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PubMed2005

Factors affecting the quantitative liver-spleen scan in normal individuals.

The quantitative liver-spleen scan (QLSS) can estimate the functional hepatic mass and the organ volumes by precise measurement of sulfur colloid (SC) distribution. The normal range determined in prior studies was estimated from patients with absence of chronic liver disease in which intense fasting appeared to produce slightly abnormal values. This study was to determine the effect of fasting or fed status and colloid particle size on quantitative measurements from the QLSS in a small cohort of normal individuals. Twelve persons without any medical problems had QLSS taken twice, 2 weeks apart, one fasting and one postprandial. Patients were scanned after injection of 5-6 mCi of SC; six patients were given solution A (5- to 12-microm particle size) and six patients solution B (2- to 12-microm particle size). SPECT and planar analysis were performed. SC distribution of total counts between the liver and the spleen {[L/(L + S)]t ratio}, liver-spleen index (LSI), and liver-bone marrow index (LBI) were calculated. The perfused hepatic mass (PHM) is the average of the LSI and LBI. Spleen and liver volumes are expressed as milliliters per pound ideal body weight (IBW). Results showed that the liver and spleen volumes (solution B postprandial, 9.27 +/- 2.48 and 1.47 +/- 0.57 ml/lb IBW, respectively) and LBI were not affected by the type of SC solution or by ingestion status. L/(L + S) total and pixel count ratios were significantly higher for solution B and postprandial studies. [L/(L + S)]t, LSI, and PHM increased significantly (P < 0.05) from fasting to postprandial for solution A (0.71 +/- 0.13 vs 0.79 +/- 0.08, 80 +/- 14 vs 91 +/- 8, and 102 +/- 10 vs 106 +/- 8, respectively) and for solution B (0.81 +/- 0.05 vs 0.90 +/- 0.02, 86 +/- 4 vs 95 +/- 3, and 101 +/- 5 vs 110 +/- 3). Neither fasting nor postprandial LSI and PHM were significantly different between solution A and solution B. We conclude the following. (1) The QLSS functional indices in "true" normal patients fall within the previously reported normal range. (2) Calculated liver and spleen volumes are not altered by fasting or sulfur colloid particle size. (3) Fasting significantly decreased the [L/(L + S)]t, LSI, and PHM. (4) A postprandial scan may be preferable since the normal values for [L/(L + S)]t, LSI, and PHM are greater, with a narrower range, than fasting values.

Adult↗
PubMed1984

Removal of the massive spleen: a surgical risk?

The results of splenectomy for hematologic disorders have been reviewed with special attention to problems possibly associated with massive spleens (1,500 g or more). The mortality rate in the group of patients with massive spleens did not differ from that in the group of patients with smaller spleens (2 percent and 3 percent, respectively). The complication rate, however, in the group of patients with massive spleens (43 percent) was twice that in the patients with smaller spleens (43 percent and 22 percent, respectively). The most frequent complication was postoperative hemorrhage in the splenic bed, usually caused by thrombocytopenia, perisplenitis , or both. Postoperative morbidity is seen as a function of the underlying disorder and of the general condition of the patient and not of the weight of the spleen per se.

Adolescent↗
PubMed1989

Differential properties of organ-specific serum opsonins for liver and spleen macrophages.

Earlier we reported that serum contains organ-specific opsonins which selectively enhance recognition of liposomes by macrophages in the specific organs of the reticuloendothelial system (Moghimi, S.M. and Patel, H.M. (1988) FEBS Lett. 233, 143-147). The results presented here describe the properties of these organ-specific opsonins which differentiate between liver-specific and spleen-specific opsonins responsible for the enhancement of phagocytosis of liposomes by Kupffer cells and spleen macrophage, respectively. Liver-specific opsonin is a heat-stable macromolecule which on heating or on freezing and thawing exhibits enhanced opsonic activity. Serum also contains a dialysable factor which inhibits its opsonic activity. On the other hand, the spleen-specific opsonin is a heat-labile macromolecule which is sensitive to freezing and thawing and requires a dialysable serum co-factor for its optimum opsonic activity on spleen macrophages. Removal of this factor from serum brings about an irreversible conformational change in the opsonin. Evidence suggests that the spleen-specific opsonin may be composed of more than one different opsonin molecule. It is suggested that the serum factor(s) that inhibits liver-specific opsonic activity and enhances the spleen-specific activity may not be the same molecule, but in both the cases the factor(s) may mediate its function by modifying the process of the opsonisation of liposomes or by influencing the interaction of the opsonised liposomes with the respective cells. We propose that purification of the organ-specific opsonins may provide an opportunity to target drug carriers selectively to a specific organ of the reticuloendothelial system, and help us to evaluate their role in the altered opsonin states known to exist in certain diseases.

Animals↗
PubMed1982

The occurrence of psychosine and other glycolipids in spleen and liver from the three major types of Gaucher's disease.

Glycolipid changes in spleen autopsy specimens were determined in four cases of Gaucher's disease type I, three cases of type II, and twelve cases of type III. These changes were also determined in liver autopsy specimens from three cases of type II and in nine cases of type III. The concentration of glucosylceramide in spleen was of the same magnitude in all three types, 36.3 +/- 11.7 mmol/kg in type I, 32.7 +/- 8.5 mmol/kg in type II, and 32.6 +/- 6.9 mmol/kg in type III. In liver there were large differences in the glucosylceramide concentration between splenectomized and non-splenectomized cases. Thus, in the non-splenectomized type III cases it was 9.9 +/- 3.0 mmol/kg, while in the splenectomized type III cases it was 24.1 +/- 6.1 mmol/kg. The accelerated deposition of glucosylceramide in liver after splenectomy was also demonstrated by analyses of liver biopsy specimens. A 2-6-fold increase of gangliosides was found in liver and spleen from the three types, with no significant differences between the types. The increase of gangliosides was limited almost exclusively to GM3. Glucosylsphingosine, never detected in normal tissue, was demonstrated in all samples from Gaucher's livers and spleens. The concentration in spleen was in type II, 0.16 +/- 0.05 mmol/kg, in type III, 0.19 +/- 0.05 mmol/kg, while in type I it was significantly lower, 0.07 +/- 0.03 mmol/kg. In liver, the highest concentrations occurred in the splenectomized type III subjects, 0.16 +/- 0.08 mmol/kg, while in the non-splenectomized type III cases it was 0.06 +/- 0.02 mmol/kg and in type II 0.09 +/- 0.02 mmol/kg. The demonstration of high concentrations of the cytotoxic compound glycosylsphingosine may be a contributing factor behind the tissue necrosis and fibrosis commonly seen in spleens and livers from Gaucher's patients.

Adolescent↗
PubMed1984

Spontaneous proliferation in unfractionated spleen cell cultures: autologous mixed-lymphocyte reactions (AMLR) which can be differentially regulated by prostaglandins and lymphokines.

The present studies were undertaken to define the contribution of the autologous or syngeneic mixed-leukocyte reactions (AMLR/SMLR) to the cellular proliferation observed in unfractionated spleen cell cultures. Proliferation was studied in whole, untreated 6-day murine spleen cell cultures supplemented with syngeneic serum. These cultures exhibited relatively low but significant levels of cellular proliferation as measured by uptake of radioactive thymidine ([3H]TdR). Treatment of spleen cells with monoclonal anti-Thy 1.2 antibody and complement before culture, the addition of specific anti-I-A monoclonal antibodies to the cultures or removal of Ia+ adherent cells before initiation of culture all inhibited the proliferative response significantly. Thus, the autologous proliferation of untreated and unfractionated spleen cells manifests the main characteristics of the AMLR/SMLR, namely, its dependence on T (responder) and Ia+ (stimulator) cells and specific inhibition by anti-I-A antibodies. A marked augmentation in cellular proliferation was observed in unfractionated spleen cell cultures treated for the initial 24 hr of culture with 5 X 10(-6) M indomethacin, an inhibitor of prostaglandin synthesis. Conversely, the addition of 7 X 10(-9) M prostaglandin E1 (PGE1) to these cultures depressed cellular proliferation. This suppression of autologous splenic cell proliferation induced by PGE1 could be partially reversed by the addition of concanavalin A-induced lymphokine (LK) preparations early in the culture. These findings indicate that (a) the proliferation of unfractionated spleen cell cultures occurring in the absence of exogenous stimulatory signals is due largely to an ongoing AMLR, and (b) biologically active mediators with opposing influences, namely, prostaglandins and immunostimulatory LK, participate in the regulation of the AMLR.

Alprostadil↗
PubMed1984

Immunoregulation in experimental Schistosomiasis. III. Role of macrophages in soluble egg antigen-induced chronic spleen cell augmentation of baseline lymphocyte reactivity.

Spleen cells from mice infected for 20 weeks with Schistosoma mansoni, exposed in vitro to soluble schistosomal egg antigens (SEA), treated with mitomycin C (Mc), and cocultured with syngeneic responder spleen cells increased the baseline proliferation of the otherwise unstimulated responder cells in cocultures. The role of macrophages in this "spontaneous" thymidine incorporation was studied directly by removal of macrophages on Sephadex G-10 columns. Removal of esterase-positive, Sephadex G-10-adherent cells (macrophages) greatly reduced the amount of SEA-induced, chronically infected spleen cell-mediated stimulation observed in cocultures. It also reduced an elevated background of spontaneous DNA synthesis seen with control cultures of spleen cells from infected animals. Depletion of T lymphocytes from chronic spleen cell populations by treatment with anti-Thy 1.2 serum and complement prior to exposure to SEA partially abrogated the augmentation effect. Comparison of these results with mitogen (concanavalin A)-induced spleen cell-mediated stimulation (which is elevated, rather than reduced, by macrophage removal) and with known alterations in splenic T- and B-lymphocyte ratios in chronic murine schistosomiasis suggests that antigen-stimulated, chronically infected splenic macrophage-dependent baseline augmentation may depend on specific T-lymphocyte-derived lymphokine induction. These results may reflect a general mechanism whereby animals harboring a persistent, chronic infection can respond quickly to a second or challenge infection or a flareup of the primary infection.

Animals↗
PubMed1985

Activation of suppressor T cells by low-molecular-weight factors secreted by spleen cells from tumor-bearing mice.

The spleens of mice bearing large M-1 fibrosarcomas have been shown to contain several populations of cells which nonspecifically suppress antibody synthesis by cocultured normal spleen cells. It has now been shown that the spleens of tumor-bearing mice also contain inducer cells which secrete soluble factors capable of activating suppressor T cells from unprimed precursor cells. The activated suppressor cells are Thy 1+, Lyt 1+2+ and secrete a soluble suppressive factor. They inhibit the in vitro generation of antibody-forming cells by cocultured normal spleen cells stimulated by T-cell-dependent antigens. They do not, however, suppress the antibody response to T-cell-independent antigens and do not inhibit antibody synthesis by cocultured nude mouse spleen cells cultured with T-cell-dependent antigens and exogenous helper factors. In addition, suppression is blocked if conditioned medium containing T-cell growth factors is added to the suppressor cell assays. These data suggest that cells in the spleens of tumor-bearing mice secrete inducing factors which activate suppressor cells. These activated suppressor cells in turn secrete soluble suppressor factors which inhibit antibody synthesis, possibly by interfering with the synthesis or release of T-cell growth factors.

Animals↗
PubMed1988

Impaired interleukin 1 and interleukin 2 production following in vitro abortive infection of murine spleen mononuclear cells by Semliki Forest virus.

The effect of Semliki Forest virus (SFV) infection of murine spleen mononuclear cells was investigated in vitro. A small percentage of spleen macrophages expressed viral antigens, but no infectious virus particles were released, indicating an abortive-type infection. Wild-type SFV infected a higher percentage of macrophages than the attenuated, demyelinating mutant A7. The proliferation of spleen mononuclear cells under Con A stimulation was inhibited by the viral infection. The supernatant (SN) harvested from infected and Con A-stimulated spleen adherent cells could not stimulate thymocytes in an interleukin 1 (IL-1) assay and indomethacin treatment of infected cultures had no effect. The stimulatory effect of SN from noninfected cultures in the IL-1 assay was reduced when SN from infected cultures was added, suggesting the presence of an IL-1 inhibitor. Interleukin 2 (IL-2) production by splenocytes also decreased after viral infection, but exogenous IL-2 restored the response to Con A stimulation of infected spleen cells. This study demonstrates that abortive SFV infection of spleen macrophages has an immunosuppressive effect which may lead to an aberrant immune regulation.

Animals↗
PubMed1989

Altered immune response patterns in murine syngeneic pregnancy: presence of natural null suppressor cells in maternal spleen identifiable by monoclonal antibodies.

Expression of certain autologous lymphocyte-activating antigenic determinants on the developing embryo is known to provide a stimulus for maternal anti-fetal autoproliferative responses. If left unregulated these responses could exert negative influences on the reproductive process by converting to autoaggressive forms of immune reactivity. In normal circumstances, immunological reactions of this nature are therefore likely to be under the control of pregnancy-associated immunoregulatory elements found within the maternal/fetal environment. In the present investigation we describe a naturally occurring splenic inhibitory cell type devoid of conventional T, B, and macrophage surface markers associated with syngeneic murine pregnancy that is capable of exerting potent immunosuppressive effects on an in vitro expression of fetal/newborn T cell autoreactivity, namely the autologous mixed lymphocyte reaction (AMLR). Maternal spleen cells inhibitory for AMLR were found to be highly resistant to cytotoxic pretreatment with a panel of conventional antisera directed against T cell-specific antigenic determinants. The non-T nature of the natural splenic suppressor cell was further indicated by experiments showing that purified spleen T cells had no inhibitory activity. Pregnancy spleen cell populations that were effectively depleted of macrophages retained full ability to inhibit AMLR. Maternal suppressor activity could be localized to the spleen cell population bearing receptors for the B cell-specific lectin, soybean agglutinin (SBA). A panel of monoclonal antibodies prepared against enriched populations of suppressor cells was screened and selected for specific reactivity using an ELISA against glutaraldehyde-fixed SBA+ spleen cell subpopulations from pregnant versus virgin animals. Several of the monoclonals developed against suppressor-enriched spleen cell populations from isopregnant as well as allopregnant animals were effective in reducing or eliminating suppressor cell activity following cytotoxic pretreatment in the presence of complement. The novel set of anti-suppressor monoclonal antibodies described here should prove useful in furthering the isolation and characterization of pregnancy-associated suppressor cells and in determining their relationship to natural suppressor cell populations described in other systems.

Animals↗
PubMed1991

NZB serum factor (NZB-SF): B precursor cell maturation factor identified in murine lupus. I. Identification of 60-kDa glycoprotein as the major component from both spleen cell supernatant and serum.

NZB serum factor (NZB-SF), initially identified in sera of very young NZB mice, can enhance maturation and proliferation of sIg- pre-B cells in marrow. In the present study, spleen cell supernatant from young NZB mice was used as a source of NZB-SF. NZB mice were treated with Corynebacterium parvum 2 weeks prior to sacrifice, and harvested spleen cells obtained at sacrifice were cultured for 24 hr in serum-free medium. One liter of spleen cell supernatant prepared in this way contained NZB-SF-like activity equivalent to that present in 10 ml of serum collected from young NZB mice. NZB-SF was purified on an affinity chromatographic column conjugated with mouse IgG1 monoclonal antibody (mAb) against NZB-SF. The purified NZB-SF had pI 7.8 and showed one major band of 60 kDa and a faintly stained 35-kDa band upon SDS-PAGE under nonreducing conditions. The 60-kDa NZB-SF extracted from the gel slice was also more potent in dot blot ELISA (greater than 100 times) than the 35 kDa NZB-SF and was biologically active. After endoglycosidase F treatment, but not after treatment with a reducing agent (2-ME), the two bands merged into a single band at the 15-kDa position. Amino acid sequence analysis of endo-F treated NZB-SF indicated that the N-terminus of this protein is blocked. Serological and functional studies of affinity-purified NZB-SF have revealed that NZB-SF is distinguishable from IL-1 alpha, IL-2, IL-3, IL-4, IL-5, IL-6, CSF-GM, IFN-gamma, and TNF alpha. Therefore, a major component of NZB-SF(s) in the spleen cell supernatant may be an apparently novel 60-kDa glycoprotein with a single amino acid backbone. Sera and spleen cell supernatants from normal strains of mice (DBA/2, B6, or BALB/c) were also applied to the immuno-affinity column used to purify NZB-SF. It was found that trace amounts of NZB-SF are present also in serum of normal strains of mice and that spleen cells of these mice can also produce NZB-SF in vitro following stimulation with C. parvum. In SDS-PAGE, the 60-kDa NZB-SF is also the major component of NZB-SF in normal strains of mice. These results suggest that the 60-kDa NZB-SF may be of physiological importance in B cell differentiation and that this physiological factor is autoimmune-prone NZB mice.

Animals↗
PubMed1991

Possible mechanism of the preventive effect of BCG against diabetes mellitus in NOD mouse. I. Generation of suppressor macrophages in spleen cells of BCG-vaccinated mice.

With the aim of clarifying the mechanism of the suppressive action of BCG against insulitis and overt diabetes in NOD mice, we studied the effects of BCG on spleen cell populations and on the in vitro immune responses of spleen cells. The spleen cells of BCG-vaccinated mice showed much lower responsiveness to various mitogens such as Con A, PHA, PWM, and LPS than those of saline-treated mice. Low responsiveness to alloantigens was also observed. Flow cytometric analysis of the spleen cells revealed that Mac-1+ and Mac-2+ cells had increased while T and B cells had decreased in the BCG-vaccinated mice compared with the saline-treated mice at the time when the maximum level of inhibition of mitogen responses of BCG-vaccinated mice was observed. This suggests that the decreased in vitro immune response was due to the increase in macrophages which suppress lymphocyte functions. Support for this interpretation comes from the following two findings: (1) the restoration of mitogen responses of spleen cells when macrophages were eliminated by plastic adhesion or FACS sorting and (2) resuppression of PHA and Con A responses of plastic-nonadherent spleen cells by addition of adherent cells or flow cytometrically sorted Mac-1+ cells obtained from BCG-vaccinated mice. These results indicate the generation of suppressor macrophages after BCG vaccination and suggest that these macrophages prevent the autoimmune pathogenesis leading to diabetes in NOD mice.

Animals↗
PubMed1992

Inhibition of experimental autoimmune uveitis by retinal photoreceptor antigens coupled to spleen cells.

Experimental autoimmune uveitis (EAU) and experimental autoimmune pinealitis (EAP) are CD4+ T cell-mediated inflammatory diseases of the uveal tract and retina of the eye and of the pineal gland. EAU and EAP can be induced by several retinal autoantigens including S-antigen (S-Ag) and interphotoreceptor retinoid binding protein (IRBP). In this study we investigated the effect of intravenous administration of S-Ag and IRBP coupled to syngeneic spleen cells on the development of EAU and EAP. Injection of S-Ag or IRBP coupled to spleen cells 5 days prior to immunization with native S-Ag or IRBP, respectively, was effective in preventing the induction of EAU and EAP in LEW rats. Conversely, LEW rats receiving S-Ag-coupled spleen cells and challenged with IRBP or LEW rats receiving IRBP-coupled spleen cells and challenged with S-Ag developed a severe EAU within 10 days to 2 weeks following immunization, as did all control animals receiving sham-coupled spleen cells and challenged with the two retinal antigens. The results show that the administration of retinal autoantigens coupled to spleen cells effectively protects against the development of EAU when animals are subsequently challenged with the tolerizing antigen but not when challenged with another unrelated pathogenic retinal autoantigen.

Animals↗
PubMed1976

Uptake and release of catecholamines in sympathetic nerve fibres in the spleen of the cod, Gadus morhua.

The effects of drugs known from mammalian experiments to interfere with uptake and release of adrenergic transmitters in the sympathetic nerve terminals have been investigated on perfused spleen and isolated spleen strips from the cod. Cocaine and desipramine inhibit the accumulation of 3H-noradrenaline in the perfused spleen, probably by interfering with uptake mechanisms. Both drugs also shift to the left the dose-response curves for noradrenaline and adrenaline on isolated strips, cocaine being most potent. The maximal contraction force of isolated strips also increases after cocaine when noradrenaline is the agonist, but not when methacholine is used or on chronically denervated strips. This effect of cocaine is therefore not due to a general postsynaptic effect. Tyramine and amphetamine both release stored 3H-noradrenaline from the perfused spleen, and tyramine also contracted the spleen strips. In contrast to the situation in mammals, the dose-response curve for tyramine is not affected by cocaine, and tyramine (up to 10(-3) M) present in the bath does not potentiate the dose-response curve for noradrenaline on isolated strips. Different uptake mechanisms for tyramine and noradrenaline into the nerve terminal are therefore suggested for the cod sympathetic fibres. The alpha-adrenoceptor blocking agent phentolamine produces an increase in overflow of label during nerve stimulation at 5Hz in the perfused spleen preloaded with 3H-noradrenaline. An alpha-adrenoceptor-mediated control of the release of catecholamines, similar to that in mammals, appears to be present in the cod.

Amphetamine↗
PubMed1989

Histological changes in the spleen and liver of C57BL/6 and A/J mice during Plasmodium chabaudi AS infection.

The level of resistance to infection in inbred mice with the murine malaria species Plasmodium chabaudi AS is genetically determined. Resistant C57BL/6, which are able to eliminate the parasite by 4 weeks, develop marked splenomegaly and survive the infection. Susceptible A/J mice, which succumb to infection (mean survival time = 10 days), develop only minimal splenomegaly. In order to determine if gross differences in the organization, number, and type of spleen cells are related to the outcome of infection with P. chabaudi AS, the development of splenomegaly was examined by enzyme and immunohistochemical methods during the first week after infection. Cryostat sections of spleens removed from normal animals of both strains and at 4 and 7 days after intraperitoneal infection with 10(6) parasitized erythrocytes were stained for enzyme (acid phosphatase and nonspecific esterase) and immunohistochemistry with conventional monoclonal antibodies against T cells, B cells, and macrophages as well as with novel rat anti-mouse monoclonal antibodies which define discrete subpopulations of macrophages in the mouse spleen. The livers of normal and infected animals of each strain were also examined. The results of this study demonstrate (1) differences between normal, uninfected B6 and A/J mice in the organization and number of one subpopulation of macrophages in the spleen, the marginal metallophilic macrophages, and (2) marked histological changes in the spleen and liver during the course of infection in both resistant C57BL/6 and susceptible A/J mice. These changes include depletion of cells from the marginal zone of the spleen which, in the case of the marginal metallophilic macrophages, appears to be more severe in susceptible A/J mice.

Animals↗
PubMed1991

Developmental kinetics of hemopoietic progenitors in the avian embryo spleen.

By means of plasma clot clonal cultures, the content of the avian spleen in granulomonocytic progenitors was studied during ontogeny. Serum-free media were used that were supplemented with growth activities produced either by embryonic fibroblasts or adult spleen cells. These two conditioned media not only permitted the growth of M-CFC, G-CFC, and GM-CFC but also F-CFU (fibroblast colony-forming units) from quail or chick embryonic spleen cells. The presence of spleen cell-conditioned medium promoted the development of large colonies of immature granulocytes. In the chick the first hemopoietic progenitors appeared at E9 and their number displayed two peaks, one at E15 and a smaller one at E18. In the quail the first progenitors were detected as early as E7 and their number peaked at E10. In this species, hemopoietic progenitors disappeared definitively before hatching while in the chick some were still present at P3. The progenitor content of the chick embryo spleen was compared to that of the bone marrow. This content remained stable during all of embryonic life, while the bone marrow exhibited a very different profile, where a sharp peak at E16 was followed by an acute decline and a stabilization at a rather low level. The particular profile in the spleen speaks in favor of a special role of this organ in the development of the hemopoietic system.

Animals↗
PubMed1994

Heat-damaged red cell scan for intraoperative localization of the accessory spleen.

Destruction of platelets by the reticuloendothelial system in immune thrombocytopenia purpura (ITP) is enhanced by platelet-associated IgG. Relapse after splenectomy may result from IgG produced in the accessory spleen. These structures may be located at any site between Gerota's fascia and the left ovary or testicle as well as adjacent to the spleen. The heat-damaged red cell scan (HDRCS) has been demonstrated to be an accurate method for identifying accessory spleens. HDRCS using semi-in vitro labeling of the patient's red blood cells with technetium 99m pertechnetate delineated accessory splenic tissue as the etiology of post-splenectomy relapse three times in two patients 3 to 9 months postoperatively. A labeled intraabdominal probe and HDRCS were subsequently used by the surgical team for identification and excision of the accessory spleen. Four additional patients underwent splenectomy for ITP between 1989 and 1992; heat-damaged red blood cells were injected after the major splenic tissue was removed. Accessory spleens were identified in two patients. All patients were discharged within 6 days, without perioperative complications. Two patients currently require steroids. The techniques of intraoperative HDRCS allow rapid localization and removal of the accessory spleen at the time of laparotomy. Evidence of growth of accessory splenic tissue postsplenectomy was demonstrated.

Child↗
PubMed1986

Simultaneous expression of multiple immune complex receptors on murine thymocytes and spleen cells.

Mixed rosette studies were performed to evaluate the coexpression of IgG Fc. IgM Fc, and complement receptors (C3R) by thymocytes obtained from mice 7 days after cortisone injection and by spleen cells. Indicator cells coated with IgM, IgG, or C3 independently were mixed and could be distinguished by morphology or by a fluorescein label. In double-marker studies, 36% of spleen cells formed rosettes with IgG- and/or IgM-sensitized red blood cells. Among this population there was a 24% overlap of cells binding IgM and IgG complexes simultaneously. Of the spleen cells, 78% bound IgM- and/or C3-sensitized cells. Of the spleen cells forming rosettes with IgM and C3 indicator cells, 15% coexpressed these receptors. With IgG and C3 indicator cells, 58% of spleen cells bound to one or both kinds of complexes with an 18% overlap. Of cortisone-resistant thymocytes, 14% formed rosettes with IgM- and/or IgG-sensitized red blood cells; within this population there was an overlap of 21%. With IgM- or C3-sensitized cells, 19% of cortisone-resistant thymocytes bound to one or both, among which there was a coexpression of 21%. With IgG- or C3-sensitized cells, there was a 14% overlap of rosette-forming cells binding both. In triple-marker studies 79% of spleen cells formed rosettes with C3-, IgG-, and/or IgM-sensitized indicator cells, out of which 11% coexpressed IgM and IgG FcR, 20% coexpressed IgG and C3R, and 10% coexpressed IgM FcR and C3R. Of rosette-forming cells, 13% coexpressed all three receptors. With cortisone-resistant thymocytes, 19% bound one or more kinds of immune complexes. Among these, 9% coexpressed IgG FcR and C3R, 14% coexpressed IgM FcR and C3R, and 14% bound IgG and IgM complexes. We could not detect the simultaneous expression of all three receptors on cortisone-resistant thymocytes. Using Isopaque-Ficoll fractionation of cells binding C3-sensitized cells, cortisone-resistant thymocytes were enriched and depleted of C3-receptor-bearing cells and their Lyt phenotypes were determined by immunofluorescence microscopy. The C3-receptor-enriched population contained 56% C3R+ cells which were 79% Lyt-1 positive and 100% Lyt-2 positive. The C3R-depleted population contained 1.3% C3R+ cells with 10% Lyt-1 positive and 22% Lyt-2 positive among the total. Surface phenotypic expression of normal and cortisone-resistant thymocytes was also evaluated by direct and indirect fluorescence by fluorescence-activated cell sorter (FACS).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Age-associated differences in cannabinoid-induced suppression of murine spleen, lymph node and thymus cell blastogenic responses.

The effects of delta 9-tetrahydrocannabinol (THC) and 11-OH THC on the proliferative responses of murine thymus, spleen and lymph node cells were examined. Specifically, weanling and adult mouse lymphocytes were stimulated in vitro with the T-cell mitogens concanavalin A and phytohemagglutinin. Thymus cells were suppressed at lower cannabinoid concentrations than cells from either spleen or lymph nodes. However, splenic cells from weanling mice were much more readily suppressed than were those from adult animals. Lymphoid cell numbers were varied from 1 x 10(6) to 8 x 10(6) cells/ml/culture and treated with a constant dose of THC or 11-OH THC. The smallest number of cells from the spleen or lymph nodes resulted in the greatest suppression. Thymus cells, however, were more readily suppressed than spleen or lymph node cells, regardless of the number of cells in culture. Furthermore, 11-OH THC suppressed the responses of the thymus cells to phytohemagglutinin more than to concanavalin A. The proliferative responses of spleen and lymph node cells from weanling mice to concanavalin A and phytohemagglutinin were much more readily suppressed than were cells from adult mice. This age-related difference was seen in the dose-response studies as well as in the studies with varying cell numbers in culture. In all cases, spleen and lymph node cells from younger mice were more readily suppressed to concanavalin A and phytohemagglutinin than those from older mice when treated with the cannabinoid preparations.

Age Factors↗