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PubMed1993

Evidence for a bone marrow B cell transcribing malignant plasma cell VDJ joined to C mu sequence in immunoglobulin (IgG)- and IgA-secreting multiple myelomas.

Multiple myeloma is a B cell malignancy characterized by the expansion of plasma cells producing monoclonal immunoglobulins (Ig). It has been regarded as a tumor arising at the B, pre-B lymphocyte, or even stem cell level. Precursor cells are presumed to proliferate and differentiate giving rise to the plasma cell clonal expansion. Antigenic features and specific Ig gene rearrangement shared by B lymphocytes and myeloma cells have supported this hypothesis. However, the existence of such a precursor is based upon indirect evidence and is still an open question. During differentiation, B cells rearrange variable (V) regions of Ig heavy chain genes, providing a specific marker of clonality. Using an anchor polymerase chain reaction assay, these rearranged regions from five patients with multiple myeloma were cloned and sequenced. The switch of the Ig constant (C) region was used to define the B cell differentiation stage: V regions are linked to C mu genes in pre-B and B lymphocytes (pre-switch B cells), but to C gamma or C alpha in post-switch B lymphocytes and plasma cells (post-switch B cells). Analysis of bone marrow cells at diagnosis revealed the presence of pre-switch B cells bearing plasma cell V regions still joined to the C mu gene. These cells were not identified in peripheral blood, where tumor post-switch B cells were detected. These pre-switch B cells may be regarded as potential myeloma cell precursors.

B-Lymphocytes↗
PubMed2005

Early appearance of germinal center-derived memory B cells and plasma cells in blood after primary immunization.

Immunization with a T cell-dependent antigen elicits production of specific memory B cells and antibody-secreting cells (ASCs). The kinetic and developmental relationships between these populations and the phenotypic forms they and their precursors may take remain unclear. Therefore, we examined the early stages of a primary immune response, focusing on the appearance of antigen-specific B cells in blood. Within 1 wk, antigen-specific B cells appear in the blood with either a memory phenotype or as immunoglobulin (Ig)G1 ASCs expressing blimp-1. The memory cells have mutated V(H) genes; respond to the chemokine CXCL13 but not CXCL12, suggesting recirculation to secondary lymphoid organs; uniformly express B220; show limited differentiation potential unless stimulated by antigen; and develop independently of blimp-1 expression. The antigen-specific IgG1 ASCs in blood show affinity maturation paralleling that of bone marrow ASCs, raising the possibility that this compartment is established directly by blood-borne ASCs. We find no evidence for a blimp-1-expressing preplasma memory compartment, suggesting germinal center output is restricted to ASCs and B220(+) memory B cells, and this is sufficient to account for the process of affinity maturation.

Adoptive Transfer↗
PubMed1992

Immunophenotype and DNA content of myeloma cells in primary plasma cell leukemia.

To clarify the biological characteristics of the myeloma cells in primary plasma cell leukemia (PCL), we studied the immunological phenotype and DNA content of cells from five patients with primary PCL as compared to those from the patients with typical multiple myeloma (MM). In two of five patients with PCL myeloma cells had B-cell-associated antigens (B1, J5) and surface immunoglobulin in addition to plasma cell associated antigens, suggesting that these cells are immunologically immature as compared to mature plasma cells. Concerning the DNA content of myeloma cells, two of four patients had hypodiploid while two had diploid myeloma cells. In contrast, 24 of the 37 (65%) patients with typical MM had hyperdiploid and 1 had hypodiploid myeloma cells. These observations suggest that the myeloma cells in PCL are immunologically heterogeneous. The increased incidence of hypodiploidy in PCL may explain its relatively poor prognosis as previously shown in those with typical MM and hypodiploid DNA content.

Adult↗
PubMed1994

Fine-needle aspiration of plasma cell disorders: special emphasis on plasma cell subtype.

Fine-needle aspiration cytology and clinical presentations of 16 cases of plasma cell dyscrasias (PCD) have been studied in a period of 6 yr. There were seven cases of solitary plasmacytomas of bones, two cases of extramedullary plasmacytomas, and seven cases of multiple myelomas. Differential counts of mature and immature plasma cells along with presence of cell clumps, mitosis, and bi/multinucleations were studied. The cytological findings revealed no correlation with the different subtypes of PCDs; however, it was helpful in the differential diagnosis. Bone marrowing findings, immunological parameters, available histopathology, and X-ray appearances were analysed. Clinical diagnosis of PCDs were made in only three cases. Thus fine-needle aspiration biopsy was considered as an important diagnostic modality in tissue diagnosis of plasma cell tumors, particularly in solitary plasmacytoma of bone and extramedullary plasmacytoma.

Adult↗
PubMed2005

Regulation of plasma-cell development.

Plasma cells are the terminally differentiated, non-dividing effector cells of the B-cell lineage. They are cellular factories devoted to the task of synthesizing and secreting thousands of molecules of clonospecific antibody each second. To respond to microbial pathogens with the necessary specificity and rapidity, B cells are exquisitely regulated with respect to both development in the bone marrow and activation in the periphery. This review focuses on the terminal differentiation of B cells into plasma cells, including the different subsets of B cells that become plasma cells, the mechanism of regulation of this transition, the transcription factors that control each developmental stage and the characteristics of long-lived plasma cells.

Animals↗
PubMed2004

A common clonal origin of nodal marginal zone B-cell lymphoma and plasma cell myeloma demonstrating different immunophenotypes: a case report of composite lymphoma.

We demonstrated an 83-year-old male case of composite lymphoma. Before 18 years, he was diagnosed with nodal marginal zone B-cell lymphoma in the cervical lymph node. Peripheral blood showed anemia and IgA (kappa)-type monoclonal gammopathy (IgA; 3,625 mg/dL). Bone marrow aspiration biopsy exhibited plasma cell myeloma, in which atypical plasma cells were positive for cytoplasmic IgA (kappa) and atypical lymphoid cells intermingled were positive for CD20. In contrast, cervical lymph node biopsy revealed nodal marginal zone B-cell lymphoma, in which lymphoma cells were positive for cytoplasmic IgG (lambda). Southern blotting analysis of the IgH gene showed same clonal rearrangement band in both lymph node and bone marrow samples and additional band in the bone marrow. Sequence analyses of the IgH gene showed an identical sequence of CDR3 in both samples. Thus, we demonstrated a common clonal origin of composite lymphoma comprising nodal marginal zone B-cell lymphoma and plasma cell myeloma. Nodal marginal zone B-cell lymphoma recurred in cervical lymph node and involved into the bone marrow, differentiating into plasma cell myeloma in which Ig isotype switched and monoclonal gammopathy developed. Sequence analysis of the IgH gene was a powerful tool for determination of clonal origin.

Aged↗
PubMed2002

NPM-ALK transgenic mice spontaneously develop T-cell lymphomas and plasma cell tumors.

Anaplastic Large Cell Lymphomas (ALCLs) carry translocations in which the anaplastic lymphoma kinase (ALK) gene is juxtaposed to various genes, the most common of which is the NPM/B23 gene. ALK fusion proteins result in the constitutive activation of ALK tyrosine kinase, thereby enhancing proliferation and increasing cell survival. A direct role for NPM-ALK in cellular transformation has been shown in vitro with immortalized cell lines and in vivo using retroviral transfer experiments. Nonetheless, there is no direct evidence of its oncogenic potential in T lymphocytes, which represent the most common target of ALK chimeras. Here, we describe a new mouse model of lymphomagenesis in which human NPM-ALK transcription was targeted to T cells. NPM-ALK transgenic (Tg) mice were born with the expected mendelian distribution, normal lymphoid organs, and a normal number and proportion of helper and suppressor T cells. However, after a short period of latency, all NPM-ALK Tg mice developed malignant lymphoproliferative disorders (mean survival, 18 weeks). NPM-ALK Tg thymic lymphomas displayed a T-cell phenotype characteristic of immature thymocytes and frequently coexpressed surface CD30. A subset of the NPM-ALK Tg mice also developed clonal B-cell plasma cell neoplasms. These tumors arose in peripheral lymphoid organs (plasmacytomas) or within the bone marrow and often led to peripheral neuropathies and limb paralysis. Our NPM-ALK Tg mice are a suitable model to dissect the molecular mechanisms of ALK-mediated transformation and to investigate the efficacy of new therapeutic approaches for the treatment of human ALCL in vivo.

Animals↗
PubMed1993

Analysis of the B-cell compartment in plasma cell leukemia and multiple myeloma: immunoglobulin gene rearrangement of EBV-infected B-cell lines.

Multiple myeloma (MM) is defined as a tumoral expansion of plasma cells occurring in the bone marrow and sometimes in the peripheral blood (plasma-cell leukemia, PCL). Many reports have demonstrated a clonal expansion of B cells bearing the same idiotypic determinants as the myeloma protein (idiotypic B cells) in MM, suggesting that they could belong to the malignant clone. In order to investigate whether the B-cell population is a malignant component or not, either in the peripheral blood of patients with PCL or in the bone marrow of patients with MM, we derived B-cell lines by infecting, with the Epstein-Barr virus (EBV), cultures in limiting dilution of mononuclear cells from six patients. A limiting dilution culture was used to prevent the elimination of slowly proliferating clones by the more rapidly dividing ones, and thus to get the most exact representation of the B-cell repertoire of these patients. The cloning efficiency of the EBV-infected cells was similar in patients and healthy individuals (range: 1 in 100 to 1 in 1650 B cells). All of the clones obtained from a single patient exhibited different clonal immunoglobulin gene rearrangements (IGR), proving the validity of our cloning technique. No tumoral clones (61 clones analysed) showed the IGR pattern specific of autologous myeloma cells. These results indicate that malignant plasma cells cannot be immortalized with EBV. These results show that, if malignant B cells (pre-switch or post-switch) exist, they could be present only in a minor population, and the corollary of this is that there is a major population of non-malignant B cells in the sites of tumoral proliferation of patients with MM. This is remarkable in view of numerous reports showing a profound defect of the polyclonal B lymphopoiesis in these patients, and even an absence of B lymphocytes. Thus, these results challenge the existence of a major compartment of malignant idiotypic B cells and favor the hypothesis of non-malignant B cells sharing cross-reactive idiotypes with the autologous myeloma protein.

Antigens, CD↗
PubMedDate not supplied

Interaction between clonal plasma cells and the immune system in plasma cell dyscrasias.

The term "monoclonal gammopathy" (MG) includes a group of clonal plasma cell disorders, which show heterogeneous clinical behavior. While multiple myeloma (MM) and plasma cell leukemia (PCL) are incurable malignant diseases, most patients with MG of undetermined significance (MGUS) show an indolent/benign clinical course. Evidence has accumulated which supports the role of the bone marrow microenvironment in MG. Accordingly, the survival, drug-resistance and proliferation of MM cells have been shown to be largely dependent on a supportive microenvironment. Among the different environment-associated parameters, those related to the status/activity of the immune system are particularly relevant. This review focuses on the different ways clonal plasma cells (PC) interact with the immune system in different models of MG, to characterize crucial events in the development and progression of MG. These advances may support the design of novel therapeutic approaches in patients with MG.

Bone Marrow↗
PubMed1989

Monoclonality and polyclonality of plasma cells in Castleman's disease of the plasma cell variant.

Castleman's disease of the plasma cell variant observed in 21 patients was investigated morphologically and by immunohistochemistry. The male to female ratio was 2.5:1. The age ranged from 18 to 71 years (mean age 47.6 years). Histologically, the lesions were characterized by numerous, evenly distributed germinal centres ranging from large hyperplastic to small hyaline-vascular types with moderate to extensive sheets of plasma cells in between. In all cases with generalized lymph node enlargement dilated sinuses could be found. Immunohistochemical studies demonstrated a polyclonal plasma cell population in 11 of 18 lesions. Seven lesions contained a monoclonal plasma cell population, five with IgG/lambda and two with IgA/lambda; clinically, two of these patients had generalized lymphadenopathy; in none could manifestation of a plasmacytoma be found outside the lymph node lesion; only two of the seven patients exhibited a paraproteinaemia (IgG/lambda and IgA/lambda, respectively) corresponding to the Ig type of the proliferated plasma cells. Six patients with polyclonal lesions had constitutional symptoms such as fever, anaemia, polyclonal hypergammaglobulinaemia; one of these six patients manifested symptoms consistent with a diagnosis of Takatsuki syndrome. The monoclonal plasma cell type of Castleman's disease did not progress to a generalized disease. This monoclonal variant may be a lymph nodebased type of benign monoclonal gammopathy.

Adolescent↗
PubMed1997

CD31 (JC70) expression in plasma cells: an immunohistochemical analysis of reactive and neoplastic plasma cells.

AIMS: To investigate the immunohistochemical expression of CD31 (JC70) in normal and neoplastic plasma cells. METHODS: Plasma cells in bone marrow biopsies and extramedullary locations were examined. All extramedullary biopsies were formalin fixed and paraffin embedded. The bone marrow biopsies were fixed in formal acetic acid and embedded in paraffin wax. Twenty multiple myelomas (12 bone marrow and eight extramedullary deposits), 10 extramedullary plasmacytomas, and 30 biopsies with reactive plasma cells (10 bone marrow, 20 extramedullary biopsies) were stained with anti-CD31 (JC70) using the streptavidin-biotin detection system with diaminobenzidine as a chromogen. Antigen retrieval in bone marrow biopsies was achieved by pressure cooking. In all other biopsies, antigen retrieval was achieved by microwave pretreatment. RESULTS: All 20 extramedullary cases with reactive plasma cells showed intense membrane staining. Focal staining was detected in reactive plasma cells in bone marrow biopsies. Five of 10 plasmacytomas showed membrane staining. None of the cases of multiple myeloma, either medullary or extramedullary, showed any immunoreactivity for CD31. CONCLUSIONS: CD31, a member of the immunoglobulin supergene family of cell adhesion molecules, is strongly expressed in extramedullary reactive plasma cells, focally in bone marrow reactive plasma cells, and occasionally in extramedullary plasmacytomas.

Cohort Studies↗
PubMed1992

[IgG-lambda-type multiple myeloma with plasma-cell pericardial effusion and terminal plasma-cell leukemia].

Monoclonal gammopathy of type IgG-lambda (IgG concentration 27.8 g/l) was discovered by chance in a 66-year-old woman with aortic and mitral valve disease. The patient declined any further diagnostic procedures. Three months later she experienced severe pain in the lumbar spine and developed decompensated cardiac failure with pulmonary and ankle edema. The IgG concentration had risen to 50.5 g/l. Echocardiography showed a large pericardial effusion and 600 ml of bloodstained fluid containing numerous plasma cells was aspirated (total protein 81.8 g/l, gamma-globulin 38.9%). Iliac crest biopsy showed diffuse infiltration with polymorphic plasma cells, but the differential count in peripheral blood was unremarkable. Multiple myeloma of Stage IIa was diagnosed and she was given cytostatic therapy with 17.5 mg melphalan and 112 mg methylprednisolone daily by mouth (for 4 days at intervals of 6 weeks). Though at first the IgG concentration fell, it later rose again. The beta 2-microglobulin level was raised at 30 mg/l. After three cycles of chemotherapy the patient complained of severe pain in the hips and thighs. The blood film now showed numerous, predominantly immature plasma cells. A few days later, having been ill for four months in all, she died, showing all the signs and symptoms of plasma cell leukaemia.

Aged↗
PubMed1999

Frequent expression of haemopoietic and non-haemopoietic antigens by reactive plasma cells: an immunohistochemical study using formalin-fixed, paraffin-embedded tissue.

Unlike other B cells, plasma cells (PC) react with only a few antibodies against haemopoietic antigens. We investigated 36 specimens exhibiting a reactive increase in PC numbers (i.e. plasmacytosis, PC hyperplasia) with a broad panel of antibodies suitable for use on formalin-fixed, paraffin-embedded tissue, and compared the findings with those obtained in 51 cases of multiple myeloma (plasmacytoma). Regardless of the immunostaining pattern for immunoglobulin light and heavy chains, reactive PC reacted with at least two and at most six of seventeen antibodies detecting haemopoietic antigens [Ber-H2/CD30 (91%), anti-leucocyte common antigen (LCA)/CD45 (86%), KP1/CD68 (64%), MB2 (57%), 4KB5/CD45RA (37%), DF-T1/CD43 (28%), UCHL1/CD45RO (20%), L26/CD20 (17%), MT2 (14%) and Mac387 (8%)], and with at least one and at most four of six antibodies against non-haemopoietic antigens [anti-epithelial membrane antigen (EMA) (94%), anti-vimentin (77%), anti-pan-cytokeratin/KL1 (74%), BMA120 (51%) and HMB45 (14%)]. Five antibodies stained reactive PC significantly more often than neoplastic PC: Ber-H2/CD30 (p < or = 0.0000), KP1/CD68 (p < or = 0.0000), anti-LCA/CD45 (p < or = 0.0000), anti-EMA (p < or = 0.0339) and anti-pancytokeratin/KL1 (p < or = 0.0000). The more frequent and more heterogeneous expression of antigens by reactive PC suggests that the aberrant immunoreactivity of neoplastic PC in plasmacytoma is not due to the process of malignant transformation in an early step of B-cell differentiation, but could reflect the heterogeneity of antigen expression by normal PC.

Fixatives↗
PubMed2002

Detection and characterization of plasma cells in peripheral blood: correlation of IgE+ plasma cell frequency with IgE serum titre.

In atopic patients and patients with hyper-IgE syndrome (HIE) highly elevated IgE serum levels can be detected. Due to their very low frequency little is known about IgE-producing plasma cells (PC) in peripheral blood. We used CD138 MACS microbeads to enrich plasma cells from peripheral blood of normal donors, atopic patients and one HIE patient. CD138+ cells were mainly CD45+, CD44++, CD19dim, CD38++, CD27++, CD86+, HLA-DR+/++, CD71dim, VLA-4+, VLA-5-, CD28-, CD25-, CD69-, CLA-, CD20-, CD21- and CD22-. They show weak expression of surface Ig but high levels of intracellular Ig and they secrete Ig in culture. Thus CD138+ cells from peripheral blood show characteristics of early plasma cells. IgE+ CD138+ plasma cells could be detected in 19 of 24 normal donors with an average frequency of 0.06% IgE+ cells among CD138+ cells. Higher frequencies were detected in atopic patients, atopic patients with markedly elevated serum IgE levels and the hyper-IgE patient with an average of 0.32%, 7.21% and 6.54%, respectively. Additionally, using the recently developed cellular affinity matrix technology, we were able to detect IgE secreting plasma cells and thereby could demonstrate that most of the IgE secreting cells express CD138. The frequency of IgE+ CD138+ cells among PBMC correlated highly significantly with serum IgE titres (r = 0.8532***), indicating that IgE secreting CD138+ cells in peripheral blood are directly related to the plasma cell pool contributing to the IgE titre.

Antibody Affinity↗
PubMed1975

Needle-like crystals in plasma cells in a patient with a plasma cell proliferative disorder.

A patient with a plasma cell proliferative disorder and a monoclonal IgG-kappa protein in the serum was observed over a period of four years. Two unusual features were seen in this patient: (1) An apparently benign course in spite of relatively large and slowly increasing amounts of Bence Jones protein (monoclonal kappa light chains) in the urine, and (2) crystalline structures located outside the cisternae of the endoplasmic reticulum in a large number of bone marrow plasma cells. The crystals, which ultrastructurally appeared to be composed of protein material, were not stained by immunofluorescent antisera to immunoglobulins. They were, however, observed only in cells staining for gamma heavy and kappa light chains. This suggest an association between the crystalline structures and the synthesis of monoclonal immunoglobulin proteins.

Bence Jones Protein↗
PubMed2001

Gingival plasma cell granuloma.

Plasma cell granulomas (pseudotumors) are rare benign, tumor-like proliferations composed chiefly of plasma cells that manifest primarily in the lungs, but may occur in various anatomic locations. We report this case of a 54-year-old male who presented with an unusual maxillary anterior gingival overgrowth treated by excisional biopsy. Histological examination revealed a dense inflammatory cell infiltrate containing mainly plasma cells. Immunohistochemistry for kappa and lambda light chains showed a polyclonal staining pattern confirming a diagnosis of plasma cell granuloma. Intraoral plasma cell granuloma is exceedingly rare, although case reports documenting such lesions have been reported. This case highlights the need to biopsy unusual lesions to rule out potential neoplasms.

Diagnosis, Differential↗
PubMed1980

2 translocations, t(11;14) and t(1;6), in a patient with plasma cell leukaemia and 2 populations of plasma cells.

2 translocations, t(11;14) and t(1;6), were found in 24 out of 46 metaphases in bone marrow cells from an untreated patient with plasma cell leukaemia. The predominating cell population produced only kappa chains while a minute population produced IgG kappa. All serum Ig's were low and only minimal amounts of monoclonal IgG kappa were found in the serum and very small amounts of kappa light chains in the urine. Analyses of ours and 2 other reported patients indicated the possibility that the location of breakpoints on the chromosomes may be of etiologic importance for the type of light chain and perhaps for the class of heavy chain.

Aged↗