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At least 19 recordsLinked to original sources
PubMed1975

[Spleen enhancement reactions in chick embryo after homografting adult chicken spleen fragments: changes in spleen cell population in relation to rate of spleen enhancement].

A method using the comparison between the modifications of spleen weight and on spleen smears visible modifications of the distribution into categories of cells which are classified by the mean of their maturation degree, suggested that these both types of modifications are bound. Therefore, the classic cytological study seems to be a really good tool for analysing the effects of this kind of grafting on the haemopoietic organs, the weight modifications of which are difficult to measure. On the other hand, this method allowed us to see that the distribution of the cell population in the weakly enlarged spleens is very different from both distribution of the population in the strongly enlarged spleens and the controls ones ; this heterogeneity of the stimulating effect of the graft asked us the question whether this one could exerce its influence by the mean of two different ways, at least, or by only one.

Animals↗
PubMed1979

A cell population in nu/nu spleen can prevent generation of cytotoxic lymphocytes by normal spleen cells against self antigens of the nu/nu spleen.

Spleen cells from athymic nu/nu mice contain two kinds of physically separable active cells that can have very different effects on the generation of CL (cytotoxic lymphocytes) by normal LN cells in an in vitro response against allogeneic stimulator cells. They can provide an accessory cell required for the activation of CLP (cytotoxic lymphocyte precursor cells) which need not be H-2 identical to the CLP and will function normally even when H-2 identical to the stimulator cells. They can also provide a suppressor cell that prevents the activation of CLP that can recognize the H-2 of the nu/nu mouse. Thus, with A, B, and C to represent three H-2 differnt mouse strains, a culture containing CLP from strain A and nu/nu spleen cells from strain B or strain (A x B)F1 will produce CL against strain C or (A x C)F1 stimulator cells but not against strain B or strain (A x B)F1 stimulator cells unless the suppressor cell is first removed. It is proposed that the in vivo role of the suppressor cell in a normal mouse is to prevent the activation of CLP reactive against self.

Animals↗
PubMed1975

In vitro proliferative response of BALB/c mouse spleen cells stimulated with trinitrophenylated syngeneic spleen cells.

Spleen cells from normal BALB/c mice showed in vitro proliferative response against hapten-conjugated syngeneic spleen cells. Trinitrophenylated (TNP) spleen cells were prepared by treating normal spleen cells with sodium 2,4,6-trinitrobenzenesulphonate (TNBS). Four-day cultures of TNP-labelled spleen cells incorporated 2.5-7.4 times more [3H]thymidine than similar cultures of untreated spleen cells. An obviously positive mixed lymphocyte reaction (MLR) by normal spleen cells against mitomycin C (MC) treated TNP-labeled syngeneic spleen cells was observed after 4 days of culture. The MLR to TNP-labelled syngeneic cells was inhibited in the presence of epsilon-TNP-L-lysine by 23-37%. The spleen cells from the mice injected intraperitoneally with TNP-labelled syngeneic spleen cells showed a higher MLR against TNP-labelled spleen cells than normal spleen cells. The sensitized spleen cells also showed an increased response to MC-treated spleen cells. These results suggest that normal spleen cells include cells which can recognize the hapten and new antigenic determinants introduced into syngeneic spleen by chemical modification.

Animals↗
PubMed1976

Pyruvate kinase isozymes in various tissues of rat, and increase of spleen-type pyruvate kinase in liver by injecting chromatins from spleen and tumor.

Pyruvate kinase [EC 2.7.1.40] in various tissues of rats was separable into seven kinds of pI-isozymes by isoelectric separation with Ampholine carrier ampholytes; pI 5.4-isozyme, pI 5.6-isozyme, pI 6.2-isozyme (2 kinds), pI 6.6-isozyme, pI 7.4-isozyme, and pI 7.8-isozyme. Some of these pI-isozymes contained bound fructose 1,6-diphosphate (FDP). The bound FDP was completely dissociated when the pI-isozymes were salted out with ammonium sulfate. In the FDP-free form, pyruvate kinase was classified into three types, liver-type (type L) of pI 6.2, muscle-type (type M) of pI 7.4, and spleen-type (type M2) of pI 7.8. The liver-type isoenzyme had two kinds of FDP-binding sites; the pI 5.6-isozyme and pI 5.4-isozyme were obtained when one and two kinds of sites were bound with FDP, respectively. The association and dissociation of FDP at both sites were reversible in the presence and absence of 0.15 M KC1 (high ionic strength). The muscle-type isoenzyme had no FDP-binding site. The spleen-type isoenzyme had two kinds of FDP-binding sites, like the liver-type isoenzyme. When the ionic strength of solutions containing the enzyme and FDP was sufficiently low, one and two kinds of the sites could bind with FDP, converting the enzyme into pI 6.6-isozyme and pI 6.2-isozyme, respectively. FDP bound with one kind of site (the 2nd site) was easily dissociable, but FDP bound with the other kind of site (the 1st site) was not. Provided that the 1st site carried bound FDP, the 2nd site was associable at high ionic strength. The liver-type isoenzyme free of FDP and the spleen-type isoenzyme bound with FDP at both sites had similar pI values of 6.2 and were not separable by isoelectric separation. Some properties of these pI-isozymes were compared. When Rhodamine sarcoma was transplanted in rats, the content of spleen-type isoenzyme in the livers increased. When rats were injected with chromatin prepared from either Rhodamine sarcoma or spleen, the content of spleen-type isoenzyme in the livers again increased. This was not observed on the injection of chromatin prepared from liver, indicating that the factor capable of controlling the gene expression was present in chromatins of sarcoma and spleen but barely or not at all in chromatin of liver.

Animals↗
PubMed1976

Graft-versus-host reactivity and renal allograft survival in rats given allogeneic spleen cells or spleen allografts.

Selective recruitment of antigen-sensitive cells (ASC) into the spleen as a method of inducing specific suppression was attempted by intravenous injection of either DA or Lewis spleen cells 24 hr before a (DA X Lewis)F1 renal allograft into a Lewis or DA recipient, either with or without a splenectomy. This led to suppression of rejection in the DA recipient and delayed rejection in the Lewis recipient. Splenectomy produced a minimal augmentation effect. Assay of graft-versus-host (GVH) reactions in (DA X Lewis)F1 rats by a popliteal node assay showed that injection of allogeneic DA or Lewis spleen cells 48 hr before the assay significantly reduced the reaction produced by node lymphocytes but not spleen lymphocytes, suggesting a loss of ASC from the lymph nodes. Lewis spleen allografts did not produce such a significant reduction in the GVH reactivity of DA node lymphocytes as intravenous Lewis cells, whereas DA spleen allografts led to an increased GVH reactivity of Lewis node lymphocytes. From these studies, it is not possible to attribute the suppression produced by the intravenous injection of allogeneic cells to selective recruitment of antigen-sensitive cells to the spleen.

Animals↗
PubMed1978

Morphological studies of the spleen in splenomegalic liver cirrhosis comparing with the spleen in idiopathic portal hypertension (so-called Banti's syndrome without liver cirrhosis).

Morphological changes of the spleen in splenomegalic liver cirrhosis (SLC) were studied. Comparisons with the normal spleen and the spleen of idiopathic portal hypertension (IPH) were made by (1) light microscopy with histometry, (2) scanning electron microscopy (SEM) with histometry, and (3) SEM of the spleen vascular replica. Histometrical studies by light microscopy showed that in both SLC and IPH, the white pulp volume was decreased in random units of splenic tissue but increased in the whole spleen, whereas the red pulp volume was increased both in random units of splenic tissue and in the whole spleen. The increase in the total volume of the white pulp was less marked in SLC than in IPH. SEM histometry demonstrated in the red pulp an increase in small venous sinuses and narrowing of the Billroth cord in SLC and IPH. Narrowing of the Billroth cord was more marked in SLC than in IPH. SEM of the white pulp showed channels formed by reticulum cells around the central artery in SLC and IPH. The channels are thought to correspond to so-called "follikuläre Fibroadenie" or periarterial fibrosis. The spleen vascular replica demonstrated open arterial termination into the tissue spaces in the Billroth cord in SLC, IPH and the normal. Venous sinuses were arranged in bundles in SLC and IPH.

Adult↗
PubMed1975

Immune complexes in the spleen. Replacement of immune complexes trapped in spleen follicles by new immune complexes from the circulation.

The fate of intravenously injected 125I-BGG-anti-BGG in the spleen of mice was studied using autoradiography. Part of the labelled immune complexes was trapped in the follicles of the spleen as could be expected. In a first experiment it was found that injections with unlabelled immune complexes were followed by a partial release of the labelled immune complexes from the follicles. In a second experiment unlabelled immune complexes retained in spleen follicles appeared to inhibit the trapping of intravenously injected labelled immune complexes to some degree and for some time. The conclusion was drawn from these experiments that immune complexes, which normally remain in part of the lymphoid follicles for a long period, may be replaced by new immune complexes from the circulation. This seems important since trapping in lymphoid follicles of antigen complexed by antibody is the only known mechanism by which small amounts of antigen may be preserved in the body for a long time after the initiation of antibody production. The bulk of antigen and antigen-antibody complexes is removed by phagocytosis followed by destruction. It appeared also that, although all spleen follicles in the mouse spleen is able to retain the complexes for a longer time. Possible explanations for these individual differences between the follicles of one spleen are discussed.

Animals↗
PubMed1979

Correlation between sectional area of the spleen by ultrasonic tomography and actual volume of the removed spleen.

The sectional area of the splenotomogram scanned parallel to the ribs provides useful information for differential diagnosis and determination of prognosis in liver diseases. To establish a relationship between sectional area and actual spleen volume, 10 spleens obtained at splenectomy or autopsy were studied. A good linear correlation (r = 0.956) was present between the sectional area (S) and the actual spleen volume (V). The spleen volume could be calculated as V = 7.5S - 77.5. Therefore the value of the sectional area obtained from one ultrasonic splenotomogram has practical application as a parameter reflecting the spleen volume in vivo.

Adult↗
PubMed1976

The spleen in Friend leukemia. II. Nonleukemic nature of spleen stroma.

Pieces of Friend leukemic spleens implanted sc into mice regenerated into normal-appearing spleens if animals were protected against the leukemia. In unimmunized animals, the implant regenerated normally, but was subsequently infiltrated by leukemia cells. This leukemia cell infiltration required at least 30% stromal regeneration of the implant. The hematopoietic regeneration was primarily a repopulation with cells from the host animal, not with cells indigenous to the donor spleen. The development of the implant, whether normal or leukemic, was retarded by the presence of the host spleen, whether leukemic or normal. These studies strongly suggested that the stromal cells of the spleen are not directly involved in the virus-induced leukemic process but acted as supporting structure for the malignant cells.

Animals↗
PubMed1978

Immune response-associated antigens on mouse leukemia cells. II. Anti-Ia sera inhibit the MLR reaction between normal GR spleen cells and syngeneic spleen cells of GRSL tumor-bearing mice.

Mitomycin C-treated ascites cells of Ia antigen-positive GRSL14 tumor cells and spleen cells from GRSL14 tumor-bearing mice stimulated lymphocyte proliferative responses in normal syngeneic GR spleen cells. Furthermore, mitomycin C-treated T cells purified from spleen cells of tumor-bearing mice also stimulated normal GR spleen cells. Anti-Ia sera inhibited the stimulating ability of tumor cells and of spleen cells of tumor-bearing mice. These data suggest a role for I region gene products in immune surveillance for syngeneic tumors.

Animals↗
PubMed1975

The predominant role of the spleen in lymphocyte recirculation. I. Homing of lymphocytes to and release from the isolated perfused pig spleen.

Lymphocyte recirculation through the isolated pig spleen was studied by means of a perfusion system which kept the organ alive for a prolonged period of time. By changing the perfusate to a leucocyte-enriched or cell-free perfusate and taking serial arterial and venous samples, the numbers of lymphocytes which homed to or were released from the spleen were measured. In all experiments more lymphocytes homed than were released per minute. There was no apparent difference when autologous or allogeneic cells were used. The number of lymphocytes released depended on the number of lymphocytes homed previously. During the phase of constant release up to 3-3 X 10(6) lymphocytes were released per gram spleen per minute. From these values it can be extrapolated that up to 270 X 19(9) lymphocytes recirculate through the isolated pig spleen per day. Based on kinetic data from other species it is estimated that in the entire pig a total number of 300-400 X 10(9) lymphocytes recirculate per day. Thus, it can be concluded that the spleen is the most important organ for lymphocyte recirculation in the pig.

Animals↗
PubMed1975

Specific partial depletion of graft-vs-host activity by incubation and centrifugation of mouse spleen cells on allogeneic spleen cell monolayers.

Spleen cells (from BALB/c mice immunized with the C57BL/6 lymphoma EL4, or from non-immune BALB/c) were incubated on monolayers of [C57BL/6 times BALB/cF1 (B6CF1) spleen cells on polylysine-coated polystyrene Petri plate, for 1/2 hr or for 1 hr at 37 degrees C followed by centrifugation of the monolayers for 5 min at 70 times G to 110 times G at 34 to 37 degrees C. Control monolayers were BALB/c spleen cells. As measured by the Simonsen spleen weight assay in neonatal mice, graft-vs-host (GVH) activity was partially depleted in cell populations nonadherent to B6CF1 monolayers. Residual GVH activity of these nonadherent cells was about half that of cells incubated on the control syngeneic monolayers (the mean of eight experiments was 49% +/- 11% S.D.). Two or three consecutive cycles of incubation and centrifugation did not significantly diminish the residual GVH activity, suggesting that spleen cells with GVH activity are heterogeneous with respect to binding to allogeneic target cells under the above conditions. Cell populations nonadherent to third-part [A times AL]F1 monolayers retained full activity, and cell populations partially depleted of GVH activity in B6CF1 neonates had full activity in third-party [BALB/c times AL]F1 neonates.

Animals↗
PubMed1977

Immunologic tolerance to HGG in mice. I. Suppression of the HGG response in normal mice with spleen cells or a spleen cell lysate from tolerant mice.

Adoptive transfer of spleen cells or spleen cell lysates from mice tolerant to human-gamma-globulin (HGG) specifically suppressed the response of normal syngeneic recipients to HGG. The suppressive activity could be transferred for over 100 days after tolerance induction. The suppression induced by both spleen cells and spleen cell lysate was found to be specific as evidenced by a normal response to a challenge with turkey-gamma-globulin or goat erythrocytes. The activity of the suppressive lysate could be removed by passing the material through an HGG immunoadsorbent column but not by passing it through an anti-HGG column or a BSA column. These results indicated that the factor had antigen specificity and was probably not antigen-antibody complexes. That this suppression was not due to a shifting of the kinetics of the antibody response has also been demonstrated. The antigen-specific suppressor factor in the tolerant spleen cell lysates was a protein with a m.w. of approximately 45,000 daltons. The kinetics of the appearance of both suppressor cells and suppressor factor were consistent with a mechanism of active suppression functioning in the maintenance of tolerance to HGG.

Animals↗
PubMed1978

Growth of Trypanosoma musculi in cultures of murine spleen cells and analysis of the requirement for supportive spleen cells.

Growth of Trypanosoma musculi in vitro has been achieved. The number of parasites increased by more than 1,500-fold in less than 8 days under the most suitable conditions. The rate and magnitude of growth was comparable to that which occurs in inoculated murine hosts. Maximum growth was displayed in cultures composed of RPMI 1640 medium supplemented with fetal calf serum, murine spleen cells, and foreign erythrocytes (sheep). No growth occurred in the absence of spleen cells. The adherent, macrophage-rich population supported parasite growth much better than did the nonadherent population. Parasite growth was excellent in the presence of irradiated spleen cells or of cells from thymectomized, irradiated, bone marrow-reconstituted mice. The important cells appeared to be macrophages. The beneficial effect of sheep erythrocytes probably resulted from preoccupation or stimulation of phagocytes. Soluble substances released by spleen cell cultures promote parasite growth, as was shown by experiments with double-compartment culture vessels. The utility of this culture system for analysis of host immune responses against the trypanosome was demonstrated.

Animals↗
PubMed1979

Cell killing by spleen necrosis virus is correlated with a transient accumulation of spleen necrosis virus DNA.

Spleen necrosis virus productively infects avian and rat cells. The average number of molecules of unintegrated and integrated viral DNA in cells at different times after infection was determined by hybridization and transfection assays. Shortly after infection, there was a transient accumulation of an average of about 150 to 200 molecules of unintegrated linear spleen necrosis virus DNA per chicken, turkey, or pheasant cell. No such accumulation was seen in infected rat cells. Soon after infection there was in chicken cells, but not inturkey, pheasant, or rat cells, also a transient integration of an average of 35 copies of viral DNA per cell. By 10 days after infection, the majority of this integrated viral DNA was lost from the population of infected chicken cells. At the same time, the majority of the unintegrated viral DNA was also lost from infected chicken, turkey, and pheasant cells. The transient cytopathic effect seen in these infected cells also occurred at this time. Late after infection about five copies of apparently nondefective spleen necrosis proviruses were stably integrated at multiple sites in chicken, turkey, pheasant, and rat DNA. These results demonstrate a correlation between the transient accumulation of large numbers of spleen necrosis virus DNA molecules and the transient occurrence of cytopathic effects.

Animals↗
PubMed1976

The spleen in Friend leukemia. I. Prolonged survival of leukemic mice after autoimplantation of spleen tissue.

Friend virus infection of susceptible mice led rapidly to fulminant erythroleukemia and death. Subcutaneous implantation of leukemia spleen bits into splenectomized normal animals led to their early death from Friend leukemia. In contrast, bits of leukemic spleen implanted sc into splenectomized leukemic mice prolonged the survival of these animals. Concomitant with this survival was a reversal of the virus-induced immunosuppression and an increase in the levels of circulating, neutralizing, antivirus activity. This marked difference in response to leukemic spleen implants by leukemic as compared to normal mice reflected previous contact of the former with Friend Virus. Our studies indicated that the Friend virus-infected mouse mounted a resistance to the virus infection, which under certain conditions is capable of reversing the disease process.

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