Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IgE antibodies can produce a late inflammatory response 6--12 h after allergen challenge which is characterized by diffuse edema, erythema, pruritus, tenderness and heat. That IgE is involved in inducing the late reaction was shown by the abolition of both immediate and late responses by passive transfer tests: (1) by heating atopic serum at 56 degrees C for 4 h; (2) by removing IgE from the atopic serum by a solid phase anti-IgE immunoabsorbent, and (3) by competitively inhibiting the binding of IgE antibodies to cells by an IgE myeloma protein. Also, both responses were induced by affinity chromatography-purified IgE antibody followed by antigenic challenge. Very similar lesions could be induced by intradermal injection of Compound 48/80. The late phase is characterized by edema and a mixed cellular infiltration, predominantly lymphocytic but also containing eosinophils, neutrophils and basophils. Direct immunofluorescent staining did not show deposition of immunoglobulins or complement components, except IgM in two of 15 and C3 in one of 15 patients, respectively.
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PMID:Late cutaneous reactions due to IgE antibodies. 33 13

S-sulfonated human IgG (S-sIgG) was prepared by treating IgG with sodium sulfite and sodium tetrathionate. The treatment resulted in the selective cleavage of interchain disulfide bonds of the IgG to give S-sulfonate groups. Complement fixing activities of aggregated S-sIgG and the immune complex formed with the S-sIgG antibody were very weak. S-sIgG at a high dose reduced the activity of the first complement component (C1) in normal human serum without any reduction of other complement components activites, but S-alkylated IgG at the same dose did not. Loss of C1 activity was not caused by either S-sulfonated myeloma proteins (IgA and IgE) or urea-treated S-sIgG, in which both inter- and intra-chain disulfide bonds were cleaved. These results suggest that the selective reduction of C1 by S-sIgG is due to a conformational change of the immunoglobulin.
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PMID:Interaction of S-sulfonated human IgG with human complement and its components. 33 17

The role of the mouse homocytotropic antibodies in passive cutaneous anaphylaxis reaction was investigated. One class of antibody was heat stable, detected at 2 h but not at 48 h after passive transfer, and belonged to a sublcass of mouse IgG. The other was heat labile, detected at 2 h and 48 h after passive transfer, and belonged to the IgE class of mouse immunoglobulins. In the presence of IgG, IgE homocytotropic antibody was not detected early after passive transfer. This was thought to be due to a masking of IgE by IgG antibodies rather than a competition for mast cell surface receptors, since inhibition studies with rat IgE myeloma protein suggested that mouse IgE and IgG1 may have different receptor sites on mast cell surfaces.
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PMID:Role of mouse IgG and IgE homocytotropic antibodies in passive cutaneous anaphylaxis. 34

Human lymphocytes isolated from adult peripheral blood and cord blood, tonsils, adenoids and spleens were analysed for Fc receptors for IgE (Fcepsilon) by rosette assays. The Fcepsilon+ cells were also characterized for their class of surface immunoglobulin (sIg), complement receptors, receptors for sheep erythrocytes (E), and Helix pomatia A haemagglutinin (HP), and their abilities to phagocytoze and adhere. The average number of Fcepsilon+ cells was in adult peripheral blood 1.2 +/- 0.4%, in cord blood 3.0 +/- 1.3%, in tonsils 4.2 +/- 5.2%, in adenoids 5.8 +/- 4.2%, and in spleens varied from 0.8% to 15.8% among individual patients. Overnight culturing of the lymphocytes under conditions that allowed detection of Fc receptors for IgM (Fcmu) usually lowered the number of Fcepsilon+ cells. Neuraminidase treatment caused no change. Rosette formation was inhibited by IgE myeloma proteins and their Fc fragments, but not by mildly reduced and alkylated and heated (56 degrees C) IgE, indicating that the receptors are specific for the native configuration of the IgE Fc fragment. Double cell surface marker analyses with fluoresceinated F(ab')2 fragments of purified anti-mu, delta, and gamma antibodies used to label the Fcepsilon rosette-forming lymphocytes from peripheral adult and cord blood showed that 50-80% were sIgM+ but only 0-28% were sIgD+. In contrast, approximately 80% of the Fcepsilon+ cells from tonsils, adenoids and spleens were sIgM+ and sIgD+. The Fcesilon+ lymphocytes represented 10-20% of the sIgM+ lymphocytes in both the peripheral adult and cord blood. Depletion and enrichment experiments indicated that most of the Fcepsilon+ cells bear complement receptors. Lymphocytes having both E and Fcepsilon receptors were not found. Furthermore, the lymphocytes with HP receptors, a marker for T cells and immature B cells, were Fcepsilon-. Monocytes and neutrophil granulocytes did not form Fcepsilon rosettes. These data indicated that a minor population of human B lymphocytes have Fcepsilon receptors. The majority of the Fcepsilon+ lymphocytes in the blood differ from those in tonsils, adenoids and spleen in that the majority of the former are sIgM+/sIgD- and the latter sIgM+/sIgD+. The sIgM+/sIgD- Fcepsilon+ cells in the blood are probably relatively mature lymphocytes since they lacked HP receptors, which are found on immature B cells.
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PMID:Characterization of human lymphocytes bearing Fc receptors for IgE isolated from blood and lymphoid organs. 36 62

An 131I-labelled IgE myeloma, standardized against the WHO reference serum for IgE was bound in varying concentrations to discs bearing anti-human light chain. These were used to construct a calibration curve for the subsequent binding of 125I-labelled anti-IgE, thus relating 125I counts to WHO IgE units. The calibrated anti-IgE could then be used to measure the actual amount of specific IgE bound to an allergen disc in the radioallergosorbent test. Using this standardized system, soluble allergen extracts could then be assayed by their ability to inhibit the binding of a defined amount of specific IgE, thereby enabling their activity to be expressed in WHO IgE units.
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PMID:Standardization of radioallergosorbent test (RAST) and allergen extracts in terms of the WHO standard for IgE. 42 86

The specific binding of radiolabelled IgE to a tissue culture lymphoblastoid cell line (Wil-2WT) was confirmed. The binding of IgE and Hamburger's IgE-derived pentapeptide Asp-Ser-Asp-Pro-Arg (HEPP) to Wil-2WT cells and to human leucocytes was compared. HEPP inhibition of IgE binding to leucocytes averaged 24% but with Wil-2WT cells only 12% inhibition was observed with double the amount of HEPP. Using myeloma IgE to inhibit the binding of tritiated HEPP to leucocytes and Wil-2WT cells confirmed the specificity of the peptide binding as well as the greater affinity of HEPP for leucocytes (basophils) compared to Wil-2WT lymphoblastoid cells. Based upon the extent of binding and the maximum inhibition attainable with HEPP it is suggested that the receptors for IgE on Wil-2WT cells, basophilic leucocytes and mast cells are not identical but that they share specificities in common. A new hypothesis for the mechanism of action of HEPP is proposed.
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PMID:Inhibition of IgE binding to tissue culture cells and leucocytes by pentapeptide. 52 Oct 61

A report on two patients with osteoclerotic myeloma is presented (myeloma with osteoblastic lesions). In case one, metastatic bone tumor of unknown origin was wrongly diagnosed initially. Because of increasing neurological symptoms laminectomy was performed. Biopsy led to the correct diagnosis of multiple myeloma of IgA-type. Patient also had a very severe peripheral neuropathy. The second patient had pancytopenia and osteosclerotic lesions of the pelvis. Bone marrow aspiration revealed so-called "empty marrow". Based on these findings, myelofibrosis was wrongly diagnosed at another hospital. Bone marrow aspiration, paper- and immunoelectrophoresis subsequently produced the correct diagnosis of multiple myeloma of IgG-type. Multiple myeloma usually is characterized by osteolytic lesions of the bones. However, the literature contains some 50 cases with osteosclerotic multiple myeloma, three different forms of which are described. In a fairly large percentage osteosclerotic multiple myeloma is combined with periphereal polyneuropathy. It would appear that in IgE-myeloma the incidence of sclerotic lesions is higher. Osteosclerotic multiple myeloma is very rare. It should however be considered if the differential diagnosis of osteosclerotic bone lesions is established.
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PMID:[2 cases of multiple myeloma with osteosclerosis]. 52 5

In order to study the regulation of IgE antibody formation, isologous anti-idiotypic antisera against the phosphoryl choline (PC)-specific BALB/c myeloma proteins T 15 and M 167 were passively administered to BALB/c in the course of an anti-PC IgE response. Isologous anti-T 15 antiserum had a long-lasting suppressive effect on the formation of IgE antibodies with PC specificity, whereas administration of anti-M 167 antiserum had no or only little effect, similar to that of normal BALB/c serum. This indicates that anti-PC IgE antibodies consist mainly of the T 15 idiotype or of cross-reacting idiotypes, and that IgE response is accessible to regulation with anti-idiotypic antibodies. This murine model may permit the study of regulation of an IgE response largely restricted to few defined idiotypes characterized as tumor proteins.
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PMID:Suppression of phosphorylcholine-specific IgE antibody formation in BALB/c mice by isologous anti-T 15 antiserum. 54 76

a) Leukocyte chemotactic activity, b) cytotaxic activity of patients' sera and c) influence of patients' sera on chemotactic activity of control leukocytes was studied in 18 patients with multiple myeloma, one patient with monoclonal IgE-gammopathy of undetermined significance and 32 controls. Chemotactic activity of patient leukocytes against Zymosan-activated normal serum and against Casein was reduced significantly. In addition, in 66% of the patients a chemotaxis inhibiting serum factor was observed. The Zymosan-induced generation of cytotaxic factors did not differ in patients or control sera. These data show that leukocyte inherent defects as well as serum factors give rise to reduced leukocyte chemotactic activity in patients with multiple myeloma. This impairment is likely to contribute to the increased susceptibility to infections in that disorder.
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PMID:[Disturbances in granulocyte chemotaxis in patients with multiple myeloma]. 55 23

The dependence of serum levels of polyclonal IgA, IgM, IgD and IgE on the amount of IgG paraprotein was studied in a series of 58 IgG paraproteinaemias. A significant correlation was found for IgA (r = -0.4782, p = 0.0007), for IgM (r = -0.3296, p = 0.0237) and for IgD (r = -0.3589, p = 0.0143) in the whole series of IgG paraproteinaemias and in the subgroup of myeloma paraproteinaemias (n = 34) for IgM (r = -0.4276, p = 0.0207) and for IgD (r = -0.4384, p = 0.0196).
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PMID:Serum levels of IgA, IgM, IgD and IgE in IgG paraproteinaemias. 61 91


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