Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hebdomadis is one of the major serogroups found in China. In Sichuan, this serogroup appears to have a close relationship with local outbreak of leptospirosis. BALB/c mice were immunized intrasplenically with outer envelope of serogroup Hendomadis serovar hebdomadis strain 245. Spleen cells were fused with SP2/0 myeloma cells, two monoclonal antibodies Af2 and Bb2 were produced by hybridoma technique. McAb Af2 and McAb Bb2 were identified to be IgG1 and IgG3 by immunodiffusion respectively. Specificities of these two McAbs were determined by MAT; both reacted to 8 serovars (hebdomadis, nona, kambale, kremastos, worsfoldi, jules, maruborincana) of Hebdomadis serogroup. The agglutination titres of McAb Af2 and McAb Bb2 were 1:640-1:2,500,000 and 1:320-1:2,500,000, respectively. The two McAbs did not agglutinate with serovar kabura of Hebdomadis serogroup, they did not agglutinate with 11 serovars of Sejroe serogroup, 4 serovars of Mini serogroup, 18 representive serovars of L. interrogans in 18 serogroups, L. biflexa strain Patoc I and Leptonema illini. So it was found that McAb Af2 and McAb Bb2 showed partial serogroup specificity for Hebdomadis by agglutination.
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PMID:[The production and identification of partial serogroup--specific monoclonal antibodies against leptospires hebdomadis serogroup]. 128 91

Spleen cells of BALB/c mice immunized with whole Leptospira interrogans serogroup Australis serovar australis strain 620 were fused with myeloma cells line SP2/0. Specificities of four McAbs determined by MAT. 2E1 McAb (IgG3) reacted with 11 serovars, of the Australis serogroup, but did not react with 22 representative serovars of L. interrogans in 20 serogroups, L. biflexa strain patoc I and Leptonema illini strain 3055. 2E1 McAb showed serogroup specificity for Australis by agglutination and the other 3 McAbs showed partial serogroup specificity. We compared the outer envelope (OE) protein profiles of serovar australis strain 620 with those of two pathogenic L. interrogans serovar lai strain 601 and serovar hebdomadis strain 156 by SDS-PAGE. 63kd protein profile was only found in the OE of strain 620, and the quantity of 42kd protein of strain 620 was greater than that of strain 601 and 156. The immunoblotting revealed that 2E1 McAb reacted with a 34kd band in the OE preparation of serovar australis strain 620, but did not react with that of other two L. interrogans. 2E1 McAb also did not react with OE of non-pathogenic leptospires. It was suggested that 34kd protein might contain the antigenic determinants which were shared by leptospires of Australis serogroup.
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PMID:[Study on the production, identification of serogroup-specific monoclonal antibodies against leptospires of Australis serogroup and detection of its antigen]. 170 13

It has recently been postulated that immunoglobulin class switching is preceded by transcription from unrearranged heavy chain genes. In this report, we have investigated the conditions under which RNA transcribed from unrearranged C gamma 3, C gamma 1, C gamma 2b, C gamma 2a, C epsilon and C alpha genes are induced in normal spleen cells by mitogens and/or interleukin (IL) 4, IL 5 and interferon-gamma. Lipopolysaccharide (LPS) plus IL 4 induced germ-line gamma 1 and epsilon transcripts. LPS induced gamma 2b and gamma 3 transcripts and high doses of IL 4 suppressed these LPS-induced transcripts. Interferon-gamma induced low levels of germ-line gamma 2a transcripts and profoundly suppressed the gamma 1 and epsilon transcripts induced by LPS and IL 4. IL 5 alone or in combination with IL 4 and/or LPS did not induce germ-line alpha transcripts. Spleen cells of the partially immunodeficient mice CBA/N and C3H/HeJ, which do not express IgG3 could be induced, however, by polyclonal activators to express germ-line gamma 3 and gamma 2b transcripts. The data indicate that the capacity of a ligand to induce/suppress transcription of a particular unrearranged heavy chain gene is a good indicator of its capacity to induce switching to the corresponding Ig isotype. However, it is also clear that control of switching can be carried out at other levels.
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PMID:Induction of germ-line immunoglobulin heavy chain transcripts by mitogens and interleukins prior to switch recombination. 197 77

We investigated whether spontaneous isotype switching in monoclonal antibody-producing hybridomas always occurs with genes on the same chromosome. Spleen cells of (BAB/ 25 X AKR/J) F1 mice, immunized with dansyl-keyhole limpet hemocyanin (DNS-KLH), were hybridized with NS-1 to generate hybridomas producing monoclonal anti-DNS antibodies of either the b or d haplotype of the BAB/25 or AKR/J parent, respectively. We selected isotype switch variants of such hybridomas using the fluorescence-activated cell sorter (FACS). Although in most cases the allotypic haplotype expressed by the parent and switch-variant hybridomas are the same, in one family of variants we noted a switch in haplotype along with the switch in isotype. This was noted in the selection of IgG2a switch variants from an IgG1 switch variant originally derived from an IgG3-producing parent. Biochemical and molecular studies confirm that the allotype switch variant expresses the same heavy-chain variable region gene complex as its parent hybridomas. As such, the allotype switch represents an example of spontaneous mitotic recombination between immunoglobulin heavy-chain genes, generating a single actively transcribed gene from loci previously positioned on different chromosomes.
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PMID:Homologous chromosome recombination generating immunoglobulin allotype and isotype switch variants. 351 8

Spleen cells from BALB/c mice, immunized with SDS-acrylamide gel purified human fibroblast interferon (HuIFN-beta) were fused with mouse myeloma cells. Culture fluids from the resulting hybrid cells were screened for HuIFN-beta specificity by the following tests: a solid-phase RIA using partially purified HuIFN-beta, a protein-transfer RIA using electrophoretically resolved and immobilized HuIFN-beta, and a bioassay which tests residual HuIFN-beta activity in the supernatant following immunoprecipitation. Six HuIFN-beta-specific hybridomas were identified; two were capable of partially neutralizing HuIFN-beta activity. All six antibodies bind to the beta 1-IFN polypeptide synthesized in E. coli cells containing a cloned beta 1-IFN DNA sequence. All six monoclonal antibodies were found to be IgG3/kappa.
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PMID:Monoclonal antibodies directed against human fibroblast interferon: characterization and functional studies. 620 71

Spleen cells of BALB/c mice that were immune to the 17X strain of P. yoelii were fused with P3X63Ag8 myeloma cells. Two hundred fifty-three of 1053 hybrid cells produced antibodies reactive with disrupted 17X parasites in a solid phase radioimmunoassay. One of these antibodies, McAb 302, reacted with the merozoites of the 17X (nonlethal) and 17XL (lethal) variants of P. yoelii. Of greater significance, McAb 302 passively protected mice against challenge infection with the lethal variant. Mice treated with this antibody before infection developed low-grade parasitemia (less than 0.3%) of short duration when challenged with P. yoelii 17XL . In contrast, control mice that had been untreated or injected with ascites fluid lacking McAb 302 uniformly died with fulminating malaria upon challenge with the same parasite. In other experiments, McAb 302 was shown capable of controlling blood parasite levels when administered to mice with patent P. yoelii 17XL infections. Although all control mice died, mice protected with a single dose of McAb 302 ultimately cleared their infections. Regardless of how passive immunization was performed, mice given McAb 302 were resistant to subsequent challenge with P. yoelii 17XL , indicating they had developed significant immunity during their initial controlled infections. McAb 302 also showed pronounced passive protective activity against the nonlethal 17X strain of P. yoelii, which is a parasite of reticulocytes. The protection afforded by McAb 302 was specific, because mice passively immunized with this antibody died when challenged with the unrelated P. vinckei. McAb 302 was shown to possess the IgG3 isotype and precipitated a 230-kd protein plus several smaller polypeptides from metabolically labeled parasite antigen preparation derived from both variants of P. yoelii. It did not react with similar preparations of other murine plasmodial species.
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PMID:Passive immunization against murine malaria with an IgG3 monoclonal antibody. 672 50

Severe combined immune-defective (SCID) mice reconstituted with immunoglobulin heavy chain-disparate spleen (SP) and peritoneal cavity (PerC) B cells exhibit serologic dominance of IgM bearing the PerC allotype. Immunization fails to elicit IgM production from donor SP B cells although flow cytometric analyses indicate the presence of these cells in the spleen of (SP + PerC)-->SCID chimeras. This observation suggests that donor SP B cell function is absent or inhibited in the SCID chimera. In this report, ELISAspot and proliferation assays were employed to further investigate the functional properties of B cells in these mice. Plasma cells derived from the donor SP were present in the spleen of SCID recipients at a lower number than those derived from donor PerC B cells. Spleen cells isolated from SCID recipients could be activated with insolubilized MAbs directed against IgM or IgD allotypes expressed by either the SP or PerC B cell donor. In contrast, the peritoneal cavity of SCID chimeras lacked B cells responsive to MAbs specific for the donor SP IgM and IgD allotypes. These results demonstrate that B cells derived from the SP donor are functional in (SP + PerC)-->SCID chimeras.
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PMID:B cell function in SCID mice reconstituted with allotype-disparate spleen and peritoneal cavity B cells. 833 Mar 14

The outcome of cutaneous leishmaniasis is dependent on the balance of Th1 and Th2 cells. In the murine model, Th1 cells are host-protective whereas the Th2 cells are disease-promoting. However, the in vivo role of interleukin-4 (IL-4), a signature product of Th2 cells, is uncertain. We compared the course of Leishmania major infection in the genetically resistant 129/Sv mice and the mutant 129/Sv mice transgenic for the murine IL-4 gene under the control of the immunoglobulin heavy chain enhancer and promoter. We report here that in contrast to their wild-type parents, the IL-4 transgenic mice are susceptible to L. major infection. This is associated with the development of inexorably progressive lesions and parasite loads. Spleen cells from infected transgenic mice produced significantly higher levels of IL-4 but lower amounts of interferon-gamma when stimulated in vitro with leishmanial antigens compared to those from infected normal 129/Sv mice. Furthermore, sera from the infected transgenic mice contained higher levels of IL-4 and IgE than the sera of infected normal 129/Sv mice. These results, therefore, establish in a new animal model that IL-4 promotes disease development in murine cutaneous leishmaniasis.
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PMID:Interleukin-4 transgenic mice of resistant background are susceptible to Leishmania major infection. 843 88

IFN-gamma is critical for prevention of development of toxoplasmic encephalitis (TE). Since IL-4 down-regulates production of IFN-gamma, we examined its role in the pathogenesis of TE in IL-4-targeted mutant (IL-4-/-) mice. IL-4-/- mice all died from 6 to 20 wk after peroral infection with cysts of the ME49 strain of Toxoplasma gondii; control mice survived. At 4 and 8 wk after infection, significantly greater numbers of T. gondii cysts and foci of acute inflammation, and greater amounts of tachyzoite-specific mRNA (by reverse-transcriptase PCR) were in brains of IL-4-/- mice than controls. Toxoplasma IgG2b and IgG3 Ab levels were slightly but significantly higher in sera of IL-4-/- than control mice, whereas IgM and IgG2a levels did not differ between these mice. Toxoplasma IgG1 and IgE Abs were not detected in sera of either strain. Amounts of IFN-gamma, TNF-alpha, IL-6, and IL-10 mRNA detected by reverse-transcriptase PCR did not differ between brains of infected IL-4-/- and controls, although brains of the former mice had greater numbers of inflammatory mononuclear cell infiltrates. IL-4 mRNA was detected only in infected control mice. Spleen cells of control mice at 8 wk after infection produced significantly greater amounts of IFN-gamma following stimulation in vitro with soluble T. gondii Ags than did those from IL-4-/- mice. These results indicate that IL-4 is protective against development of TE by preventing formation of T. gondii cysts and proliferation of tachyzoites in the brain. The impaired ability of IL-4-/- mice in the late stage of T. gondii infection to produce IFN-gamma most likely contributes to their susceptibility for development of severe TE.
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PMID:IL-4 is protective against development of toxoplasmic encephalitis. 880 58

A synthetic peptide whose amino acid sequence corresponds to residues 131-142 of human cholesteryl ester transfer protein (CETP) was used as an immunogen to generate a panel of monoclonal antibodies (MAbs) specific for the intact CETP molecule. Spleen cells from BALB/c mice immunized with the peptide conjugated with keyhole limpet hemocyanin (KLH) were fused with SP2/0 myeloma cells. Two MAbs that bound fixed peptide in an enzyme-linked immunoabsorbent assay (ELISA) were partially characterized regarding their specificity and biological activity. ATM192 of the IgG1 subclass and J16-14 of the IgG3 subclass were used in a Western blot assay as well as in the ELISA. We have also shown through the use of immunoprecipitation that ATM192 can remove CETP enzyme activity from human serum without destroying the enzyme's activity. We have also shown that the antibodies can bind CETP from rabbits. The specificity studies and the lack of inhibition of enzymatic activity suggest that the MAbs bind a structural area of the CETP molecule not a part of the active binding site of the enzyme. We conclude that these antibodies can be valuable as tools for studying CETP levels in human serum as well as in tissue homogenates from rabbits and humans.
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PMID:Mouse monoclonal antipeptide antibodies specific for cholesteryl ester transfer protein (CETP). 891 85


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