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)

The role of H-2 genetic factors in the development of benign monoclonal gammopathy (BMG) was investigated in six H-2 congenic C57BL and BALB strains (C57BL/10.ScSn and BALB.B: H-2b; B10.D2 and BALB/c: H-2d; B10.BR and BALB.K: H-2k) during ageing. The frequencies of homogeneous immunoglobulins (H-Ig), both single and multiple, in the three C57BL strains were higher than those in the corresponding three BALB strains. No relationship was found with a particular H-2 haplotype. The most frequent H-Ig isotype within the C57BL strains was IgG2a, within BALB.B and BALB.K mice IgG3 and in BALB/c mice IgG1. Categorization of the monoclonal gammopathies (MG) on the basis of their origin showed a single transient monoclonal B-cell proliferation in 2-5% and 3-9% of the C57BL and BALB mice positive for H-Ig, respectively. Multiple myeloma or B-cell lymphoma were found to be responsible for about 1% of the paraproteinaemias in all strains. Persistent, non-progressive MG, most likely BMG, was detected in 70-81% and 39-46% of the C57BL and BALB mice positive for H-Ig, respectively. The remaining 14-24% and 50-58% of the, respectively, C57BL and BALB mice positive for H-Ig could not be evaluated in time. The H-2 haplotypes under investigation were not associated with the onset, occurrence, multiplicity, persistence or isotype of the MG developing in these H-2 congenic C57BL and BALB strains during ageing.
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PMID:The influence of H-2 genetic factors on the development of benign monoclonal gammopathy in ageing H-2 congenic C57BL and BALB mice. 344 48

Infection with Listeria monocytogenes stimulates T cell proliferation and T cell-derived lymphokine production. The release of lymphokines, in turn, "activates" macrophages, enhancing their bactericidal capacity. Because prior studies suggest that I-A+ accessory cells play a critical role in this pathway, we assessed the effects of an anti-I-A antibody on the murine host resistance to listerial infection. To this end, we infused Listeria into control C57BL/6 mice (I-Ab haplotype) and mice of the same strain which had been pretreated 18 hr earlier with D3137 (a monoclonal IgG2a anti-I-Ab,d antibody). Preliminary studies demonstrated that this antibody can markedly inhibit antigen-induced proliferation of Listeria-dependent T cells in vitro and (at a dose of 1 mg/animal) can markedly reduce I-A expression on splenocytes in vivo. Even though D3137 pretreatment prevented the splenomegaly normally observed after Listeria infusion into mice, it protected animals infused with otherwise lethal concentrations of Listeria. Because antibody-treated animals had sevenfold fewer organisms in their spleens 18 hr after infection and 1000-fold fewer organisms than control animals 3 days after infection, improved survival resulted from an antibody-induced increase in the bactericidal capacity of the MPS. Protection was not noted when C1.18.4 (an IgG2a myeloma protein without known antibody activity) was infused into C57BL/6 mice or when D3137 was infused in B10.BR (I-Ak) mice. D3137 also protected (B10 X B10.BR)F1 mice (which are hybrids bearing I-Ab and I-Ak), suggesting that complete blockade of antigen presentation is not a prerequisite for its protective action. Further studies into the mechanism for these effects may provide new insights into the pathophysiology of MPS activation in response to immunologic challenge.
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PMID:The effects of an anti-I-Ab antibody on murine host resistance to Listeria monocytogenes. 349 82

Two H-2-linked autosomal dominant immune response (Ir) genes Ir-IgG and Ir-IgA were demonstrated to be at separate loci. Ir-IgG controls the immune response to IgG (gamma2a) myeloma proteins and Ir-IgA the immune response to IgA meyloma proteins. Both genes are associated with the H-2K region specificities of the H-2 chromosome, specifically Ir-IgG with H-2(b) and Ir-IgA with H-2(a). Different recombinants derived from H-2(a)/H-2(b) crossovers were examined for their immune responsiveness to BALB/c IgG (gamma2a) and IgA myeloma proteins. B10 (H-2(b)) parental type responded only to IgG; B10.A (H-2(a)) responded only to IgA. All the recombinants except for B10.A (4R) responded to either IgG or IgA. B10.A (4R), however, responded to both IgG and IgA. This indicated that the crossover event giving rise to B10.A (4R) occurred between the Ir-IgG and Ir-IgA loci.
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PMID:H-2-linked immune response (Ir) genes. Independent loci for Ir-IgG and Ir-IgA genes. 411 90

The B cell hybridomas producing monoclonal antibodies (E10, D7, F4, H6, and D4) were established by the fusion of P3U1 or NS-1 murine myeloma cell lines and spleen cells of B10.A(5R) mice hyperimmunized with mitomycin C-treated B10.A(3R) spleen and thymus cells. Two types of monoclonal antibodies specific for the products controlled by a gene in the I-Jb subregion of the H-2 complex were characterized: one specific for the private type of I-Jb determinant, the other recognizing the cross-reactive determinant between the I-Jb and I-Jd products. By using these monoclonal reagents, the I-J-encoded product on the antigen-specific suppressor T cells was found to be expressed on their soluble suppressor factors. Furthermore, the I-Jb products were successfully detected not only on the T cell hybridoma with suppressor activity specific for keyhole limpet hemocyanin (KLH), but also on KLH-primed suppressor T cells enriched by antigen-coated petri dishes and concanavalin A-induced thymocyte blasts of C57BL/6 mice by complement-dependent cytotoxic assays and membrane fluorescence techniques.
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PMID:Monoclonal antibodies that recognize the product controlled by a gene in the I-J subregion of the mouse H-2 complex. 617 Jul 15

Immunization of B10.D2 Ign mice against a (BALB/c X NZB)F1 murine B lymphoma cell line (WEHI-5) and subsequent fusion of immune spleen cells with a drug sensitive myeloma (P3 X 63-Ag8) has resulted in the generation of a series of hybridoma cell lines. One of these clones, BD5-334.5, secretes an antibody which reacts with a determinant, designated Lym 7.2, which demonstrates an identical tissue and strain distribution as the conventionally defined Ly 7.2 antigen. Furthermore, anti-Ly 7.2 alloantiserum significantly blocks reaction of the anti-Lym 7.2 monoclonal antibody with BALB/c splenocytes. Lym 7.2 is present on a majority of splenocytes, peripheral blood leukocytes, and lymph node cells. However, B cells express considerably higher cell surface density of this antigen than peripheral T lymphocytes. This antigen was not detected on erythrocytes, kidney, liver, or brain. Moreover, Lym 7.2 is present on approximately 15% of normal thymocytes, and 15% of bone marrow cells, and is expressed on cortisone resistant thymocytes. Quantitative flow cytometry analysis demonstrated that the antigen is present at approximately half the cell surface density on spleen cells from F1 mice between Lym 7.2 positive and Lym 7.2 negative mice, but on the same percentage of cells as Lym 7.2 positive inbred strains. Data from backcross analysis suggest that a single locus is encoding this antigen. Mitogen blasts, induced with PHA, ConA, and LPS, all express the Lym 7.2 marker.
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PMID:Lym 7.2: monoclonal antibody defining an alloantigen similar or identical to Ly 7.2. 620 26

Spleen cells from an SJL mouse immunized with B10.S spleen cells were fused with the nonsecretor myeloma line NS.1. One established hybrid cell line continuously secreted antibody that recognized a new antigenic specificity, tentatively called "Ly-m11." This newly found antigen is detectable on nearly 100 percent of spleen and lymph-node cells, 70 percent of bone-marrow cells, and 20 percent of thymus cells by direct cytotoxicity assays, and on the cells derived from kidney and liver. Strains that are Ly-m11 (+) include C57BL/6, C57BL/10J, B10.S, C57BR/cdJ, C57L/J, and C57BL/KsJ. Other mouse strains so far tested are Ly-m11 (-). The strain distribution pattern distinguished Ly-m11 from any known murine lymphocyte alloantigens, but it follows the H-3 alpha haplotype which is defined by skin transplantation. Linkage tests of nine congenic strains of H-3 and/or H-13/alpha loci and five recombinant inbred lines including CXB, BXH, AKXL, SWXL, and BXD revealed no recombinations between H-3 and Ly-m11 loci on chromosome 2. This newly discovered Ly-m11 alloantigen could itself constitute a minor histocompatibility antigen detectable by serological means.
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PMID:Ly-m11: the H-3 region of mouse chromosome 2 controls a new surface alloantigen. 624 82

An anti-I-Ab monoclonal antibody, designated K14.83-11, was produced in a fusion between SP 2/0 Ag-14 myeloma cells and spleen cells from a B10.D2/n mouse primed in vivo against C57BL/10. Unlike other anti-I-Ab monoclonal antibodies thus far described, K14.83-11 was found to have a combination of features involving specificity, isotype, and function, unique among existing anti-I-A reagents. K14.83-11 exhibited a strong binding to the I-Ab gene product, with only slight cross-reactivity to the I-Ap/q family of allelic products and no reactivity towards I-Ak,d. When analyzed for isotype, K14.83-11 was found to be of a rare IgG3 isotype. With respect to biologic activity, K14.83-11 not only failed to produce the expected inhibition of specific anti-I-Ab T cell reactivity in vitro, but instead produced a striking enhancement of T cell responses against the I-Ab gene product. The possible relationship of IgG isotype and function was suggested when the immunoenhancing effect of K14.83-11 on reactive T lymphocytes was reversed to that of suppression with highly purified F(ab)2 fragments obtained by pepsin digestion.
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PMID:A novel anti-Ia monoclonal antibody which specifically enhances the corresponding T cell alloreactivity. 633 45

Using a monoclonal antibody raised by fusing spleen cells from A/J mice, immunized with B10.A splenocytes and lymph-node cells, with a BALB/c myeloma, we have described a new surface alloantigen, Ly-21.2, Ly-21.2 is present in varying amounts in all lymphoid tissues, is not detectable in the brain, kidney, lung or erythrocytes, and is found in only trace amounts in the liver. Strain distribution studies showed that Ly-21.2 is present in all strains examined, including B10, except the A strain and segregation analysis of (A/J x B10) F2 mice showed that Ly-21.2 expression (1) is encoded by one gene and (2) is linked to albinism on chromosome 7. Studies performed on mice developing T-cell leukemia showed that, regardless of the etiologic agent, Ly-21.2 expression increases dramatically in mice with overt leukemia. In addition, preliminary studies suggest that expression of Ly-21.2 is linked to increased susceptibility of mice to Friend-virus-induced erythroleukemia.
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PMID:A new murine lymphocyte alloantigen, Ly-21.2, mapping to the seventh chromosome. 680 49

We have examined the recognition of the variable (V) domain of the heavy (VH) and light (V lambda 2) chains of mouse myeloma protein 315 by helper T cells. Mice were primed with the isolated V domain in complete Freund's adjuvant, and carrier (V domain)-primed spleen cells were transferred together with hapten (NIP)-primed spleen cells to recipient mice that were boosted with NIP3-Fab-315. The helper cell response to both domains was governed by H-2-linked immune response (Ir) genes, and VH-315 and V lambda 2 displayed different Ir phenotypes. H-2k conferred high responsiveness to VH on three different genetic backgrounds, BALB/c, C3H, and B10; mice of the d and b haplotypes were low responders. Conversely, H-2d conferred high responsiveness to V lambda 2 on two backgrounds, BALB/c and C3H, whereas mice of the k haplotype were low responders to this domain. Non-H-2 genes of the B10 background extinguished the helper cell response to V lambda 2 in animals with the high responder d haplotype. The VH Ir gene mapped to the K-A interval of the H-2 complex. Unfolded (completely reduced and alkylated) V domains primed helper cells as efficiently as folded domains for responses to NIP3-Fab-315, indicating that the helper cells recognized an antigenic determinant that was not conformation-dependent. The data indicate that there exists helper T cells which recognize each member of the M315 pair of V domains independent of the other, and that these V domains are recognized like conventional extrinsic protein antigens.
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PMID:Helper T cell recognition of the variable domains of a mouse myeloma protein (315). Effect of the major histocompatibility complex and domain conformation. 697 21

T lymphocytes express a unique I-A subregion-controlled surface molecule that is not expressed on B lymphocytes. We produced antisera and monoclonal antibodies recognizing this structure. Exhaustive B cell adsorption (A.TH X B10.HTT)F antiserum, produced against activated A.TL T cells, left antibodies that bind an I-Ak specificity on some B10.A(4R) T lymphocytes (11 +/- 2%, mean +/- SEM). Similarly, exhaustive B cell adsorption of (A/J X B10.MBR)F antiserum, produced against activated B10.A(5R) cells, left antibodies specific for an I-Ab determinant on B10.A(5R)T cells (17 +/- 2%). We fused A.TL-immune (A.TH X B10.HTT)F splenocytes with NS-1 myeloma cells and identified antibody-producing hybrid cells by a fluorescent enzyme-linked immunosorbent microassay described herein. Eight monoclonal antibodies were selected; these lyse 7--26% of peripheral T cells from I-Ak strains. Thymocytes and bone marrow cells do not express the I-Ak T cells determinant. Exhaustive B cell adsorption did not remove I-Ak T cell-specific monoclonal antibodies.
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PMID:Murine T cell-specific Ia antigens: monoclonal antibodies define an I-A-encoded T lymphocyte structure. 698 Apr 12


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