of genetic susceptibility to experimental allergic thyroiditis (EAT) in semi‐allogeneic mice bearing thyroid grafts from resistant, parental strain donors have indicated that these grafts remain relatively resistant to EAT when this is induced in the susceptible bearer. It was concluded that genetic control of susceptibility to EAT is expressed in both the immune system and the thyroid gland.Our experiments in which thyroid grafts were transferred to fully allogeneic, but immunologically tolerant, recipient rats indicate that thyroid tissue from an EAT‐resistant strain of rat becomes entirely susceptible when transplanted into a susceptible host. The differing susceptibility of thyroid grafts in semi‐allogeneic and tolerant allogeneic hosts may result from restrictions on interaction between host lymphocytes and the graft in the former situation. The present findings call into serious doubt the proposition that genetically determined resistance to EAT is mediated, to any extent, at the level of the target organ.