The Effect of Anti‐Ia Antibody on Immunoglobulin‐secreting Cells from Healthy Individuals and Myeloma Patients

Nagai, Kenichi; Nagai, Takashi; Takatsuki, Kiyoshi; Uchino, Haruto

doi:10.1111/j.1365-3083.1982.tb00685.x

Cited by 3 publications

(1 citation statement)

References 15 publications

(11 reference statements)

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“…Historically, there has been a major emphasis on the search for B and/or T lymphocytes in the peripheral blood that bear the tumor Id. The literature is controversial in this respect, with some investigators able to detect very large numbers of surface Id+ (sId) lymphocytes (53,54), and others finding few or none (55,56). A significant problem in the detection of Id+ cells is the presence in blood of plasma cells able to secrete the Id (55 37-59).…”

Section: Introductionmentioning

confidence: 99%

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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Section: Introductionmentioning

confidence: 99%

Analysis of immunodeficiency in multiple myeloma: Observations and hypothesis

Pilarski

Mant

Ruether

1987

Clinical Laboratory Analysis

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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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Treatment of Rheumatoid Arthritis by Antibodies Directed Against Class II MHC Antigens

Sany¹

1988

Scandinavian Journal of Rheumatology

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The Effect of Anti‐Ia Antibody on Immunoglobulin‐secreting Cells from Healthy Individuals and Myeloma Patients

Cited by 3 publications

References 15 publications

Analysis of immunodeficiency in multiple myeloma: Observations and hypothesis

Analysis of immunodeficiency in multiple myeloma: Observations and hypothesis

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

Treatment of Rheumatoid Arthritis by Antibodies Directed Against Class II MHC Antigens

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