The Journal of molecular and cellular immunology : JMCI最新文献

{"title":"B-cell transplants to immunodeficient xid neonates do not imprint their helper T cells.","authors":"J Quintans,&nbsp;G A Wemhoff","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A great variety of Igh-restricted immunoregulatory phenomena have been described in responses to both haptens and carriers. The investigation of Igh-dependent T-cell functions is of considerable interest because it relates to issues such as the interdependence of the T- and B-cell networks, isotope- and idiotype-specific help, the role of Igh-linked products in the generation of the helper and cytolytic T-cell repertoires and Igh-linked effects on cell interactions among helper and suppressor cells. Helper T cells have been shown to be critically susceptible to B cell-mediated education and it is generally assumed that T cells become imprinted by B-cell idiotypes during development. It occurred to us that xid immunodeficient neonates, which lack T15+ B cells and T15 antibodies, might provide a suitable host to investigate the B-cell dependent imprinting of T cells providing help in T15+ anti-PC responses. We designed our experiments to test whether or not T15 deficient xid mice could be used as recipients of normal B cells capable of imprinting the host's helper cells. The results of our experiments demonstrate that unirradiated xid neonates are readily engrafted with normal B cells from both neonatal and adult donors. The transplanted B cells reconstitute anti-PC and anti TNP-FICOLL PFC responses in the xid hosts. However, the early engraftment of T15+ B cells in xid mice did not cause a detectable imprinting of their helper T cells, i.e., we could not detect any biases in the preference of carrier-/primed cells from reconstituted mice for primary or secondary T15+ or T15- B cells.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 2","pages":"97-103"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14111986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential induction of class II gene expression in murine pre-B-cell lines by B-cell stimulatory factor-1 and by antibodies to B-cell surface antigens.","authors":"B S Polla,&nbsp;J Ohara,&nbsp;W E Paul,&nbsp;N Nabavi,&nbsp;A Myer,&nbsp;H C Liou,&nbsp;F W Shen,&nbsp;S Gillis,&nbsp;J V Bonventre,&nbsp;L H Glimcher","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have previously reported that BSF-1 and an alloantibody to the B-cell differentiation antigen Lyb2 induce class II gene expression in two Ia negative pre-B-cell lines. Two questions were asked in these studies. The first question is whether the different stimuli which we and others have shown to induce class II expression in B-cells act via the same signal transduction mechanisms. The second question is whether the traditionally accepted pathway of B-cell differentiation, as defined by immunoglobulin (Ig) gene rearrangement, is applicable to other events that occur during B-cell differentiation. In this report, we have therefore examined a large panel of pre-B-cell lines at different stages of Ig gene rearrangement in an attempt to 1) identify the stage in B-cell development where class II gene expression occurs and where it becomes inducible by BSF-1 or anti-Lyb2, and 2) compare the signal transduction mechanisms used by these ligands. The majority of pre-B-cell lines tested did not express BSF-1 receptors and were consequently noninducible for class II by BSF-1; such cell lines were, however, inducible for class II expression by anti-Lyb2 and, in addition, by antibodies to the B220 membrane glycoprotein. The induction of class II molecules by BSF-1 and by anti-Lyb2 and anti-B220 differed in several respects: 1) Induction by anti-Lyb2 and anti-B220 did not require the presence of BSF-1 receptors; 2) BSF-1 selectively induced class II antigen expression while anti-Lyb2 and anti-B220 induced the expression of other surface markers as well; and 3) PGE2 inhibited BSF-1 but not antibody-mediated class II induction. Finally, the presence of receptors for BSF-1 and the baseline expression of cell surface Ia was shown to be unlinked to Ig gene rearrangement and expression in this series of pre-B-cell lines. The independent regulation of Ia and Ig genes observed here may reflect a branching rather than a linear pathway for B-cell differentiation. The differentiation of pre-B-cells to mature Ig-secreting cells should probably not be defined solely by rearrangement of Ig genes, since this is likely to represent an oversimplified view of B-cell differentiation.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 6","pages":"363-73"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14282109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of human IL 1 alpha and beta messenger RNAs and IL 1 activity in human peripheral blood mononuclear cells.","authors":"S Demczuk,&nbsp;C Baumberger,&nbsp;B Mach,&nbsp;J M Dayer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The macrophage-derived lymphokine interleukin 1 (IL 1) plays a critical role in modulating immune (cellular and humoral) and nonimmune responses. For example, the relative expression of IL 1 alpha and beta under various states may be crucial to the success of the immune system in response to infection. Until recently, a comparative study of IL 1 mRNA expression and IL 1 biological activity was not possible. We have cloned both IL 1 alpha and beta cDNAs and employed them as probes in Northern blot analysis to determine in mitogen-stimulated peripheral blood mononuclear cells the steady-state expression of their cognate mRNAs with respect to IL 1 activity. IL 1 was determined by the lymphocyte-activating factor (IL 1/LAF) and the mononuclear cell factor (IL 1/MCF) activities. In lectin-stimulated PBMC, maximum cell-associated activities whereas detected at 12 and 24 hr after stimulation whereas maximum extracellular activities appeared between 24-48 hr. In the same cultures, the kinetics of IL 1 mRNA steady-state expression were determined by Northern gel blot analysis with IL 1 alpha and beta cDNA probes. IL 1 mRNAs were undetectable in noncultured freshly isolated PBMC (time zero). Both IL 1 mRNAs appeared as early as 4 hr after lectin stimulation as did IL 1 beta mRNA in unstimulated cultures. Both IL 1 alpha and beta mRNA steady-state levels were barely detectable by 48 hr. At all time points, IL 1 mRNA levels were considerably lower in unstimulated cultures. IL 1 beta mRNA was always considerably more abundant than IL 1 alpha mRNA. The less abundant IL 1 alpha mRNA showed a decrease in its stead-state levels prior to the reduction in the levels of IL 1 beta mRNA. TNF alpha activity and mRNA were not detected under these culture conditions. Poly(A) + RNA injected into Xenopus oocytes revealed that the Northern blot detected IL 1 mRNAs were biologically active. To understand the precise nature of IL 1 in immune and nonimmune events, we felt it necessary to first study the kinetics of IL 1 mRNA steady-state levels with respect to its cell-associated and extracellular biological activities. The data presented here may allow for a better understanding of the etiology of various immune and nonimmune responses that are modulated through the expression of IL 1.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 5","pages":"255-65"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14633167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of murine B cells from different tissues with different mitogens. II. Isotype distribution of secreted immunoglobulins in the presence and absence of IL-4-containing T cell supernatants.","authors":"A Bossie,&nbsp;K H Brooks,&nbsp;P H Krammer,&nbsp;E S Vitetta","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In the accompanying report, we have compared a B cell-specific protein mitogen, Salmonella thyphimurium mitogen (STM), to lipopolysaccharide (LPS), dextran sulfate (DxS), and the combination of LPS/DxS with regard to their ability to induce B cell proliferation and differentiation. The results of these studies demonstrated that STM, LPS, and LPS/DxS induce significant expression of cytoplasmic immunoglobulin (Ig). In this report, we have analyzed the distribution of isotypes induced by each of these mitogens in the presence or absence of interleukin-4 (IL-4) containing T cell supernatants (SN), since IL-4 increases the secretion of IgG1 and IgE and decreases the secretion of IgG3 and IgG2b in LPS-stimulated splenic B cells. These experiments were designed to determine whether LPS was unique in its ability to \"program\" B cells to respond to IL-4 by secreting IgG1, as has been suggested in our previous studies. The current experiments also addressed the issue of whether splenic B cells were unique in their response to IL-4 by using B cells from other tissues. The efficiency of induction of cytoplasmic Ig measured in the preceding report was STM greater than LPS/DxS greater than LPS. DxS did not induce a significant level of cell proliferation, cytoplasmic Ig, or secreted IgM and inhibited the LPS-induced IgM response by approximately 50%. In contrast, STM induced an extremely high level of IgM secretion in splenic B cells. In this report, we demonstrate that the addition of IL-4-containing T cell SN to splenic B cells stimulated with LPS, LPS/DxS or STM increased the level of IgG1 and reduced the level of IgM, IgG3, and IgG2b secretion.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 4","pages":"221-6"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14634024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of murine B cells with Salmonella typhimurium mitogen (STM), lipopolysaccharide (LPS), and dextran sulfate (DxS). I. Cell-cycle analysis and induction of cytoplasmic immunoglobulin.","authors":"K H Brooks,&nbsp;E S Vitetta","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>There have been two recent reports concerning a B cell-specific mitogen that induces proliferation, but not differentiation of rat and human B cells. This mitogen, which is derived from Salmonella typhimurium (STM), appears to be providing the signals required for anti-immunoglobulin-treated (anti-Ig) B cells to enter cycle and divide, but may not be inducing responsiveness to B cell differentiation factors (BCDF). In this report, we have compared STM to the other known murine B cell polyclonal activators: lipopolysaccharide (LPS), dextran sulfate (DxS), and the combination of LPS/DxS. STM was the most potent stimulus of B cell proliferation as determined by uptake of 3H-thymidine, viable cell numbers and cell cycle analysis utilizing acridine orange (AO). STM did not induce significant proliferation of murine T lymphocytes. In addition, the proliferative effect of STM on B cells shows minimal, if any, macrophage dependence. However, in contrast to its effect on human and rat B cells, STM induces differentiation of murine B cells. The levels of cytoplasmic Ig induced by STM are equivalent or greater to those induced by LPS/DxS. Thus, in the murine system, STM will be useful as a polyclonal activator which induces proliferation and differentiation of the vast majority of the B cell population without stringent accessory cell requirements.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 4","pages":"215-9"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13619377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of help and contrasuppression as essential prerequisites for immune response.","authors":"G Andrighetto,&nbsp;M Zöller","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The network theory proposes the immune system as a self-centered defense mechanism, which continuously maintains a steady state of activity via idiotypic-anti-idiotypic interactions. In line with this hypothesis, the steady state of the immune system has been described to represent a status of suppressed activity, response being manifested by release from suppression. There is evidence that release from suppression is initiated by activation of contrasuppressor cells (TCS), which either transfer a state of resistance towards suppression on helper T-cells (TH) or interact directly with suppressor T-cells (TS). In the latter case, it was postulated that the nominal antigen of contrasuppressor T-cells are antibodies and that TS and TCS interact one with the other via idiotypic-anti-idiotypic structures. The present report examined the role of TCS in initiation of response and proved that the responding state requires activation of TH as well as TCS. While antigenic stimulation (TNP) resulted in concomitant activation of TH and TCS, it was possible to dissect these two prerequisites for response by application of a monoclonal anti-TNP antibody (AB) carrying a recurrent idiotype (Sp6) followed by application of a subimmunogenic dose of the nominal antigen. Clonal analysis of regulatory cells via limiting dilution (LD) cultures revealed that a subimmunogenic dose of antigen led to activation of help but failed to activate TCS. On the other hand application of AB, which did not initiate response, resulted in activation of TCS, but not in activation of TH, i.e., these were not released from suppression. However, consecutive activation of TCS via AB and of help via a subimmunogenic dose of antigen moved the immune system into the responding state. Activation of TCS via AB was found to be independent from the mode of application, i.e., free AB, AB coupled to syngeneic cells, or AB coupled to the nominal antigen, although most straightforward results were obtained with free AB, since syngeneic cells exerted an additional suppressive effect, and AB-antigen (TNP) conjugates activated TNP-specific TH as well as TCS. Furthermore, AB-induced activation of TCS was independent of the recipient's age. Yet, the effect was most pronounced when AB were applied neonatally, i.e., after a hyporesponsive stage, animals were hyperreactive towards the nominal antigen, and this hyperreactivity was initiated by expansion of TCS. This extends the notion of high idiotypic connectivity in the neonatal period to the level of regulatory T-cells.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 4","pages":"199-214"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14111817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The C mu gene is transcribed in IgG bearing B lymphocytes.","authors":"E A Weiss,&nbsp;P W Tucker,&nbsp;D Yuan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>During the maturation of an immune response, some IgM bearing B lymphocytes differentiate into IgG secreting cells. Similarly, a subset of normal B cells cultured in the presence of a mitogen will develop into IgG synthesizing cells, many of which continue to express IgM. The experiments described in this paper utilize such IgG3 expressing B cells present in mitogen-stimulated cultures to address the continuing controversy over the molecular mechanism(s) allowing simultaneous expression of IgM and isotypes other than IgD. Nascent transcripts were labelled in vitro in order to determine whether the C mu gene was still transcribed in these cells. If no mu transcription was detected, then this would suggest that the mu chain protein, in cells expressing both IgM and IgG3, must be derived from translation of long-lived mu mRNA. Alternatively, detection of continued mu gene transcription would provide direct evidence for alternate processing of pre-mRNA transcripts encoding both mu and gamma gene sequences. The membrane IgG3+ (mIgG3+) cells were isolated from mitogen-stimulated cultures by staining and then sorting on a Fluorescence Activated Cell Sorter (FACS). Prior to examining mu gene transcription in these cells, it was necessary to ascertain the purity of the sorted population. Accordingly, restaining of the sorted IgG3+ cells showed only a minor contamination by mIgM+IgG3- cells. Additionally, the majority of the mIgG3+ cells were also mIgM+. Most importantly, it was then demonstrated that the IgG3 detected on the cells was intrinsic to them rather than cytophilically adsorbed. By biosynthetic labelling, the sorted IgG3+ population was found to also actively secrete both IgM and IgG3. Examination of transcription showed that the IgG3+ cells were indeed transcribing the mu exons and were doing so at about 50% the level of an equal number of unseparated cells. It was determined that this level of C mu transcription is significantly higher than that which could be derived from the contaminating cells. Thus, it is clear that at least some IgG3 expressing cells have not deleted the C mu gene and therefore the gamma 3 mRNA in a portion of the cells expressing both IgM and IgG3 must be derived from pre-mRNA transcripts which contain both C mu and C gamma 3 sequences.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 2","pages":"69-81"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14281076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lymphoma models for B cell activation and tolerance. V. Anti-Ig mediated growth inhibition is reversed by phorbol myristate acetate but does not involve changes in cytosolic free calcium.","authors":"D W Scott,&nbsp;D Livnat,&nbsp;J Whitin,&nbsp;S B Dillon,&nbsp;R Snyderman,&nbsp;C A Pennell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>B cell lymphomas which can be growth inhibited by crosslinking their surface IgM receptors by anti-Ig reagents provide models for normal B cell regulation and tolerance. WEHI-231 and CH31 are two independently derived lines that are exquisitely sensitive to negative signalling by antibodies specific for mu or kappa chains, but are unaffected by antibodies against MHC class 1 or 2 antigens. In order to determine the mechanism of this growth inhibition as a model for tolerance, we have examined the roles played by protein kinase C activation and calcium mobilization/influx during negative signalling in these cells. We found that growth inhibition caused by anti-mu crosslinking was reversed in the presence of either phorbol myristate acetate (PMA) or by lipopolysaccharide (LPS) from E. coli. The effect of PMA on negative signalling was a true reversal since phorbol esters could be added after anti-mu treatment, thus allowing nearly normal cellular progression into the S phase of the cell cycle. In contrast, pretreatment with PMA did not provide protection against the growth inhibition from anti-mu. Indeed, a \"desensitization\" protocol demonstrated that PMA pretreatment actually decreased reversal by both PMA and LPS of the effects of anti-mu on B lymphoma growth. These studies suggest that both LPS and PMA act via at least one common intermediate, which is assumed to involve activation and translocation of protein kinase C. Analysis of changes in calcium ion concentration after treatment with anti-Ig reagents showed both mobilization from internal stores and influx via calcium channels in WEHI-231, as has been reported for normal B cells. However, these changes did not correlate with negative signalling for the several reasons. Firstly, anti-mu inhibition of the growth of WEHI-231 could be induced in the relative absence of extracellular Ca++ or in quin-2 loaded (buffered) cells. Secondly, pretreatment with high concentrations of PMA ablated calcium mobilization, yet failed to modulate growth inhibition in WEHI-231 cells. Moreover, LPS provided protection from the effects of anti-mu yet did not alter cellular [Cai++]. In addition, PMA posttreatment (under conditions causing a reversal of the effects of anti-mu) can be applied as long as four hours after the initial exposure to anti-mu and the rapid measurable changes in calcium flux. Indeed, such changes in intracellular free calcium occurred in elutriated WEHI-231 lymphoma cells at all phases of the cell cycle, although we have previously identified early G1 as the only critical period in which negative signalling can be delivered.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 2","pages":"109-20"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14634021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation and use of an antigen-specific hybrid to study B-cell function.","authors":"R B Bankert,&nbsp;E A Repasky,&nbsp;P K Mazzaferro,&nbsp;R T Kubo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Several important events are known to occur following the crosslinking of membrane-associated immunoglobulin (mIg) on B-lymphocytes. Among these include the internalization and re-expression of mIg. We have addressed two questions regarding the re-expression of mIg following an antigen-induced clearance of this B-cell receptor. 1) How long does it take for a cell to re-express its receptors after the first or second exposure to antigen, and 2) is this re-expression dependent upon the synthesis of new mIg? These questions, which in the past have been addressed primarily with heterogeneous populations of cells and using anti-immunoglobulin instead of antigen, are vital to understanding B-cell activation as well as antigen processing events. In order to address these questions, we have produced and characterized an antigen-specific B-cell hybrid 2C3E1 that expresses a membrane-associated form of immunoglobulin. A hybrid specific for a charged hapten (phthalate) was selected to avoid the possibility of nonspecific hydrophobic interactions of the binding ligand with the plasma membrane. After establishing the presence of mIg biochemically and demonstrating the ability of phthalate-keyhole limpet hemocyanin to induce the clearance of the phthalate-specific receptor from the plasma membrane, it was determined that re-expression of antigen-specific receptors was detected within one hour and completed by six hours after the first or second pulse with antigen and that this re-expression did not require the synthesis of new receptors. This later finding is novel and suggests that B-cell receptors are re-utilized or that a presynthesized pool of mIg exists within the cytoplasm of these cells. During the characterization of the 2C3E1 cell line, it was determined that this hybrid also produced a secreted form of the phthalate-specific immunoglobulin (sIg). An unexpected subsequent observation was that sIg was found associated with the cell surface in addition to membrane Ig. A likely source of this unexpected surface-associated sIg was observed as a vesicle on the surface of many cells that is associated with a high concentration of sIg. This finding and its possible relevance to Ig secretion per se are considered further in the paper which follows this one.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 5","pages":"279-91"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14633168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A helper T cell clone produces an antigen-specific molecule (T-ABM) which functions in the induction of suppression.","authors":"D R Green,&nbsp;B Chue,&nbsp;H G Zheng,&nbsp;T A Ferguson,&nbsp;K D Beaman,&nbsp;P M Flood","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Among Ly-1+,2-T cells there appears to be two independent modes of antigen recognition. Helper and cytotoxic Ly-1 T cells recognize antigen only in the context of I region products whereas regulatory T cells, such as T suppressor inducer cells, produce antigen-specific, antigen-binding molecules (T-ABM). These T-ABM often have been found to form a part of biologically active, antigen-specific regulatory factors. A number of environmental conditions effect whether a foreign antigen will produce a positive response leading to immunity or a negative one leading to tolerance. Many of the conditions which favor the induction of suppressor T cells simultaneously preclude the proper interaction of antigen presenting cells with helper T cells. This parallel led us to ask whether helper T cells perform at least two, apparently opposite functions: a) under conditions favoring immunity helper T cells produce lymphokines to activate immune effector cells, and b) under conditions favoring suppression they produce molecules which function in suppressor cell induction. Therefore, this question relates to the mechanisms by which an immune response is switched into either a positive (help) or negative (suppressive) track. In addition, it begins to address the relationship between the different modes of antigen recognition exhibited by helper T cells vs. T suppressor inducer cells (see above). To explore this problem we employed an antigen-specific, I-Ak restricted helper T cell clone as the purest available source of helper T cells. We presented antigen to the cloned T cells under conditions which favor suppression rather than help (for example, by ultraviolet irradiation of the antigen-presenting cells) and collected supernatants 48 hrs later. The supernatants were then examined for activity in a functional assay for antigen-specific suppressor factors. Our results indicate that under conditions favoring suppression, a T-ABM was produced which functioned in the antigen-specific induction of suppression in vitro. The T-ABM had the same antigen specificity as that exhibited by the helper T cell and was therefore probably derived from the clone. This observation introduces the possibility that the interaction between antigen-presenting cells and helper T cells is a crucial decision point in the immune response which can lead to either immunity or suppression. The latter would be achieved through the production, by helper T cells, of an antigen-specific component of T suppressor inducer factor (i.e., the T-ABM). The possible relationship between T-ABMs and the T cell receptor is discussed.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"3 2","pages":"95-108"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14111814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}