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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dendritic cells (DCs; 1) have been purified from mouse spleen in good yield. Spleen cell suspensions were floated on dense bovine plasma albumin (BPA) columns, and the low density fraction was adhered to glass (2). The adherent cells consisted of DCs and immature macrophages most of which eluted in a viable state from the culture dish after overnight incubation. The macrophages were then removed by selective rosetting with opsonized erythrocytes and recentrifugation on dense BPA. This protocol resulted in a purified DC fraction, containing 1--3 X 10(5) DCs/spleen, which was homogeneous and distinctive in its properties. All cells exhibited the phase contrast and transmission electron microscopy (EM) cytologic features that were previously described for freshly isolated adherent DCs. By scanning EM, most purified DCs exhibited a remarkable array of bulbous protrusions of varying length and shape, unlike any other lymphoid cell. All DCs expressed surface Ia and other major histocompatibility complex (MHC)-linked alloantigens. DCs, however, lacked surface Ig and T-cell antigens, and did not bind or interiorize opsonized erythrocytes. Purified DCs have been maintined in vitro for 3 days. Recovery of cultured purified cells was 70% or more of starting cell numbers. When [3H]uridine-tagged DCs were mixed with nonlabeled heterogeneous spleen cells, 70--80% of the labeled DCs were recovered as viable cells 2--3 days later. Purified DCs did not readhere to tissue culture surfaces and did not proliferate, even when cultured with mitogenic doses of concanavalin A and lipopolysaccharide. Finally, DCs did not change their cytologic or surface properties after 3 days of culture. These observations extend the evidence that DCs are a novel cell type and provide useful properties and techniques for their further study.
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PMID:Identification of a novel cell type in peripheral lymphoid organs of mice. V. Purification of spleen dendritic cells, new surface markers, and maintenance in vitro. 76 93

Spleen cells from mice inoculated with partially purified preparations of interferon (Sp. Act. 1 X 10(7) i.u./mg protein, 0.2 ml i. v./mouse) were stimulated in vitro with phytohemagglutinin, concanavalin A or lipopolysaccharide. After 2 days of stimulation, the incorporation of 3H-thymidine into TCA-insoluble radioactivity was inhibited 50-90% when compared with cells from animals inoculated with mock interferon. Maximal inhibition, with optimal doses of lectins was obtained when interferon was;inoculated 18 hours before. This effect of interferon on DNA synthesis was preceeded by inhibition of the incorporation of 3H-uridine into TCA-insoluble material. When cells were pretreated in vitro with interferon for 24 hours and subsequently stimulated with PHA, RNA synthesis was inhibited by 30-40%, whatever was the dose of the mitogen. The synthesis of 4S tRNA, 18S and 28S ribosomal RNAs were inhibited to the same degree by interferon. The incorporation of methyl groups into cytoplasmic sRNA was unaltered.
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PMID:Inhibitory effect of interferon on DNA and RNA synthesis in murine spleen cells stimulated by lectins. 93 1

The ability of T and B lymphocytes to migrate into skin allografts undergoing rejection was studied in mice. Spleen cells from CBA/J mice sensitized to transplantation antigens of A/J or C57BL/6 mice were separated on immunabsorbent columns into purified populations of T and B cells, labeled in vitro with 3H-uridine and injected intravenously into CBA/J mice with 7-day old skin iso and allografts (A/J or C57BL/6). The mice were sacrificed 24 h later and studied by autoradiography. After transfer of either unfractionated spleen cells or T cells, large numbers of labeled cells were found in the cellular infiltrate of allografts, whereas extremely few were seen in isografts. In contrast, after transfer of B cells, almost no labeled cells were detected either in the allografts or the isografts, although they, like T cells, homed normally to lymphoid tissue.
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PMID:T-cell migration into allografts. 109 94

Rapid kinetic techniques were used to study the transport and salvage of uridine and other nucleosides in mouse spleen cells. Spleen cells express two nucleoside transport systems: (1) the non-concentrative, symmetrical, Na+-independent transporter with broad substrate specificity, which has been found in all mammalian cells and is sensitive to inhibition by dipyridamole and nitrobenzylthioinosine; and (2) a Na+-dependent nucleoside transport, which is specific for uridine and purine nucleosides and resistant to inhibition by dipyridamole and nitrobenzylthioinosine. The kinetic properties of the two transporters were determined by measuring uridine influx in ATP-depleted cells and dipyridamole-treated cells, respectively. The Michaelis-Menten constants for Na+-independent and -dependent transport were about 40 and 200 microM, respectively, but the first-order rate constants were about the same for both transport systems. Nitrobenzylthioinosine-sensitivity of the facilitated nucleoside transporter correlated with the presence of about 10,000 high-affinity (Kd = 0.6 nM) nitrobenzylthioinosine-binding sites per cell. The turnover number of the nitrobenzylthioinosine-sensitive nucleoside transporter was comparable to that of mouse P388 leukemia cells. The activation energy of this transporter was 20 kcal/mol. Entry of uridine via either of the transport routes was rapidly followed by its phosphorylation and conversion to UTP. The Michaelis-Menten constant for the in situ phosphorylation of uridine was about 50 microM and the first-order rate constants for phosphorylation and transport were about the same. The spleen cells also efficiently salvaged adenosine, adenine, and hypoxanthine, but not thymidine.
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PMID:Na+-dependent and -independent transport of uridine and its phosphorylation in mouse spleen cells. 273 Sep 9

Tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 (IL-2) are reported to enhance lymphocyte binding to endothelial cells in vitro. We examined these two agents on lymphocyte migration in vivo. Spleen lymphocytes were radiolabeled with tritiated uridine (3H-UR) and then injected i.v. into mice. Each cytokine (TNF-alpha or IL-2) or both cytokines were then injected intradermally on the back of mice. The results demonstrated that TNF-alpha stimulates lymphocyte migration in vivo in dose-dependent fashion. Kinetic analysis demonstrated that migration with TNF-alpha started at 3 h, peaked at 6 h, followed by a gradual decline back to baseline at 24 h. IL-2, on the other hand, was nearly inactive, and did not augment lymphocyte migration over and above that induced by TNF-alpha when both cytokines were injected together.
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PMID:Effect of tumor necrosis factor-alpha and interleukin-2 on spleen lymphocyte migration in mouse skin. 1065