Idiotypic studies on myeloma B cells

Acker, Annette Van; Conte, Federica; Hulin, Nicole; Urbain, Jacques

doi:10.1016/0014-2964(79)90136-1

Cited by 27 publications

(7 citation statements)

References 18 publications

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“…2). Although our methods would not reveal the existence of a small population of monoclonal B cells, the results do indicate that the large numbers reported by others (up to 50% of total PBL) (7,10,15,(17)(18)(19) can not be detected in PBL from the patient population studied here.…”

Section: Resultscontrasting

confidence: 77%

“…In patients categorized by treatment status, the pattern of HLA-DRT and of 41H.16 expression parallelled those of sIg' markers (Table II, Fig. 1 myeloma patients either through the use of anti-idiotypic reagents, or analysis of K/A light chain ratios, or of surface heavy chains (7,8,(10)(11)(12)(13)(14)(15)(16)(17)(18)(19) (Fig. 2).…”

Section: Resultsmentioning

confidence: 77%

“…Other workers have detected from 3 to 15% Id' cells in PBL from multiple myeloma patients in remission (7,10,17,19) and much larger numbers in relapse patients (10-47%) (7,10,13,17 …”

Section: Resultsmentioning

confidence: 95%

“…(7)(8)(9)(10)(11)(12)(13)(14). Both an expanded monoclonal lymphocyte pool and an absence of monoclonal lymphocytes related to the malignant plasma cells have also been reported (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20).…”

Section: Introductionmentioning

confidence: 94%

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Severe deficiency of B lymphocytes in peripheral blood from multiple myeloma patients.

Pilarski¹,

Mant²,

Ruether³

et al. 1984

J. Clin. Invest.

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Abstract. A major problem in the assessment of circulating B lymphocytes in multiple myeloma is the extent to which cells with passively absorbed Ig contribute to the assay. We have analyzed peripheral blood B cell numbers in 51 patients in various treatment categories by using an assay that is not subject to artifacts involving cytophilic Ig. We have defined a B lymphocyte by three different criteria (a) expression of a high surface density of Ig (b) expression of a high density of HLA.DR and (c) expression of a marker exclusive to surface Ig' B cells. By these criteria, normal individuals have an average of 6% B cells. In multiple myeloma patients, B cell levels in purified mononuclear cell preparations are severely reduced. Untreated patients and the majority of patients on intermittent chemotherapy have 20-600-fold fewer B cells than do normal donors (average = 0.3%). This decrease was even greater in whole blood of patients as compared with normal donors (100-1,000-fold fewer B cells). The number of B cells did not correlate with disease status or paraprotein concentration. We found no evidence to support the idea that B lymphocytes in patients include a substantial monoclonal subset.

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Section: Resultscontrasting

confidence: 77%

Section: Resultsmentioning

confidence: 77%

“…Other workers have detected from 3 to 15% Id' cells in PBL from multiple myeloma patients in remission (7,10,17,19) and much larger numbers in relapse patients (10-47%) (7,10,13,17 …”

Section: Resultsmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 94%

See 2 more Smart Citations

Severe deficiency of B lymphocytes in peripheral blood from multiple myeloma patients.

Pilarski¹,

Mant²,

Ruether³

et al. 1984

J. Clin. Invest.

View full text Add to dashboard Cite

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“…Myeloma cells usually synthesize a large amount of immuno globulin (Ig), and lack detectable surface Ig (slg) and other B cell-associated anti gens [reviewed by Foon et al, 1982]. How ever, several studies have shown that pa tients with myeloma have circulating B cells bearing idiotypic Ig structures of the monoclonal protein produced by mye loma cells [Lindstrom et al, 1973;Mellstedt et al, 1974;Van Acker et al, 1979;Bast et al, 1982], The presence of Pre-B cells expressing idiotypic cytoplasmic Ig (clg) has also been reported [Kubagawa et al, 1979]. These idiotypic lymphocytes are considered to be progenitors of myeloma cells, but little is known about the process of in vivo maturation of neoplastic cells.…”

Section: Introductionmentioning

confidence: 99%

Surface Expression of Human Myeloma Cells: An Analysis Using a Panel of Monoclonal Antibodies

Katagiri¹,

Yonezawa²,

Tamaki³

et al. 1984

Acta Haematol

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Neoplastic cells of 18 patients with multiple myeloma were studied using a panel of 6 monoclonal antibodies to B cells and monospecific antisera against the light chain types of immunoglobulin. OKT10 bound to the myeloma cells of all the patients, although only a small percentage of the cells reacted in 3 instances. Monoclonal slg was present in 5 patients. HLA-DR antigen detected with OKIa-1 was found in 5 patients. B1 bound to a small percentage of the myeloma cells only in 2 patients who had received treatment. The B1+ cells were always sIg+. In 3 patients, BA-2 reacted with the myeloma cells. BA-1 and BA-3 invariably did not react with the cells. Myeloma cells with B cell markers were found more frequently in treated patients than in untreated patients. The RPMI8226 line was also studied and found to react with OKT10 and BA-2. The results of this study show the presence of phenotypic variety in myeloma cells.

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Analysis of immunodeficiency in multiple myeloma: Observations and hypothesis

Pilarski

Mant

Ruether

1987

Clinical Laboratory Analysis

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Patients with multiple myeloma suffer from often profound immunodeficiency that seriously compromises both longevity and quality of life. The cellular basis for the immunodeficiency is unknown and the mechanism(s) giving rise to and possibly maintaining it is also unknown. In this review, evidence defining cellular defects in the nonmalignant B and T peripheral blood lymphocyte pool is summarized and discussed in terms of possible mechanisms that could give rise to the abberrant immune phenotype characteristic of many patients. The abnormalities we have defined include a deficiency of mature B lymphocytes, presence of often large numbers of pre-B cells in the blood, arrested differentiation of B cells into immunoglobulin (Ig)-secreting cells, and abnormal progenitorlike T cells in blood. The specificity repertoire of the remaining B lymphocyte population is heavily skewed toward recognition of idiotypic and shared epitopes on the variable region of Ig, perhaps reflecting immune reaction with the monoclonal myeloma lg. This may begin as a response to tumor antigen that gradually progresses to autoimmunity. A second subset of B cells present at abnormally high frequency in myeloma patients is that of antigen-experienced memory B cells, which probably encountered antigen prior to the events leading to frank myeloma. In this instance, the high frequency reflects a decrease in aggregate numbers of B cells, although it seems likely that expansion of memory clones also occurs. This is exemplified by the set of memory B cells specific for tetanus toxoid, which are present at normal number but highly enriched frequency in myeloma PBL. Both the antitumor B cells (anti-idiotype, and anti-lg) and the memory cells specific for environmental pathogens appear to be arrested in their differentiation to 19-secretors as evidenced by the lack of serum antibody in patients. The above observations are interpreted in terms of the hypothesis that immunoregulatory events triggered by the monoclonal myeloma lg establish and maintain the immunodeficiency. We speculate that autoimmune suppressor T cells specific for conserved determinants of Ig prevent pre-B cell differentiation to slg+ B cells, and B cell terminal differentiation to Ig-secretors. If correct, this analysis could lead to therapeutic approaches for the reversal of the immunodeficiency and perhaps some degree of control over the malignant growth.

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Idiotypic studies on myeloma B cells

Cited by 27 publications

References 18 publications

Severe deficiency of B lymphocytes in peripheral blood from multiple myeloma patients.

Severe deficiency of B lymphocytes in peripheral blood from multiple myeloma patients.

Surface Expression of Human Myeloma Cells: An Analysis Using a Panel of Monoclonal Antibodies

Analysis of immunodeficiency in multiple myeloma: Observations and hypothesis

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