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PubMed2005

Centrocytoid plasma cells of the germinal center.

Germinal centers within the lymph node follicles are T-cell-dependent, antigen-driven B-cell proliferations that develop from the rapid clonal expansion of a few founder cells. The end results of this B-cell expansion are memory B cells or plasma cells. Two morphologic forms of plasma cell can be recognized in the germinal center: classic plasma cells, characterized morphologically by peripherally clumped arrangement of nuclear chromatin, and cells with a nuclear morphology more resembling that of the centrocytes, which the authors have termed "centrocytoid plasma cells." In this study the authors examined the distribution and immunohistochemical characteristics of these two populations of germinal center plasma cells. The centrocytoid plasma cells were arranged in a band stretching from the junction of the dark and light zone to the periphery of the germinal centers, while the classic plasma cells were mainly present at the germinal center periphery. Both marked with CD38, CD138, and VS38c, recognized markers for plasma cells; however, EMA and CD31 were present only in the classic form of plasma cell. The proliferation marker Ki67 was present in less than 1% of the cells labeling with CD138. Others have demonstrated Ki67 in 50% of the cells labeled with Blimp-1, which is consistent with Blimp-1 appearing earlier than CD138 in ontogeny. CD10 is co-expressed with CD138 in about 10% of cells and CD45 with CD138 in about 5% of cells. Their topographic features, together with the progressive acquisition of plasma cell markers, suggest that the centrocytoid plasma cells may be the precursors of the classic plasma cells. Of note, both the forms of plasma cell were absent in follicles of follicular lymphoma, which supports the concept that in this disease, lymphocytes fail to differentiate and mature beyond the centrocyte stage.

Biomarkers↗
PubMed1995

The blood B-cells and bone marrow plasma cells in patients with multiple myeloma share identical IgH rearrangements.

Previous reports have described the phenotypic and functional properties of monotypic late stage B cells in the blood of patients with multiple myeloma and have speculated that these B cells represent a malignant circulating component of myeloma. Here we show that blood B cells have IgH rearrangements identical to those expressed by the bone marrow plasma cells by using Ig Fingerprint and Allele-Specific Oligomer (ASO) polymerase chain reaction (PCR) methods. DNA from purified blood B cells and bone marrow plasma cells taken at the same time, and blood B cells taken at subsequent patient visits was amplified using consensus IgH primers, or ASO primers. In 10/16 patients, a single IgH rearrangement was amplified from the bone marrow plasma cells. In all 10 of those patients the same clonotypic rearrangement was amplified from the purified blood B cells. The relationship of these clonal blood B cells to the malignant bone marrow plasma cells remains undetermined.

Aneuploidy↗
PubMed1984

A population of resting IgM-IgD double-bearing lymphocytes in Peyer's patches: the major precursor cells for IgA plasma cells in the gut lamina propria.

The precursor cells in Peyer's patches and mesenteric lymph nodes responsible for repopulating IgA plasma cells in the gut lamina propria were identified by using cell separation and by using cell transfer in Ig allotype congeneic mice (CB-20 and BALB/cJ mice). It was found that the IgA precursor cells are mainly resting lymphoid cells bearing IgM and IgD on their surface. The IgA-bearing cells are also precursors; their repopulation efficiency, however, is remarkably low. The majority of the IgA precursor cells also bear complement receptors on their surface; this suggests that they are relatively mature B cells.

Animals↗
PubMed2003

Transcriptional regulatory cascades controlling plasma cell differentiation.

Plasma cells are the terminally differentiated effector cells of the B lymphocyte lineage. Recently, studies using genetically altered mice and analyses of global gene expression programs have significantly expanded our understanding of the molecular mechanisms regulating plasmacytic differentiation. Specific molecular components of a multistep cascade of transcriptional regulators have been identified. Furthermore, two transcriptional regulators, X box binding protein-1 (XBP-1) and B lymphocyte induced maturation protein-1 (Blimp-1), have been shown to be necessary for plasmacytic differentiation. In addition to providing a mechanistic basis for the induction of genes necessary for immunoglobulin secretion, cessation of cell cycle and other phenotypic changes characteristic of terminally differentiated plasma cells, these studies have led to the important concept that plasmacytic differentiation involves repression of regulators, such as Bcl-6 and Pax5, that are necessary to maintain the earlier developmental phenotype of activated, germinal center B cells. This review describes our current understanding of the transcriptional cascades regulating terminal differentiation of B cells.

Animals↗
PubMed2002

The role of bone marrow-derived stromal cells in the maintenance of plasma cell longevity.

Protective circulating Abs originate primarily from long-lived plasma cells in the bone marrow. However, the molecular and cellular basis of plasma cell longevity is unknown. We investigated the capacity of primary bone marrow-derived stromal cells to maintain plasma cell viability in vitro. Plasma cells purified from the bone marrow or lymph nodes died rapidly when plated in media, but a subpopulation of plasma cells survived and secreted high levels of Ab for up to 4 wk when cocultured with stromal cells. Ab secretion was inhibited by the addition of anti-very late Ag-4 to plasma cell/stromal cell cocultures indicating that direct interactions occur and are necessary between stromal cells and plasma cells. The addition of rIL-6 to plasma cells cultured in media alone partially relieved the sharp decline in Ab secretion observed in the absence of stromal cells. Moreover, when stromal cells from IL-6(-/-) mice were used in plasma cell/stromal cell cocultures, Ab levels decreased 80% after 7 days as compared with wild-type stromal cells. Further, IL-6 mRNA message was induced in stromal cells by coculture with plasma cells. These data indicate that bone marrow plasma cells are not intrinsically long-lived, but rather that plasma cells contact and modify bone marrow stromal cells to provide survival factors.

Animals↗
PubMed2005

Insertion of c-Myc into Igh induces B-cell and plasma-cell neoplasms in mice.

We used gene targeting in mice to insert a His(6)-tagged mouse c-Myc cDNA, Myc(His), head to head into the mouse immunoglobulin heavy-chain locus, Igh, just 5' of the intronic enhancer, Emu. The insertion of Myc(His) mimicked both the human t(8;14)(q24;q32) translocation that results in the activation of MYC in human endemic Burkitt lymphomas and the homologous mouse T(12;15) translocation that deregulates Myc in certain mouse plasmacytomas. Beginning at the age of 6 months, Myc(His) transgenic mice developed B-cell and plasma neoplasms, such as IgM(+) lymphoblastic B-cell lymphomas, Bcl-6(+) diffuse large B-cell lymphomas, and CD138(+) plasmacytomas, with an overall incidence of 68% by 21 months. Molecular studies of lymphoblastic B-cell lymphoma, the most prevalent neoplasm (50% of all tumors), showed that the lymphomas were clonal, overexpressed Myc(His), and exhibited the P2 to P1 promoter shift in Myc expression, a hallmark of MYC/Myc deregulation in human endemic Burkitt lymphoma and mouse plasmacytoma. Only 1 (6.3%) of 16 lymphoblastic B-cell lymphomas contained a BL-typical point mutation in the amino-terminal transactivation domain of Myc(His), suggesting that most of these tumors are derived from naive, pregerminal center B cells. Twelve (46%) of 26 lymphoblastic B-cell lymphomas exhibited changes in the p19(Arf)-Mdm2-p53 tumor suppressor axis, an important pathway for Myc-dependent apoptosis. We conclude that Myc(His) insertion into Igh predictably induces B-cell and plasma-cell tumors in mice, providing a valuable mouse model for understanding the transformation-inducing consequences of the MYC/Myc-activating endemic Burkitt lymphoma t(8;14)/plasmacytoma T(12;15) translocation.

Amino Acid Sequence↗
PubMedDate not supplied

Appearance of human plasma cells following differentiation of human B cells in NOD/SCID mouse spleen.

Relatively little is known for the differentiation and maturation process of human B cells to plasma cells. This is particularly important in reconstitution work involving transfer of autoantibodies. To address this issue, we transplanted human peripheral blood mononuclear cells (PBMC) directly into the spleen of irradiated NOD/SCID mice depleted of natural killer cell activity. Within 6 weeks, naive B cells differentiated into memory B cells and, importantly, the numbers of human CD138+ plasma cells in spleen increased by 100 fold after transplantation. Plasma cell numbers correlated with the detection of human IgM and IgG in serum, indicating that human B cells had differentiated into mature plasma cells in the murine spleen. In addition to CD19+ plasma cells, a distinct CD19- plasma cell population was detected, suggesting that downregulation of CD19 associated with maturation of plasma cells occurred. When purified human B cells were transplanted, those findings were not observed. Our results indicate that differentiation and maturation of human B cells and plasma cells can be investigated by transplantation of human PBMC into the spleen of NOD/SCID mice. The model will be useful for studying the differentiation of human B cells and generation of plasma cells.

Animals↗
PubMed1992

Rapid and simple gas chromatographic measurement of lactic acid in red blood cells, plasma, and tumor cells after hyperthermia.

The content of lactic acid in red blood cells, plasma, and Ehrlich ascites tumor cells were measured by a gas-liquid chromatography using a column with a terephtalic acid support coated with polyethylene glycol-6000. The lactic acid contents were directly determined in aqueous samples, because they were converted to a volatile derivative in the column. The method was rapid and simple, compared with previous methods which need time-consuming conversion of lactic acid to volatile derivatives. Our measurements showed the increase in the contents of intra- and extracellular lactic acid after hyperthermia.

Animals↗
PubMed1984

[A case of so-called plasma cell granuloma of the stomach--demonstration of monoclonal immunoglobulin (IgM, K) in the plasma cells].

A patient with a surgically removed plasma cell granuloma of the stomach is reported. The patient was a 54-year-old male, the lesion was IIc-like on the anterior wall of the antrum. Histologically conspicuous features were marked thickening of the submucosa by fibrosis, hyperplastic lymph follicles and massive infiltration of mature plasma cells. However, immunohistochemical study using the PAP technique demonstrated the monoclonal nature of the infiltrating plasma cells which were positive for IgM, k. This is the fourth case of plasma cell granuloma reported in the literature, however, our findings also suggested that this might be an early stage of plasmacytoma.

Granuloma↗
PubMed1991

Evolution of a case of lung plasma cell granuloma.

Plasma cell granuloma, on lung inflammatory pseudotumour, is a localized benign proliferation of plasma cells and mesenchymal cells. We report the case of a 45 yr old male, who first presented with mild pain in the left side of the chest. Chest radiography was normal. Eight weeks later he had more pain and an opacity in the left and lower zones of his left chest. After another 7 weeks he had fever and cough with yellowish-green sputum. Chest X-ray then showed a round density in the left upper lobe. The final diagnosis was established after thoracotomy histological examination.

Granuloma, Plasma Cell↗
PubMed2002

Plasma cell gingivitis.

Plasma cell gingivitis (PCG), an infrequent benign inflammatory condition of unknown etiology, is a type of plasma cell orificial mucositis, which includes a wide spectrum of conditions. We present the case of a 13-year-old girl who had PCG with an erythematous congestive plaque on the anterior maxillary gingiva for 4 years. Occasionally, the lesion became increasingly swollen and painful and bled. Results of a histopathologic examination showed dense plasmacytic infiltrate in the dermis, affecting the dermoepidermal border, with immunohistochemical positivity in the K and A light chains and vascular proliferation. "Lozenge" keratinocytes, "watery" spongiosis, and exocytosis were seen in the epidermis. Laboratory analysis showed notably low levels of both serum IgA and secretory IgA. We consider whether secretory IgA at low levels has an important etiopathogenic role favoring the development of localized subclinical repetitive infections that could lead to chronic PCG.

Adolescent↗
PubMed1986

An antigenic study of human plasma cells in normal tissue and in myeloma: identification of a novel plasma cell associated antigen.

A mouse monoclonal antibody named BU11 which detects an antigen strongly expressed on human plasma cells is described. The antibody stains plasma cells in tonsil sections, fresh and cultured plasmacytoid cells from the bone marrow of patients with multiple myeloma and cells of the plasmacytoid cell line RPMI 8226 used as the immunogen. In vitro studies of pokeweed mitogen (PWM) stimulated peripheral blood B cells and Epstein-Barr virus (EBV) stimulated tonsil B cells show that the antigen is present mainly on cells coexpressing the OKT10 antigen and containing cytoplasmic immunoglobulin (cIg). The BU11 antigen is expressed weakly on some normal B cells and is not present on T cells, monocytes or granulocytes. The antigen is of molecular weight 58kD under reducing conditions and is biochemically distinct from previously described plasma cell antigens.

Animals↗
PubMed2005

Bortezomib is an efficient agent in plasma cell leukemias.

Plasma cell leukemia (PCL) represents the most aggressive form of monoclonal gammopathy for which new treatment approaches are needed. Here we report the effect of Bortezomib on cells from 4 patients with PCL, as well as the in vivo efficacy on a patient with secondary PCL. Bortezomib reduced PCL numbers and was more efficient in cell growth inhibition than dexamethasone or doxorubicin. Treatment with Bortezomib induced procaspase-3 and poly(ADP-ribose) polymerase cleavage and decreased the amount of extracellular signal regulated kinase (Erk1/2) and phospho-Erk1/2. However, Bortezomib did not substantially affect the levels of the Erk1/2 upstream activating kinase (MEK1), p27 or p21. Finally, we had the opportunity to use Bortezomib in a heavily pretreated patient with overt secondary PCL and severe anemia and thrombocytopenia. Following Bortezomib treatment, circulating plasma cells disappeared; what is more striking, the peripheral blood counts returned to normal, becoming transfusion-independent. These data support the inclusion of Bortezomib in the therapeutic armamentarium of PCL.

Anemia↗
PubMed2006

Transcription factor IRF4 controls plasma cell differentiation and class-switch recombination.

B cells producing high-affinity antibodies are destined to differentiate into memory B cells and plasma cells, but the mechanisms leading to those differentiation pathways are mostly unknown. Here we report that the transcription factor IRF4 is required for the generation of plasma cells. Transgenic mice with conditional deletion of Irf4 in germinal center B cells lacked post-germinal center plasma cells and were unable to differentiate memory B cells into plasma cells. Plasma cell differentiation required IRF4 as well as the transcriptional repressor Blimp-1, which both acted 'upstream' of the transcription factor XBP-1. In addition, IRF4-deficient B cells had impaired expression of activation-induced deaminase and lacked class-switch recombination, suggesting an independent function for IRF4 in this process. These results identify IRF4 as a crucial transcriptional 'switch' in the generation of functionally competent plasma cells.

Animals↗
PubMed1997

CD154/CD40 and CD70/CD27 interactions have different and sequential functions in T cell-dependent B cell responses: enhancement of plasma cell differentiation by CD27 signaling.

CD40, a TNF receptor family member, plays a central role in T cell-mediated B cell activation. We have recently demonstrated that CD27, another TNF receptor family member, was also involved in B cell regulation and enhanced Ig production. In this report we compare CD27 and CD40 signals in B cell function. We selectively mimicked the effect of T cell help by addition to peripheral blood B cells activated with Staphylococcus aureus Cowan I strain and IL-2 of irradiated 300-19 cells transfected with either the CD70 (CD27 ligand) gene or the CD154 (CD40 ligand) gene, the vector alone, or both CD70 and CD154 genes. CD27 ligation induced only a slight increase in B cell proliferation compared with the dramatic enhancement induced by CD40 ligation; double ligation proved to be less efficient than CD40 ligation alone. In contrast, IgG production was increased only by CD27 ligation alone. Moreover, the CD27 signal was more efficient when it was given on day 2 of the culture rather than on day 0. Phenotypic analysis of the activated cells showed that CD27 ligation increased the percentage of cells showing a plasma cell profile (CD19-, CD38+), whereas upon CD40 ligation most of the cells still had a germinal center-like phenotype (CD19+, CD38+). Our results suggest that the CD27 and CD40 signals are not synergistic but, rather, are complementary and involve distinct steps of T cell-dependent B cell activation. CD27 may be more important in the induction of plasma cell differentiation at a time when the expansion phase has already occurred.

B-Lymphocytes↗
PubMed1989

[Acute plasma cell leukemia].

Plasma Cell Leukemia is a very rare form of plasmocytic dyscrasia, whose clinical and pathological characteristics warrant its recognition as a distinct subentity. We report the case of a 60 years old man who presented a rapidly fatal acute plasma cell leukemia, with multiple osteolytic lesions, hipercalcemia, renal and cardiac failure.

Acute Disease↗
PubMed1995

T cell-induced B cell blasts differentiate into plasma cells when cultured on bone marrow stroma with IL-3 and IL-10.

B lymphocytes activated by T cells in secondary lymphoid organs mature into plasma cells after migration into the medullary cords of these organs, mucosal lamina propria or bone marrow. To analyze each step leading to plasma cell generation, we set up a two-step culture system of purified tonsillar B cells. In a primary stage, B cell blasts were generated by co-culturing B cells with an irradiated T cell clone activated with immobilized anti-CD3. In a secondary step, culturing these blasts on bone marrow stromal cells (BMSC) induced them to secrete large amounts of IgG, as well as some IgM and IgA. Other fibroblast-like cell lines were less efficient at sustaining the differentiation of blasts into Ig-secreting cells, suggesting that these are specific properties of BMSC. Addition of IL-3 and IL-10 further stimulated IgG secretion by B cell blasts cultured on BMSC, mostly the IgG1 subclass. These two cytokines probably acted through different pathways, as (i) the effect of IL-3 but not IL-10 was dependent upon prolonged T cell pre-activation and (ii) their combined stimulatory effect was additive. B cell blasts cultured on BMSC with a combination of IL-3 and IL-10 differentiated into non-proliferating plasma cells as determined by poor thymidine incorporation, typical cellular morphology, intense expression of intracytoplasmic Igs, very high levels of surface CD38 and lack of surface CD20.

Adult↗