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

{"title":"Class II MHC molecules are spontaneously internalized in acidic endosomes by activated B cells.","authors":"D A Weber,&nbsp;L B Buck,&nbsp;T M Delohery,&nbsp;N Agostino,&nbsp;B Pernis","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The antibody response to protein antigens requires specific cooperation between B and T cells. In order to deliver the helper signal, T cells must recognize, in the context of Class II MHC, processed antigen on the membrane of B cells. Processed antigen is in the form of peptides bound in a given site of the Class II MHC molecule; in order to address the question of where, in the B cell, the complex of Class II MHC and processed antigen is formed, we studied the subcellular localization of these two molecules. Since the formation of this complex is the crucial step in antigen processing and presentation, the answer to this question is central to the whole problem of the physiology of antigen handling by B cells. To collect information pertinent to the question, we have compared, in B cells, the intracellular traffic of Class II MHC and of monovalent and divalent anti-immunoglobulin antibodies used as protein ligands of the membrane immunoglobulins. We have done so by two-color immunofluorescence microscopy, and we have detected extensive confluence of Class II MHC molecules with the immunoglobulin ligand, both mono- and bi-valent, in the endosomes of LPS-activated murine B cells. Whereas the ligand clearly reaches the endosomes by internalization from the cell membrane, the Class II MHC molecules could reach the same location either by endocytosis from the membrane or through targeting to the endosomes of newly synthesized Class II MHC molecules. We have collected quantitative evidence for endocytosis of Class II MHC by following, with the fluorescence activated cell sorter, the quenching of the fluorescence of fluoresceinated Fab' anti Class II MHC in LPS-activated murine B cells; this quenching indicates the entry of the label into an acidic intracellular compartment. Together with the results of others, obtained with different methods, our observations support the concept that, at least in mature activated B cells, Class II MHC molecules reach the organelles where they meet processed protein antigens, mainly through the endocytic route. Since activated B cells endocytose their membrane Class II MHC, and not their membrane Class I, our results contribute to the understanding of how B cells present antigens, that have bound to their membrane immunoglobulins, to Class II-restricted helper T cells and not to Class I-restricted cytolytic T cells.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 5","pages":"255-66; discussion 266-8"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13324073","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 CD5+ B cell hybridoma derived factor(s), which induces maturation of CD5+, idiotype-specific B-cell populations.","authors":"M Gibson,&nbsp;J A Hardin,&nbsp;D H Sherr","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A number of investigators have demonstrated the association of CD5+ (Ly-1/Leu-1) B cells with autoimmunity, excessive B-cell proliferation, and transformation. Previous work from our laboratory, among others, suggests that the selective advantage of this frequently autoreactive B-cell subset is to provide activation signals to conventional antigen-specific B cells. If one current hypothesis is correct then the overrepresentation of CD5+ B cells in some diseases and their novel capacity to act as helper cells reflect the activities of a separate B-cell lineage. Because of these observations it is of particular interest to evaluate the factors which contribute to the maturation of the CD5+ B-cell subset. The possibility that CD5+ B cells produce a factor or factors capable of influencing their own development was the focus of the present investigation. Rather than attempt to obtain soluble factors from heterogeneous CD5+ B-cell populations which could be contaminated with cytokine secreting monocytes or which could require as yet undefined activation signals in order to secrete putative factors, we chose to evaluate the production of CD5+ B-cell inducing factor(s) by monoclonal CD5+ B-cell hybridomas. Added incentive to this approach was provided by the observation that these hybridomas elaborate a factor(s) which, together with (NPb) idiotype-specific antibody produced by the hybridoma, substitutes for CD5+ B-cell populations in activating antigen-specific (NPb idiotypic) B cells in vitro. Furthermore, because of the low percentage of CD5+ B cells in the spleen and their relatively low level of CD5 antigen expression, we employed a sensitive functional assay rather than surface antigen expression alone to detect small numbers of mature CD5+ B helper cells. With this previously described system it was possible to observe the induction of functional CD5+ B cells following a 40 h culture of apparently CD5- B-cell populations with a 19-22 kd factor or factors derived from a CD5+ B hybridoma. Data presented here and elsewhere suggest that this CD5+ B-cell inducing activity is not mediated by IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IFN-gamma, GM-CSF, or TNF. The role that such a B cell derived, B-cell directed factor may play in immunity and disease is discussed.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 5","pages":"241-51; discussion 251-3"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12862591","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":"Adrenocorticotropin (ACTH) functions as a late-acting B cell growth factor and synergizes with interleukin 5.","authors":"K H Brooks","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In recent years there has been considerable discussion of possible cross-regulatory mechanisms involving the immune system and the neuroendocrine system. Certainly, evidence of hormonal communication between these two systems would provide at least a partial explanation for the many anecdotal observations of physical and mental stress affecting disease course. In previous studies of a neoplastic lymphokine-responsive B cell clone, BCL1-3B3, we noted that these cells produced a lymphokine which could affect normal B cell growth and viability. Physical characterization of this lymphokine indicated that its molecular weight was identical to that of the neuroendocrine hormone adrenocorticotropin (ACTH). Since Blalock and colleagues had reported the production of ACTH by virally-infected B cells, we have investigated whether ACTH can functionally mimic the BCL1-3B3-derived lymphokine. The neuroendocrine hormone adrenocorticotropin (ACTH) can increase in vitro murine B lymphocyte proliferation when added at physiologically relevant concentrations between 10(-9) to 10(-11) M. ACTH does not mimic the action of any lymphokine known to be required for B cell proliferation such as IL-2, IL-4, or IL-5. ACTH requires the presence of one or more of these known B cell stimulatory factors for its action and the most marked increase in B cell proliferation were noted in assays for IL-5 activity where 10(-10) M ACTH increased thymidine incorporation up to five-fold. Using two-stage assays, we determined that ACTH acts during the latter stages of B cell activation (i.e., 3-4 days after initial stimulation with either the combination of IL-4, GAMIg-Sepharose, and IL-1 or the combination of DxS and IL-5). These data indicate a direct role for a stress-induced neuroendocrine hormone in modulating the course of a humoral immune response.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 6","pages":"327-35; discussion 335-7"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13122228","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":"Isolation and characterization of NK cell or NK/T cell-specific cDNA clones.","authors":"J P Houchins,&nbsp;T Yabe,&nbsp;C McSherry,&nbsp;N Miyokawa,&nbsp;F H Bach","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Natural killer (NK) cells are cytotoxic lymphocytes that share numerous cell surface antigens and functional components with T cells. However, in comparison with our knowledge of T cells, little is known about the molecular mechanisms of NK cell activation and function. The following study was initiated as an effort to obtain further information about similarities and differences between NK and T cells at the level of gene expression and also to identify NK-specific cDNA clones for future functional studies of the corresponding gene products. The study used cDNA libraries prepared from an NK clone and from an Epstein-Barr virus transformed B cell lymphoblastoid cell line (LCL). We employed a combination of differential and subtractive hybridization methodologies, which can successfully identify cell-specific cDNA clones representing medium to high abundance transcripts, to identify genes that are expressed in NK cells but not in the LCL. We were particularly interested to ascertain to what extent genes isolated in this manner would be expressed only in NK cells as opposed to being expressed in NK and T cells. Twelve different cross-hybridizing groups were identified that were not expressed in the LCL, and these groups were further characterized: (1) they were used to probe Northern blots prepared from a panel of cells including NK cells, T cells, and B cells: (2) changes in the steady-state level of message following T cell growth factor (TCGF)-induced activation of an NK cell clone were examined for selected isolates; and (3) a partial DNA sequence was determined for each cross-hybridizing group. The DNA sequences of seven groups were identical to previously reported sequences. One group was highly homologous with but not identical to what has been reported as a T cell specific gene, named 519. The DNA sequences of four groups showed no significant homology with the sequences in the GenBank and EMBL databases. The mRNA expression of the newly-identified groups demonstrated several different regulation patterns with respect to cell distribution and level of expression in response to TCGF-activation. Expression of the twelve different genes was examined in three populations of NK cells all of which were CD3- and possessed NK activity. Although these cells differentially expressed the prototype NK markers CD16 and CD56 (the cells were CD16+, CD56-, CD16-, CD56+ and CD16+, CD56+), the expression of all groups of cDNA clones was comparable in the three different types of NK cells despite the phenotypic differences.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 6","pages":"295-304; discussion 305-6"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13236862","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":"Characterization of a neoplastic B cell clone that secretes IgM in response to Th2-derived lymphokines.","authors":"K H Brooks,&nbsp;C S Oakley,&nbsp;H Takayasu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Recent advances of T cell cloning have allowed the classification of T helper cells in terms of the lymphokines they secrete. The functional significance of segregating lymphokine production to unique T cell subsets is still being evaluated, but undoubtedly plays a key role in the regulatory mechanisms of the immune system. Initial studies have indicated that the Th1 cells which secrete IL-2 and IFN-gamma may be primarily responsible for augmenting cell-mediated responses, whereas Th2 cells, which release IL-4, IL-5, and IL-6, provide help for humoral responses. However, it is also known that B cells can respond to both IL-2 and IFN-gamma. This raises the question of the homogeneity of B lymphocyte activation requirements. Are all B cells responsive to all of the lymphokines with the end-result of stimulation depending largely on the relative concentrations of the various lymphokines, or are there B cell subsets which only respond to Th1-derived lymphokines and others which respond to Th2-derived lymphokines? Such differential activation requirements might be present to allow these subsets to play unique roles in immunological responses. Since B cell cloning techniques have not yet been developed to obtain a homogenous B cell population for studies of activation requirements, regulation of lymphokine receptors, and regulation of gene expression, we must utilize lymphokine-responsive neoplastic B cells. The vast majority of spontaneous B cell lymphomas appear to belong to a minor B cell subset which expresses the Ly1 marker. This subset is clearly not representative of the majority of splenic B cells.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 6","pages":"339-47; discussion 347-8"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13304581","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 regulatory role for the soluble IL-2 receptor via competition with the p75 cell-surface form of the receptor for IL-2.","authors":"M S Loughnan,&nbsp;G J Nossal","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Murine T and B lymphocytes can be induced to release soluble interleukin 2 receptors (sIL2R). This receptor is believed to be a truncated form of the p55 chain of the cell membrane-associated receptor. It has been speculated that this receptor may play an immunoregulatory role via competition for IL-2 with the high-affinity (p55/75 heterodimer) IL-2 receptor. Of crucial importance to this hypothesis are both the concentration of the receptor and its affinity of binding for interleukin 2. We report the measurement of the affinity of sIL2R derived from stimulated normal murine splenocytes for IL-2. We also report the quantification of an enzyme linked immunosorbent assay (ELISA) for sIL2R via measurement of the sIL2R concentration in normal murine splenocyte conditioned medium using a radioimmunometric assay and Scatchard analysis. This method of sIL2R quantification is preferable to sIL2R purification and subsequent concentration estimation as used by previous investigators as any purification process risks destruction of some epitopes. Using the above conditioned medium as a standard we have tested supernatants from several cell lines and sera from several different mouse strains for sIL2R. As would be expected this method of quantification yielded a markedly different value for serum sIL2R levels in normal mice than that obtained by previous investigators. Our results indicate that it is very unlikely that sIL2R competes with the high-affinity form of the IL-2 receptor for IL-2. However, it is possible that it competes for IL-2 with the medium-affinity p75 form of the IL-2 receptor and as such is important in restricting unwanted non-specific (bystander) activation of p75 expressing cells. Evidence from both our previous work as well as from the literature is presented to support this hypothesis.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 6","pages":"307-15; discussion 316"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13237467","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":"Antibody-activated immunoregulatory T cells are defective in B cell deprived mice.","authors":"W Ptak,&nbsp;P Flood,&nbsp;C A Janeway","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have previously shown that antibody bound to hapten-conjugated macrophages influences the contact sensitivity response to the hapten, the effect depending upon the isotype of antibody used. In the present experiments, we have examined the regulation of the contact sensitivity response of mice lacking B cells, in order to determine whether B cells and/or their products play a role in regulating such responses in situ. We have observed that contact sensitivity is normally induced in such B cell depleted mice, in contrast to the previously described failure of such mice to mount proliferative T cell responses to protein antigens. However, virtually all of the immunoregulatory activities previously defined in the contact sensitivity reaction, including those induced by antibody bound to hapten-coupled macrophages, cannot be elicited in these animals. In particular, intravenous injection of either hapten-coupled PEC, or antigen-antibody complexes of the IgG2a isotype on the surface of a hapten-coupled PEC (both of which induce unresponsiveness to contact sensitization in normal mice due to the activation of suppressor T cell activity) actually sensitize B cell deficient mice. Thus, we conclude that B cells or their products play a central role in the development and/or functioning of immunoregulatory cells involved in the control of contact sensitivity responses.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 5","pages":"281-9; discussion 289-90"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13298590","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":"Class I and class II MHC gene products differentially affect the fate of V beta 5 bearing thymocytes.","authors":"J Bill,&nbsp;O Kanagawa,&nbsp;J Linten,&nbsp;Y Utsunomiya,&nbsp;E Palmer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have previously shown that T cells bearing V beta 5+ T-cell receptors (TCRs) are frequent in B10 (H-2b) and B10.Q (H-2q) mouse strains but are rare in the congenic strain B10.BR (H-2k). Furthermore, we have found that V beta 5 bearing T cells appear to be excluded from the B10 alloresponse to I-Abm12 despite the participation of most other V beta bearing cells. To further study MHC effects on V beta 5 expression, we have generated two V beta 5 specific monoclonal antibodies and show here that V beta 5 expressing T cells are clonally deleted from strains expressing a class II, I-E molecule. Furthermore, I-E- strains generate few CD4+ V beta 5+ T cells despite significant numbers of V beta 5+ T cells in the CD8+ subset. Thus, V beta 5 bearing T cells are positively selected by class I MHC molecules, clonally deleted by class II I-E molecules, and poorly selected by class II I-A molecules.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 5","pages":"269-79; discussion 279-80"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13135203","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 PMA-induced specific association of LFA-1 and talin in intact cloned T helper cells.","authors":"A Kupfer,&nbsp;P Burn,&nbsp;S J Singer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Previous experiments with individual cell couples formed between cloned T helper (Th) cells and antigen-presenting cells have led us to suggest that the cytoskeletal protein talin may be associated with the cell surface protein LFA-1 in the Th cell. In order to examine this suggestion, we induced the surface capping of LFA-1 with suitable specific antibody reagents on the intact Th cells, and then determined by double immunofluorescence microscopic experiments, whether talin was co-clustered with the LFA-1 caps. With untreated Th cells, capping of LFA-1 did not result in any redistribution of intracellular talin. However, if the intact Th cells were treated with the phorbol ester PMA, the capping of LFA-1 resulted in a co-clustering of talin with the LFA-1 caps, but not a alpha-actinin. The capping of TCR or CD4 on the Th cells with or without pretreatment with PMA did not lead to any such co-clustering of talin with these caps. PMA treatment of the Th cells therefore induces a direct or indirect association of talin with LFA-1 underneath the Th cell surface. PMA treatment of the Th cells also increased their polarized spreading and adherence to substrata, as had been observed before. We found, furthermore, that this increased adherence upon PMA-treatment was inhibited by the presence of antibodies to LFA-1. The association of talin, and very likely also F-actin microfilaments, with LFA-1 appears to mediate a generalized increased adhesivity of the Th cells. The relevance of these findings with isolated Th cells to the interaction of Th cells with specific antigen-presenting cells is discussed.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 6","pages":"317-25"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13304580","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":"Constitutive production of lymphokines by cloned murine B-cell lymphomas--CH12 B lymphoma produces interleukin-4.","authors":"A O'Garra,&nbsp;D Barbis,&nbsp;N Harada,&nbsp;F Lee,&nbsp;M Howard","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>B cells can be activated by T-independent antigens or mitogens such as lipopolysaccharide (LPS) which will induce proliferation and differentiation of the B cells into Ig-secreting cells, without the intervention of T cells. The precise mechanism of T-independent proliferation and differentiation of B cells is still unclear. It is possible however that antigen-stimulated B cells may produce some factors which play a role in T-independent B-cell responses. In addition, since it has now been established that B cells can function as antigen-presenting cells, it is possible that they too secrete a molecule which is involved in the activation of T cells, analogous to IL-1 production by antigen-presenting macrophages. A number of human B-cell lines, as well as human normal B cells activated appropriately, have been shown to produce various cytokines, and similar studies are now being undertaken in the mouse. In the present study, six cloned murine B-cell lymphomas of different origin were analyzed for the presence of mRNA encoding a number of lymphokines by hybridization of specific cDNA probes to poly-A RNA, followed by the sensitive S1 nuclease digestion technique. The lymphokines included (IL-) 1, 2, 3, 4, 5, and neuroleukin. Whereas none of the lines expressed detectable levels of IL-2, IL-3, or IL-5 mRNA, all the lines expressed high levels of neuroleukin mRNA. Three of the lymphomas (CH12, CH31, and NBL) expressed low levels of IL-1 mRNA. The most striking finding was that one lymphoma, CH12, constitutively expressed IL-4 mRNA. This mRNA appeared to be functional, as IL-4 activity measured by the HT-2 T cell proliferation assay could be detected in supernatants collected from CH12 cells. The growth-inducing activity of CH12 supernatant on HT-2 cells could be completely blocked by an anti-IL-4 monoclonal (11B11), but not by an anti-IL-2 antibody (S4B6), consistent with our observations that CH12 cells produce IL-4 but not IL-2. CH12 cells were also found to express high affinity receptors for IL-4. Proliferation of CH12 cells was not affected by the addition of exogenous IL-4. Addition of anti-IL-4 antibodies to CH12 cells in culture caused a slight but reproducible increase in their proliferation at low cell numbers, which is probably not highly significant. These findings open the possibilities that murine B lymphocytes are capable of lymphokine production or alternatively that aberrant lymphokine production underlies B-lymphocyte transformation.</p>","PeriodicalId":77639,"journal":{"name":"The Journal of molecular and cellular immunology : JMCI","volume":"4 3","pages":"149-58; discussion 158-9"},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13927452","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}