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PubMed2003

Plasmacytoid dendritic cells, antigen, and CpG-C license human B cells for plasma cell differentiation and immunoglobulin production in the absence of T-cell help.

It has been reported that interferon alpha (IFN-alpha) enhances humoral immunity and that dendritic cells of the myeloid lineage promote B-cell differentiation. Here we studied whether the plasmacytoid dendritic cell (PDC), a subset of dendritic cells specialized for the production of IFN-alpha, is involved in regulating B-cell differentiation and immunoglobulin production. The recently identified class of CpG oligonucleotides (CpG-C) was used to activate both B cells and PDCs via Toll-like receptor 9 (TLR9). The presence of PDCs synergistically enhanced CD86 expression, cytokine production (interleukin 6 [IL-6], tumor necrosis factor alpha, and IL-10) and plasma cell differentiation of isolated human peripheral blood B cells stimulated through CpG-C and B-cell antigen receptor (BCR) ligation. This stimulation protocol was sufficient to drive purified naive B cells into IgM-producing plasma cells and to trigger IgG synthesis in memory B cells. PDCs contributed to B-cell activation via IFN-alpha secretion. Up-regulation of TLR9 on B cells was not involved. These results demonstrate that CpG-stimulated PDCs induce plasma cell differentiation in naive and memory B cells in the absence of T-cell help, providing an explanation for the excellent activity of CpG oligonucleotides as a humoral vaccine adjuvant.

Antigens↗

PubMed2007

Immunophenotypic differentiation between neoplastic plasma cells in mature B-cell lymphoma vs plasma cell myeloma.

Some non-Hodgkin lymphomas show marked plasmacytic differentiation. In such cases, it may be difficult to differentiate these lymphoma from plasmacytoma or myeloma, especially with limited diagnostic material. However, there may be immunophenotypic differences in the plasma cells in these disorders that distinguish them. This study characterizes the immunophenotypes of neoplastic plasma cells in 41 cases of B-lineage non-Hodgkin lymphoma and compares them with those in plasma cell myeloma. We found that plasma cells in lymphoma were significantly more likely to express CD19, CD45, and surface immunoglobulin and less likely to express CD56 than those in myeloma. We further show that CD 19 and CD56 expression can be used reliably to distinguish these entities. Myeloma-associated osseous lesions and solitary plasmacytoma of bone showed myeloma-like immunophenotypes. However, some extramedullary plasmacytomas showed lymphoma-like phenotypes, suggesting that, in reality, they may represent non-Hodgkin lymphomas with extensive plasmacytic differentiation.

ADP-ribosyl Cyclase 1↗

PubMed2002

Eotaxin expression by epithelial cells and plasma cells in chronic asthma.

Chemoattractants such as eotaxin are believed to play an important role in the recruitment of eosinophils into the airways in asthma. We investigated expression of eotaxin in the airway wall in a model of chronic human asthma, in which systemically sensitized mice were exposed to low mass concentrations of aerosolized antigen for 6 weeks. In these animals, the number of intraepithelial eosinophils in the airways was significantly increased 3 hours after exposure and declined by 24 hours. In parallel, immunoreactivity for eotaxin was strikingly up-regulated in airway epithelial cells and in inflammatory cells in the lamina propria. The latter were identified as plasma cells by double immunofluorescent labeling. Increased expression of eotaxin by epithelial cells and plasma cells was also demonstrated in a case of fatal human asthma. In contrast, sensitized mice that received a single exposure to a high mass concentration of aerosolized antigen exhibited delayed eosinophil recruitment, which did not correlate with eotaxin expression. Furthermore, in sensitized chronically exposed interleukin-13-deficient mice there was virtually no recruitment of eosinophils into the airways, although eotaxin expression was greater than or equal to that in wild-type mice. These results indicate that there are striking differences between acute and chronic exposure models in the time course of eotaxin expression and eosinophil recruitment. Although high eotaxin levels alone are not sufficient to cause recruitment of eosinophils into the airways, recurrent exposure may generate or up-regulate additional signals required for eosinophil chemotaxis.

Allergens↗

PubMed1989

T-cell and plasma cell populations in coeliac small intestinal mucosa in relation to dermatitis herpetiformis.

Differential lymphocyte and plasma cell counts and measurements of mucosal architecture were studied in small intestinal biopsies from 17 controls and 17 patients with untreated uncomplicated coeliac disease of whom five also had dermatitis herpetiformis. Intraepithelial T-cell and plasma cell counts and measurements of mucosal architecture were not significantly different in the two coeliac groups but both groups differed from the controls. Lamina propria T-cell counts were significantly higher in the patients who also had dermatitis herpetiformis than in uncomplicated coeliac disease, with a significant increase in the Leu 2 (CD8) positive (cytotoxic/suppressor) T-cell subset. This suggests a specific abnormality of T-cell control of immune responsiveness in the pathogenesis of the skin manifestations of dermatitis herpetiformis which is not found in uncomplicated coeliac disease.

Adolescent↗

PubMed1983

Neutral maltase: the first human B-cell enzymatic marker reflecting terminal differentiation of mature B cells into plasma cells.

Neutral maltase activity (alpha-D-glucoside glucohydrolase; EC: 3.2.1.20) was measured in B and T lymphocytes from peripheral blood of normal subjects and patients suffering from chronic or acute lymphoid leukemias. Neutral maltase activity is undetectable in T cells from normal subjects as well as in patients with chronic or acute T-lymphoid leukemias. Conversely, whereas this enzyme activity is always undetectable in chronic or acute B-lymphoid leukemia, neutral maltase activity is expressed in mature B cells from normal subjects. The detection of higher neutral maltase activity in plasma cells from myelomas than in normal B cells supports the concept that the expression of neutral maltase activity is related to the stages of differentiation and maturation reached by lymphocytes of the B-cell lineage. Neutral maltase therefore appears as the first B-cell enzymatic marker described that is expressed in the course of terminal differentiation of mature B cells into plasma cells.

B-Lymphocytes↗

PubMed2004

Developmentally distinct Th cells control plasma cell production in vivo.

Differential Ly6C expression identifies a major phenotypic division in CD44loCD62LhiCD4+ Th cells. Using two separate models of single subset adoptive transfer, we demonstrate the unique capacity of Ly6Chi Th cells to promote antigen-specific plasma cell production in vivo. In contrast, both compartments support germinal center formation and proliferate to equivalent levels upon TCR triggering in vivo and in vitro. Developmentally, CD4+CD8- thymocytes leave the thymus expressing low levels of Ly6C; 3 days later approximately 50% stably upregulate Ly6C without cell division or TCR engagement in the periphery. Interestingly, antigen-specific Th cell clonotypes unevenly assort into these peripheral compartments, creating separate TCR repertoires that underpin peripheral functional diversity. Taken together, these data reveal a developmentally distinct Ly6Chi naive Th cell compartment subspecialized to regulate plasma cell production in vivo.

Adoptive Transfer↗

PubMed1989

Transcriptional control of MHC class II gene expression during differentiation from B cells to plasma cells.

In this study we investigated the molecular mechanisms responsible for the extinction of the constitutive MHC class II gene expression of human B cells on somatic cell hybridization with murine plasmocytoma cells. We found that this event is due to trans-acting suppressor functions of mouse origin pre-existing in the plasmocytoma cells and acting at transcriptional level. Transcription of the entire family of human class II genes is suppressed, including genes as DO beta for which a distinct regulation of expression in B cells had been previously demonstrated. Suppression appears specific for class II genes because in the hybrids expression of MHC class I genes of mouse is unaffected and of human only partially reduced. Interestingly, also murine invariant chain gene is expressed in both parental plasmocytoma and hybrid cells although at reduced amounts as compared to a murine class II positive B cell line. The class II negative phenotype of hybrid cells and parental plasmocytoma cells is highly stable and unaffected by treatment with protein synthesis inhibitors, suggesting that the transcriptional suppressor function is not mediated by rapid, labile turning-over proteins. Possible mechanisms responsible for transcriptional regulation of MHC class II gene expression during terminal differentiation of B cells to plasma cells are discussed.

B-Lymphocytes↗

PubMed2006

Identification of rare Epstein-Barr virus infected memory B cells and plasma cells in non-monomorphic post-transplant lymphoproliferative disorders and the signature of viral signaling.

BACKGROUND AND OBJECTIVES: In early and polymorphic post-transplant lymphoproliferative disorders (PTLD) Epstein-Barr virus (EBV), through its latency proteins, drives the proliferation of B lymphocytes, a process which in immunocompetent individuals leads to the establishment of latently infected memory B cells. DESIGN AND METHODS: We analyzed 11 cases, which included early and polymorphic PTLD, and 12 controls for latency of EBV infection and their antigenic profile. RESULTS: We identified a minority of terminally differentiated EBER+ IRTA1+ memory B cells and EBER+ CD138+ PRDM1+ plasma cells in these samples. These elements were identified both in PTLD and in tumor-free tonsils from post-transplant patients but not in EBV- control tonsils. The expression of EBV latency proteins is heterogeneous, and is associated with activation of the NF-kB pathway. EBV signaling (through EBNA2, LMP1 and LMP2A) and NF-kB activation correlated with upregulation of target proteins: cMYC, JunB, CCL22, TRAF1 and IRF4. EBV-infected lymphocytes in early and polymorphic PTLDs represent a mixture of latencies II, III and, in at least 1/3 of infected cells, of latency 0. INTERPRETATION AND CONCLUSIONS: EBV infection correlates with NF-kB activation, with EBV-dependent cell signaling, and lastly, with the presence of EBV-infected plasma cells and memory cells.

Adolescent↗

PubMed2004

Stressed-out B cells? Plasma-cell differentiation and the unfolded protein response.

Plasma cells operate as factories where large quantities of Ig heavy and light chains are made and assembled into functional antibodies. The finished products are shipped out with impressive efficiency. A major component of the machinery necessary for high-rate antibody secretion is an elaborate network of endoplasmic reticulum (ER), the site of antibody biosynthesis. Recent discoveries have provided insights into how this expansive secretory machinery is built, equipped and maintained. The unfolded protein response (UPR) pathway, a stress-induced signaling cascade emanating from the ER, regulates the expression and activity of X-box binding protein 1, a transcription factor required for plasma-cell development. The UPR pathway therefore senses conditions in the ER--the very compartment where antibodies are formed--and directs events required for humoral immunity.

Animals↗

PubMed1980

Tumor immunity to murine plasma cell tumors. V. Genetic control of the in vitro cytotoxic T-cell response to plasma cell tumor-associated antigens of NZB mice.

Cytotoxic T-lymphocytes (Tc) were induced in vitro to plasmacytoma tumor-associated antigens (TAA) by coculture of irradiated cells of plasma cell tumors (PCT) from NZB mice and viable nonimmune or PCT-immune spleen cells from NZB. (NZB X C57BL)F1, (NZB X B10.D2)F1, and (NZB X B10,BR)F1 mice. When nonimmune spleen cells were used, major histocompatibility complex (MHC)-linked genetic control of te primary in vitro induction of Tc to NZB PCT was demostrated for a shared TAA expressed on NZB and BALB/c PCT. Evidence was also obtained for a non-MHC-linked genetic control of the primary in vitro induction of Tc to a second TAA that ws expressed on both PCT and T-lymphomas. When the spleen cells were obtained from mice preimmunized to an NZB PCT, a secondary in vitro Tc response was observed, and a PCT-specific and strain-specific TAA or NZB mice was identified. In addition, results with the F1 hybrids also indicated an MHC-linked genetic control of the in vitro Tc response to this strain-specific TAA.

Animals↗

PubMed1998

CD27/CD70 interaction augments IgE secretion by promoting the differentiation of memory B cells into plasma cells.

The induction of IgE switching in B cells requires several signals given by cytokines and cell contact-delivered signals. Here, we investigated the role of CD27/CD70 interaction in B cell IgE synthesis. The addition of CD27 ligand (CD70) transfectants to B cell cultures increased the IgE synthesis synergistically in the presence of IL-4 plus anti-CD40 mAb (anti-CD40). The effect of CD70 transfectants was dose dependent and was completely blocked by anti-CD70 mAb. CD27+ B cells had the ability to produce IgE, which was increased by contact with CD70 transfectants, whereas CD27- B cells did not produce IgE. CD27/CD70 interaction enhanced B cell proliferation in the presence of IL-4 or IL-4 plus anti-CD40. The augmentation of B cell proliferation by CD70 transfectants was apparent in CD27+ B cells, but was mild in CD27- B cells. The helper activity for IgE synthesis by the CD27/CD70 interaction did not contribute to the enhancement of germline epsilon transcripts. Flow cytometric and morphological analyses demonstrated that the addition of CD70 transfectants to B cell cultures remarkably promoted differentiation into plasma cells in the presence of IL-4 and CD40 signaling. Finally, CD27 cross-linking resulted in the up-regulation of positive regulatory domain I-binding factor-1. Taken together, our findings indicate that signaling via CD27 on B cells induces IgE synthesis, in cooperation with IL-4 and CD40 signaling, by promoting the generation of plasma cells through up-regulation of positive regulatory domain I-binding factor-1.

Adult↗

PubMed1983

Ten percent of normal B cells and plasma cells share A VH determinant(s) (J606-GAC) with a distinct subset of murine VHIII plasmacytomas.

Our findings indicate that a subset of VHIII antibodies, which we refer to as J606-GAC, contains a determinant(s) that is present on 5 to 15% of normal splenic B cells and plasma cells as detected by immunofluorescence. This subpopulation is detected by purified antibody, 0-1, which was prepared against a murine anti-group A carbohydrate (anti-GAC) hybridoma antibody. The J606-GAC subset includes the beta 2, 1 fructosan myelomas J606, EPC109, W3082, ABPC4, and UPC61, as well as 13 anti-GAC hybridomas. The 0-1 antiserum failed to react with hybridoma and myeloma immunoglobulins from murine VH groups I and II or other VHIII antibodies. By Western blot analysis, it was observed to react with isolated heavy, but not light, chains of J606-GAC-bearing antibodies. 0-1 failed to react with myelomas XRPC44 and J539, which have the same J region as J606 but a very different VH region. These observations indicate that 0-1 is detecting a VH region determinant. The J606-GAC marker recognized by 0-1 was expressed as early as 4 days after birth and was expressed at similar frequencies in germfree and conventional mice. Immunoprecipitation of both surface and biosynthetically labeled proteins from spleen cells or J606-GAC-positive hybridoma cell lines, respectively, confirmed that 0-1 was recognizing an immunoglobulin determinant.

Animals↗

PubMed1988

PB76: a novel surface glycoprotein preferentially expressed on mouse pre-B cells and plasma cells detected by the monoclonal antibody G-5-2.

A monoclonal antibody (mAb) G-5-2 was isolated which binds to transformed as well as normal cells of the B lineage but not to cells of the T cell, myeloid lineages nor to fibroblasts. mAb G-5-2 reacts with pre-B and plasma cell-transformed lines, and it preferentially recognizes normal pre-B cells from fetal liver and bone marrow as well as plasma cells from spleen of mice. G-5-2+ fetal liver cells isolated by cell sorter express mRNA for mu heavy chain Ig gene and generate in vitro antibody-producing cells when co-cultured with lipopolysaccharide and rat thymocyte filler cells. During development the frequency and staining intensity of G-5-2+ cells in fetal liver from normal mice increases from 1% G-5-2+ cells at day 14 to approximately 7% positive cells at day 18 of gestation. Several strains or normal mice contain comparable numbers of G-5-2+ cells as well as B-220+ and BP-1+ B cell precursors in the fetal liver. Mice carrying the xid mutation have 3-4-fold less G-5-2+ as well as B-220+ and BP-1+ cells in the fetal liver, suggesting that the effects of the xid mutation may be manifested from early stages of B cell development. Fetal liver cells from mice carrying the scid mutation were found to contain normal numbers of G-5-2+ as well as B-220+ and BP-1+ pre-B cells. These results indicate that differentiation from progenitors to pre-B cells in scid mice may occur normally; the scid mutation would thus appear to affect the process of rearrangement and expression of the Ig genes in the developing pre-B cells. mAb G-5-2 precipitates a 76-kDa glycoprotein from surface-radiolabeled pre-B cells and plasma cells. Taken together, these results indicate that G-5-2 mAb recognizes a novel B cell lineage-specific surface molecule called PB76 which is preferentially expressed by pre-B cells and plasma cells.

Animals↗

PubMed2005

Selecting B cells and plasma cells to memory.

Humoral immunity appears to be based on immunological memory provided by memory plasma cells, which secrete protective antibodies, and memory B cells, which react to antigen challenge by differentiating into plasma cells. How these differentiation pathways relate to each other, how cells are selected into these memory populations, and how these populations are maintained remains enigmatic.

Animals↗

PubMed2001

Increased frequency of pre-germinal center B cells and plasma cell precursors in the blood of children with systemic lupus erythematosus.

We have analyzed the blood B cell subpopulations of children with systemic lupus erythematosus (SLE) and healthy controls. We found that the normal recirculating mature B cell pool is composed of four subsets: conventional naive and memory B cells, a novel B cell subset with pregerminal center phenotype (IgD(+)CD38(+)centerin(+)), and a plasma cell precursor subset (CD20(-)CD19(+/low)CD27(+/++) CD38(++)). In SLE patients, naive and memory B cells (CD20(+)CD38(-)) are approximately 90% reduced, whereas oligoclonal plasma cell precursors are 3-fold expanded, independently of disease activity and modality of therapy. Pregerminal center cells in SLE are decreased to a lesser extent than conventional B cells, and therefore represent the predominant blood B cell subset in a number of patients. Thus, SLE is associated with major blood B cell subset alterations.

ADP-ribosyl Cyclase↗

PubMed2001

Comparative characteristics of mu chain and alpha chain transcripts expressed by individual tonsil plasma cells.

Plasma cells (PCs) are one of the two major cell types generated during germinal center reactions. To test the hypothesis that PCs express a unique repertoire of immunoglobulin (Ig) genes resulting from intensive antigenic stimulation and selection, the mutational pattern and distribution of V(H) gene segments within 178 transcripts amplified from individual IgM and IgA secreting tonsil PCs were analyzed. The results demonstrated that both mu and alpha transcripts expressed repertoires with limited diversity. Moreover, both mu and alpha transcripts were heavily mutated, with a significantly increased mutational frequency noted for alpha compared to mu transcripts (5.0 x 10(-2) vs 1.8 x 10(-2), P<0.001). In addition, both mu and alpha transcripts showed significantly greater targeting of mutations to RGYW motifs (purine/guanine/pyrimidine/A or T) compared to memory B cells. Finally, clonally expanded cells were detected in alpha but not mu PC compartments. These results indicate that antigen driven stimulation and selection shape the entire expressed PC repertoire, but the impact is greater in alpha expressing PCs.

Base Sequence↗

PubMed2005

Molecular case report: IgVH analysis in acute humoral and cellular liver allograft rejection suggests a selected accumulation of effector B cells and plasma cells.

Acute cellular (CLR) and humoral liver allograft rejection (HLR) are the most important immunological obstacles to successful liver transplantation. In HLR, serum antibodies play the central pathogenetic role. In CLR, CD3+ T lymphocytes drive the destructive immune response. Although CLR and HLR show different clinical symptoms and can be kept apart in most cases, they share histomorphological similarities. In CLR, hepatic B lymphocytes and plasma cells as well as B-cell-activating cytokines have recently been described, indicating that, in addition to T cells, antibody-mediated mechanisms might be involved. To analyze the impact of hepatic B cells in CLR and HLR, the immunoglobulin (Ig) variable (V)-region gene repertoire was determined from tissue of one case of CLR and one case of HLR. Complement deposits and lymphocytic infiltrate were determined using immunohistochemistry. T cells, B lymphocytes and plasma cells could be detected in both cases, whereas C3c and C4d deposits could only be demonstrated in the HLR case. The molecular analysis of 63 V-region genes showed that B cells in both allografts expressed selected V-gene repertoires. All sequences differed from the putative germline sequences by multiple somatic mutations. This suggests a clonal expansion of selected effector B cells in the portal tracts of liver allografts. Locally accumulated B cells and their antibodies might be involved in IgG-mediated complement activation in CLR and HLR.

Adult↗

PubMed1994

Semiquantitative, nonradioactive RT-PCR detection of immunoglobulin mRNA in human B cells and plasma cells.

Quantification of mRNA is important for studies of gene expression and gene regulation. We investigated the utility of the reverse transcriptase polymerase chain reaction (RT-PCR) approach in the quantification of mRNA from small cell numbers. To take into account the complex kinetics of the PCR amplification process and the nonlinear signal development during detection of PCR products, calibration curves were established on the basis of different, known, starting concentrations of cDNA fragments, different PCR cycle numbers, and different signal intensities. Detection of digoxigenin-labeled PCR products via an enzymatically generated chemiluminescent signal was found to give a reproducible and wider range of signal intensities compared to simple ethidium bromide staining. We applied this methodology to the quantification of immunoglobulin M (IgM) mRNA levels in human B cells. Using an in vitro culture system in which B cells differentiate into plasma cells, the kinetics of IgM mRNA expression were established during a 10-day culture period and a 180-fold mRNA increase was found.

B-Lymphocytes↗