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)

Spleen cells from BDIX-rats bearing either GVlAl-tumor (a syngeneic mixed glioma) or NVlAc-tumor (a cloned syngeneic neurinoma of the peripheral nervous system) were cytotoxic to both tumor cells in vitro. However, the tumors displayed individually distinct antigenic specificities by in vivo rejection tests. Their in vitro cross-reactivity disappeared when a particular subpopulation of the spleen cells was used. The procedure of lymphocyte purification included three consecutive steps: treatment with carbonyl iron and magnetism, passage through a nylon wool column, and finally removal of complement receptor-bearing cells present in the colum-excluded population. Cross-reactivity between the syngeneic tumors persisted after the first two steps of lymphocyte purification. In contrast, specific cytotoxic reactions were observed against each individual tumor subsequent to the removal of the remaining C3 receptor-positive but surface Ig-negative cells. While killer cells were present in normal spleen-cell populations, these were almost completely eliminated by passage through the nylon wool column.
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PMID:Spleen-cell reactivity against transplanted neurogenic rat tumors induced by ethylnitrosourea: uncovering of tumor specificity after removal of complement-receptor-bearing lymphocytes. 5 Feb 96

Spleen cells at various times after inoculation of W/Fu rats with a syngeneic Gross virus-induced lymphoma, (C58NT)D, were tested for their in vivo activity in adoptive transfer experiments and for their in vitro reactivity in a 4-hr 51Cr release cytotoxicity assay and in a mixed lymphocyte-tumor cell interaction assay. In adoptive transfer, the best protection against tumor growth was observed with immune spleen cells taken at 30 days after tumor cell inoculation (the peak of reactivity in the mixed lymphocyte-tumor cell interaction assay) whereas cells taken at 10 days (the peak reactivity in the 51Cr release cytotoxicity assay) gave only partial protection. The protection detected in the adoptive transfer experiments was specific for (C58NT)D associated antigens, and this correlated well with the specificity observed in the in vitro cell-mediated immunity assays. T cells, but not complement receptor-bearing cells or macrophages, were essential for the protection against tumor growth in vivo, and also for the in vitro reactivity in the 51Cr release cytotoxicity and the mixed lymphocyte-tumor cell interaction assays.
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PMID:In vivo protection against syngeneic Gross virus-induced lymphoma in rats: comparison with in vitro studies of cell-mediated immunity. 5 36

Serum from bacillus Calmette-Guerin-infected mice injected with endotoxin induces the appearance of surface immunoglobulin, Ia antigen, and complement receptor on the surface of precursor bone-marrow-derived (B) cells. While endotoxin itself causes phenotypic conversion of both thymus-derived (T) cells and B cells in vitro, the endotoxin-induced serum factor was found to be a selective inducer of B cell differentiation. Spleen cells rendered immunodeficient by removal of B cells bearing the complement receptor regained the capacity to cooperate with helper T cells and to produce antibody against red cell antigens in vitro upon upon addition of the serum factor to the culture medium. Thus, a factor that controls selective phenotypic and functional differentiation of B cells has been identified and can now be characterized,
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PMID:Endotoxin-induced serum factor controlling differentiation of bone-marrow-derived lymphocytes. 32 50

Spleen cells from 8-week-old, nonimmunized donor chickens can transfer resistance to a supralethal dose of the JMV leukemia line of Marek's disease (MD) to newly hatched, highly susceptible, histocompatible recipients. The population of cells transferring resistance has previously been shown to be non-T, non-B, and nonmacrophage in nature. We present data here showing that heavily x-irradiated spleen cells were unable to protect recipients from leukemia challenge. Both complement receptor-bearing and -lacking cells could confer resistance to newly hatched recipients. Fc receptor-bearing cells conferred significant protection to recipients, whereas spleen cells depleted of Fc receptor-bearing cells were unable to protect chickens from death after JMV challenge. This indicates that the population of spleen cells, which is moderately radiosensitive and which possesses Fc receptors, is responsible for the transfer of natural resistance to the malignancy in vivo.
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PMID:Transfer of natural resistance to Marek's disease (JMV) with nonimmune spleen cells. II. Further characterization of protecting cell population. 739 77

The effect of systemic complement depletion by cobra venom factor (CVF) was evaluated in adoptive transfer experimental allergic neuritis (AT-EAN). Spleen cells of rats immunized with a neuritogenic peptide SP26 were injected into naive rats. On days 3 and 6 after cell transfer AT-EAN rats were treated with CVF or saline intraperitoneally. AT-EAN rats treated with CVF had significantly lower scores for histological inflammation (0.25 +/- 0.25 vs 1.9 +/- 0.4, mean +/- SEM, P < 0.03) and demyelination (0.13 +/- 0.13 vs 1.6 +/- 1.4, P < 0.02) than saline-treated AT-EAN rats. Immunocytochemistry of lumbosacral nerve roots showed significantly less ED1-positive macrophages (0.5 +/- 0.3 vs 1.6 +/- 0.6, P < 0.04) and CD11bc-positive (expressing complement receptor 3 or CR3) inflammatory cells (0.6 +/- 0.4 vs 1.7 +/- 0.5, P < 0.03). Our data suggest that complement plays a crucial role in inflammatory demyelination since systemic complement depletion significantly reduces recruitment of macrophages into the nerve and subsequent macrophage-mediated demyelination.
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PMID:Systemic complement depletion reduces inflammation and demyelination in adoptive transfer experimental allergic neuritis. 954 96