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

BALB/cJ X C57BL/10Sn F1 (hereafter called B10F1) hybrids resist challenge with the BALB/c plasmacytoma, MPC-11, by a radiation-sensitive, silica-insensitive mechanism, whereas BALB/cJ X BALB.B F1 (hereafter called BALB.BF1) hybrids are as susceptible to MPC-11 as are homozygous BALB/c mice themselves. To investigate the mechanism of resistance, we have compared anti-MPC-11 immune responses by these F1 hybrids both before and at various times after tumor challenge. Resistance is not determined by natural killer cell reactivity inasmuch as neither hybrid harbors splenic natural killer cells with lytic activity directed against MPC-11. Nor is it determined by antibody-dependent cell-mediated cytotoxicity since neither hybrid produces an appropriate anti-MPC-11 antibody. Spleen cells and lymph node cells from both hybrids are capable of generating high levels of anti-MPC-11 cytotoxic T-lymphocyte activity in both primary and secondary mixed-lymphocyte tumor cell cultures. Such cytotoxic T-lymphocytes protect susceptible hybrids from tumor growth in Winn assays. The susceptible but not the resistant hybrids lose the ability to generate high levels of cytotoxic T-lymphocytes activity in spleen mixed lymphocyte tumor cell cultures by 28 days, and in lymph node mixed-lymphocyte tumor cell cultures by 14 days postchallenge. The reduction in spleen cell reactivity is due to suppression mainly by adherent cells and can be abrogated by pretreatment of the susceptible hybrids with a low dose of Cytoxan 2 days before challenge. This pretreatment does not, however, protect the mice. They develop tumor at the same rate and die at the same time as do controls. Both the late appearance of suppression and the lack of effect on survival of its ablation suggest it to be a concomitant of tumor growth rather than its cause. Resistance to tumor growth in this model system may reflect an enhanced ability of the resistant hybrid to deliver effector cells to the site of tumor implantation.
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PMID:Hybrid resistance to BALB/c plasmacytomas: F1 hybrid anti-MPC-11 immunological responses correlated with resistance to tumor challenge. 348 80

Spleen cells from an unimmunized autoimmune NZB/NZW F1 female mouse were fused to the BALB/c MPC-11 drug-resistant clone 45.6 TG 1.7. One hybrid clone (D4) produced IgG-3 immunoglobulin that bound ribosomal RNA. A high concentration of this antibody was produced in the ascitic fluid of NZB/NZW male mice. DNA, tRNA, and synthetic single- and double-stranded polynucleotides could not bind significantly to the antibody. A Scatchard analysis showed that the rRNA-binding immunoglobulin is monoclonal and has a high affinity (10(9) liter/mole) for the RNA antigen.
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PMID:A hybridoma from an autoimmune NZB/NZW mouse producing monoclonal antibody to ribosomal-RNA. 735 11