Biomedical subjects
Publications and source records attributed to T Schulz.
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Incorporation of [3h]thymidine ([3H]TdR) into concanavalin A (Con A)-stimulated murine splenocytes was found to be enhanced by addition of certain concentrations of ethanol, 2-propanol and acetone. The alcohol/acetone-induced enhancement of the Con A response was found to be accompanied by an increase of the percentage of living cells as assessed by trypan blue exclusion. Concentrations of ethanol and 2-propanol which caused maximum [3H]TdR uptake in Con A cultures were also found to lead to higher percentages of aggregated cells than in comparison to Con A cultures without alcohol. The data suggest that alcohols in certain concentrations are capable to achieve optimum Con A stimulation.
Raji cells were described to carry receptors for iC3b, C3d, C3b-beta 1 H and beta 1 H. Controversial opinions, however, exist whether or not these cells carry also receptors for C3b. Using highly purified C3, definitely devoid of beta 1 H and C5, for preparation of C3b intermediates, it could be shown that Raji cells bound to C3b cells. Furthermore, Raji cells reacted with monoclonal antibodies that interfered with binding of C3b to human erythrocytes, lymphocytes and renal cells. The receptor for C3b on Raji cell, however, exhibited some special properties and, therefore, required some distinct experimental conditions for its detection: (1) The origin of the erythrocytes used for preparation of the C3b intermediates seemed to be important; this was not the case when iC3b and C3d receptor reactivity was assessed. (2) Rosettes already formed between Raji cells and EAC1423b showed the tendency to disintegrate within the first 30 min after the rosette formation assay. Again, this effect could not be observed with iC3b- and C3d-dependent rosette formation. (3) Incubation of the Raji cells at 37 degrees C as well as 4 degrees C before rosette formation resulted in a rhythmic loss and reappearance of C3b receptor reactivity. At room temperature (19-22 degrees C) this effect was much less expressed. There was no influence of preincubation at 4 and 37 degrees C, respectively, on the iC3b and C3d receptor reactivity of Raji cells. (4) Diisopropylfluorophosphate (DFP) present during rosette formation enhanced, within a certain range of concentration, the percentage of C3b-dependent rosette formation. iC3b and C3d receptor reactivity was not influenced. A similar reaction pattern was observed with pokeweed mitogen (PWM)-stimulated tonsil lymphocytes. In the concentrations tested, DFP showed no effect on the rosette formation between C3b, iC3b, and C3d cells, respectively, and unstimulated tonsil lymphocytes. The data presented suggest that C3b receptors on Raji cells undergo some special metabolism, possibly controlled by fluid phase or cell-bound proteases. This might be a common property of C3b receptors on blast-like and transformed cells, differing from that of unstimulated small lymphocytes.
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Mouse mastocytoma cells (P 815) formed rosettes with normal mouse spleen lymphocytes which had been coated with uncleaved human C 3; this interaction was clearly dependent on the amount of C 3. Lymphocytes treated with C 3 b or buffer alone were ineffective. Formation of cell contact could be inhibited by the presence of protease inhibitors such as diisopropyl fluorophosphate, phenyl methyl sulfonyl fluoride and tosyllysyl chloromethyl ketone. Seve n out of 13 different cell lines behaved like P 815 cells. The results strongly suggested that a proteolytic activity on mouse tumor cells led to a cooperation with uncleaved C 3 on a carrier cell to connect these two cells. We interpreted these data in analogy to the complement-dependent bridge formation mechanism (M. P. Dierich and B. Landen, J. Exp. Med. 1977. 146: 1484): uncleaved C 3, attached to mouse spleen lymphocytes as carriers, becomes cleaved by enzymes associated with the tumor cells tested; by this cleavage, the labile binding site is released on C 3 (nascent C 3 b) and anchors the C 3-carrying cell to the protease-carrying cell; since this labile binding site is short-lived, this process can be induced by membrane-associated proteases only. The nature of the proteases and the biological implications of this process are as yet uncertain.
Monolayers of primary rabbit kidney cells infected with HSV type I bound lymphoblastoid (Raji) cells, to which the third component (C3) of the complement system had been attached (Raji-C3). This induction of cell contact did not occur on non-infected monolayers and was dependent on C3. The interaction could be suppressed by the presence of protease inhibitors (1 mM-TLCK or-PMSF). The results are interpreted as indicating de novo expression of protease activity on the surface of HSV-infected cells. This protease is characterized by its potential to activate C3 and its inhibition by TLCK.
The effects of an intravenous infusion of cholecystokinin-pancreozymin on bile secretion were studied in 13 unanesthetized and cholecystectomized piglets. The results demonstrate that CCK-PZ induces a significant increase of bile flow and bile salt excretion. The excretion patterns for bilirubin and Ioglycamide, however, showed a slight but not significant decrease. Peripheral hemodynamic parameters remained unchanged. A detailed analysis of these results suggests that CCK-PZ induces an increase of biliary bile salt secretion by stimulation of intestinal motility and enhancement of bile salt circulation within the enterohepatic circulation (EHC). In combination with previous studies on the effects of spasmolytics on biliary bile salt excretion these results therefore emphasize, that the intestinal motility and transit time might play a role in the physiology and pathophysiology of biliary bile salt secretion.
The in vitro synthesis of EF-Tu was studied using the transducing phage lambdarifd18 DNA as template. The EF-Tu synthesized was identified by its immunological properties, gel analysis, and its ability to interact with GDP and EF-Ts. Two other unidentified polypeptides were also precipitated from the incubation mixture by EF-Tu antiserum. The synthesis of total EF-Tu immunoprecipitable material was depressed about one-half by guanosine-5'-diphosphate-3'-diphosphate which was shown to inhibit the transcription process.
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Three restriction points control the cell cycle of activated B lymphocytes. The first occurs directly after mitosis and is controlled by the occupancy of surface-bound immunoglobulin. The second is observed approximately 4 h after mitosis in the G1 phase of the cycle, that is, before DNA replication, and is controlled by growth factors that are produced by macrophages which we have previously classified as alpha-type factors. The third restriction point occurs in the G2 phase, 2-4 h before mitosis, and is controlled by beta-type growth factors probably produced by helper T lymphocytes. The third component of complement, C3, has long been implicated in the control of B-cell responses. C3 is secreted by monocytes and macrophages. We have found recently that crosslinked, but not soluble, human C3 stimulates activated, but not resting, murine B cells to thymidine uptake. Here we investigate the role of C3b and C3d in the progression of the cell cycle of activated, synchronized murine B cells. We find that crosslinked C3d replaces the action of alpha-factors within the cell cycle of these cells and allows entry into S phase. In contrast, soluble C3d inhibits the action of alpha-factors. This implies that a C3d-specific receptor, probably the murine analogue to the human complement receptor CR2, is a growth factor receptor on activated B cells that will give the cell a growth-positive signal when it is crosslinked, while occupancy by the soluble form of C3d will result in inhibition of the action of alpha-factors or of crosslinked C3b or C3d. A stretch of weak homology between the cDNA sequence of murine C3d and those of murine growth factors indicates that an insulin-like growth factor could be the active principle of C3d that controls the cell cycle of activated B cells.
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