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The majority of the polyclonal plasma cells identified in the synovial tissues of rheumatoid arthritis patients contain immunoglobulins that express a common idiotype related to that of the monoclonal cryoglobulins of the Wa group (RCRI). In these same tissues, there are twice as many plasma cells which are marked by a common idiotype yet do not show binding of aggregated IgG. These plasma cells are members of an idiotypically parallel set relative to those which produce rheumatoid factor. Direct comparison of rabbit polyclonal RCRI+ plasma cells with murine monoclonal RCRI+ plasma cells using two color fluorescent counterstains shows that the epitope recognized by the monoclonal anti-RCRI exists among a set of epitopes present in the RCRI. Since all the monoclonal RCRI+ plasma cells are not also positive with the polyclonal anti-RCRI antisera, the epitope characterized by the monoclonal antibody Glo 86.3 is not included among the set of epitopes the polyclonal antiserum identifies. A suitably absorbed anti-idiotypic polyclonal antiserum is superior to monoclonal antibodies for the purpose of detection of molecules (and cells) that are part of a polyclonal reaction involved in a given immune response.
Primary plasma cell leukemia (PPCL) is a rare form of disease accounting for 1-2 percent of myelomas. Between September 1990 and November 2000, among 540 patients with myeloma studied, 24 fulfilled the criteria of PPCL (4.4 percent). We found high frequencies of female patients (62 percent), Bence Jones proteinuria (79 percent), anemia (88 percent), bleeding (54 percent), confusional syndrome (42 percent), weight loss (71 percent), hepatomegaly (25 percent), splenomegaly (21 percent), leukocytosis (62 percent), and thrombocytopenia (71 percent). High serum levels of creatinine, calcium, lactate dehydrogenase (LDH), and beta(2)-microglobulin were detected in 50 percent, 37 percent, 58 percent, and 71 percent, respectively. Four patients were treated with vincristine, melphalan, cyclophosphamide, prednisone, and adriamycin (VMCPA), 12 with vincristine, adriamycin, and dexamethasone (VAD), and 8 with M-80 (oral melphalan 80 mg/m(2) plus dexamethasone 40 mg/m(2)). There was a trend toward lower values of Karnofsky score (P=0.07) and higher values of LDH (P=0.2) in the VAD group. Other clinical characteristics were comparable among the three groups. Complete plus partial responses were achieved in one and six patients treated with VMCPA and M-80, respectively. All patients treated with VAD failed to respond to treatment. Patients receiving the M-80 regimen experienced higher platelet toxicity (P=0.05), vomiting (P<0.0003), and mucositis. Also, the need for red blood cell transfusions was higher in the M-80 group. Median overall survival was 60 days. Overall survival was better in patients achieving complete or partial response. In conclusion, our study illustrates that intermediate doses of melphalan plus dexamethasone are an effective chemotherapy regimen for this aggressive disease. Response to treatment is the only prognostic factor for survival in these patients.
Circulating plasma cells from six patients who had plasma cell leukemia were examined by transmission and scanning electron microscopy. In all cases, leukemic plasma cells constituted more than 60% of the total cell population in the peripheral blood. Transmission electron microscopy confirmed that the leukemic cells were plasmacytic and that many of them contained parallel arrays of rough endoplasmic reticulum and a prominent Golgi apparatus. Scanning electron microscopy confirmed previous observations of cultured myeloma cells and showed that plasma cells display varying numbers of surface blebs in addition to short stublike microvilli. The microvilli were frequently clustered together in one area of the surface. Bleb formation appears to be characteristic of plasma cells, but its nature is still obscure. Current knowledge of this phenomenon is briefly reviewed.
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UNLABELLED: Multiple myeloma plasma cells are actively dividing cells with the long surviving ability in the ex-vivo culture. In the effort for better understanding of the proliferative potential of malignant myeloma cells and establishment of permanent myeloma cell lines we performed long term cultures of human myeloma cells ex-vivo. During the last two years we cultured 41 bone marrow samples from 39 patients with multiple myeloma. Cells were cultured in the RPMI 1640 culture medium with 15% fetal calf serum at 37 degrees C in 5% CO2 and approximately one third of the culture medium was changed regularly twice a week. Most of the marrows cultures died by apoptosis within 30 days. Four bone marrow samples were cultured for more than 11 months, however, no culture can be qualified as an established cell line. In three cases permanent B-lymphoblastoid cell lines were established (UHKT-55, UHKT-56 a UHKT-57) but secondary immortalization by Epstein-Barr virus was suggested. CONCLUSIONS: Presented results suggest that myeloma plasma cells can survive and are able to proliferate in the ex-vivo culture for several months up to one year independently on the addition of any external growth factor without spontaneous apoptosis or necrosis. The probability of the establishment of a permanent cell line of plasma cell origin is, however, low. Presence of accessory bone marrow cells was the most important factor for the long-term survival of myeloma cells.
Considerable progress has been made in identifying the transcription factors involved in the early specification of the B-lymphocyte lineage. However, little is known about factors that control the transition of mature activated B cells to antibody-secreting plasma cells. Here we report that the transcription factor XBP-1 is required for the generation of plasma cells. XBP-1 transcripts were rapidly upregulated in vitro by stimuli that induce plasma-cell differentiation, and were found at high levels in plasma cells from rheumatoid synovium. When introduced into B-lineage cells, XBP-1 initiated plasma-cell differentiation. Mouse lymphoid chimaeras deficient in XBP-1 possessed normal numbers of activated B lymphocytes that proliferated, secreted cytokines and formed normal germinal centres. However, they secreted very little immunoglobulin of any isotype and failed to control infection with the B-cell-dependent polyoma virus, because plasma cells were markedly absent. XBP-1 is the only transcription factor known to be selectively and specifically required for the terminal differentiation of B lymphocytes to plasma cells.
BACKGROUND: Plasma cell infiltration of the liver can be detected in 25 to 40% of patients with multiple myeloma. However, there are only rare cases of multiple myeloma clinically presenting as acute liver disease. CASE REPORT: We report an 88-year-old woman with painless jaundice and abnormal liver function tests, resembling acute cholestatic hepatitis. Viral hepatitis as well as autoimmune hepatitis could be excluded. Liver biopsy revealed a diffuse portal and sinusoidal infiltration of plasma cells with lambda light chain restriction. Serological immune fixation disclosed monoclonal gammopathy of IgG lambda with bone marrow infiltration of 25% plasma cells. After administration of 60 mg prednisolone per day, the elevated liver enzymes declined considerably. CONCLUSION: Hepatic plasma cell infiltration of multiple myeloma can, in rare cases, manifest as acute cholestatic hepatitis, which may respond to treatment with corticosteroids.
Plasma cell granuloma occurs most frequently in the lung and upper respiratory tract; fewer than ten cases have been reported to occur in the central nervous system. A case of intracranial plasma cell granuloma in a 69-year-old male was reported. He visited our clinic, complaining of progressive visual disturbance. The CT in this patient showed a suprasellar mass, diagnosed as a tuberculum sellae meningioma. Over a 10-year observation period the tumor grew remarkably and, when finally removed, it proved to be a plasma cell granuloma. This report presents CT scans and MR images and a review of the literature relevant to this rare intracranial lesion. The most common preoperative diagnosis in these cases, as reported here, was meningioma. Although plasma cell granuloma rarely occurs intracranially, the existence of this entity should be borne in mind in the differential diagnosis of meningioma.
Plasma cell granuloma of the lung is an uncommon and non-malignant neoplasm that may present difficulties in both diagnosis and management. We report a 52-year-old male who was admitted to our hospital due to fever and an abnormal shadow on chest roentgenography. Chest computed tomography revealed a tumor shadow with a cavity in the left upper lobe. However, neither bronchofiberscopy nor serum examinations suggested a diagnosis. Video-assisted thoracoscopic surgery (VATS) was performed and postoperative pathological examination of the resected specimen showed plasma cell granuloma. The postoperative course was uneventful. No recurrence was observed 10 months after the operation. As plasma cell granuloma of the lung is histologically benign, surgery should be performed to preserve the maximal residual lung with no lesion. VATS is the method of choice for treatment of pulmonary plasma cell granuloma.
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The majority of immunoglobulin in tears in various species is of the IgA isotype and is produced mainly by plasma cells of the lacrimal gland. The mechanism responsible for lodging of IgA committed cells in lacrimal gland is unknown, but could occur as a result of retained T helper cells in the lacrimal gland. The present experiments use an in-vitro adherence assay to examine the interaction of various murine lymphocyte populations with frozen sections of mouse lacrimal gland. Splenic and Peyer's Patch lymphocytes, as well as T-cell enriched and T-cell depleted lymphocyte populations were incubated with thin sections of lacrimal gland. Adherent lymphocytes were counted in randomly selected fields for each experiment. Each lymphocyte population was tested at least three times. It was found that more Peyer's Patch cells adhered to lacrimal gland than did spleen cells, and this increase was due to T-cells. The T-cell population responsible for adherence was localized to the helper T-cell population which appeared greater with Peyer's Patch T helper cells than splenic T helper cells. The data suggest that a lacrimal gland-T-cell interaction could retard the migration of a subpopulation of T helper cells as they migrate through the lacrimal gland. It is speculated that such T helper cells could be responsible for the terminal differentiation of IgA B cells to plasma cells, thus explaining the predominance of IgA plasma cells in the lacrimal gland.
Plasma cell granuloma of the thyroid is an uncommon lesion; only 6 cases have been reported in the English literature to date. All reported cases occurred in women, mostly after the age of 50 years. We report a case of plasma cell granuloma of the thyroid in a 46-year-old woman with a 20-year history of euthyroid goiter and a positive family history of goiter in 3 close relatives. The lesion was composed of sheets of plasma cells involving the entire parenchyma that histologically resembled plasmacytoma. Plasmacytoma was excluded by demonstration of polyclonal kappa/lambda light chain immunostaining and by lack of evidence of clonal bands by polymerase chain reaction for immunoglobulin heavy-chain gene rearrangement. Similarly, the predominant histologic pattern in all previously reported cases is that of marked plasma cell infiltration. A family history of thyroid disease (goiter, thyroiditis) was associated with diffuse involvement of the thyroid. Prognosis after surgery is excellent, and to our knowledge no cases of malignant transformation or recurrence have been described.
The intramedullary solitary plasma cell tumour is an invasive tumour of plasma cells. Three cases of solitary intramedullary plasmacytoma and one case of follicular lymphoma with marked plasma cell component are described. The diagnostic and therapeutic difficulties are discussed.
The origin of human ileal lamina propria (LP) plasma cells has been investigated using a technique based on microdissection of cells from immunohistochemically stained tissue sections. We have sequenced rearranged IgVH4.2 1, IgVH 5 family and IgVH6 genes from Peyer's patch germinal center (GC) cells and plasma cells from the ileal LP. Clonally related cells were identified by comparison of their complementarity determining region (CDR) 3 sequences and patterns of somatic mutation. We observed Ig genes from B cells in the GC of Peyer's patches which were related to Ig genes from plasma cells in the ileal LP, demonstrating that clonally related cells span these sites. In addition, groups of clonally related. but diversified plasma cells were common in the lamina propria. All Ig genes isolated from LP plasma cells were heavily mutated. The distribution of mutations in the CDR of the Ig heavy chain variable region (VH) genes which were considered to be the expressed alleles in LP plasma cells was consistent with an affinity-matured response. These observations provide compelling evidence for the origin of human ileal plasma cells from the Peyer's patches.
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Plasma cells represent the final stage of B lymphocyte differentiation. Most plasma cells in secondary lymphoid tissues live for a few days, whereas those in the lamina propria of mucosa and in bone marrow live for several weeks. To investigate the regulation of human plasma cell survival, plasma cells were isolated from tonsils according to high CD38 and low CD20 expression. Tonsillar plasma cells express CD9, CD19, CD24, CD37, CD40, CD74, and HLA-DR, but not CD10, HLA-DQ, CD28, CD56, and Fas/CD95. Although plasma cells express intracytoplasmic Bcl-2, they undergo swift apoptosis in vitro and do not respond to CD40 triggering. Bone marrow fibroblasts and rheumatoid synoviocytes, however, prevented plasma cells from undergoing apoptosis in a contact-dependent fashion. These data indicate that fibroblasts may form a microenvironment favorable for plasma cell survival under normal and pathological conditions.