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PubMed1980

Functional Thy-1+ cells in cultures of spleen cells from nu/nu mice.

Thy-1+ lymphocytes, detectable by quantitative serum absorption, arise in cultures of spleen cells from congenitally athymic (nu/nu) mice supplemented with supernatants from cultures of normal spleen cells stimulated with the T cell mitogen concanavalin A. Pretreatment of nu/nu spleen cells with appropriate anti-Thy-1 alloantibody and complement prior to culture reduces their capacity to generate Thy-1+ cells by about 90%. This shows that the majority of cells proliferating in these cultures are descendants of Thy-1+ cells which can be detected in the original nu/nu spleens. Experiments aimed at exploring the function of these Thy-1+ cells after culture in conditioned medium revealed that within one or two days after culture initiation, strong cooperative activity for a humoral response to xenogeneic erythrocytes can be detected. In mixtures of bone marrow-derived lymphocytes from various mouse strains with cultured nu/nu spleen cells, it was observed that T-B cooperation is not H-2-restricted. Attempts at inducing T cell-mediated cytotoxicity to alloantigens in such cultures of nu/nu spleen cells were unsuccessful. In contrast, nonspecific cytotoxicity which was attributed to natural killer cells was regularly observed and could be maintained in these cultures over extended periods.

Animals↗
PubMed1985

The selective localization of B lymphocytes in the spleen and the role of complement receptors.

The role of complement receptors on the localization of T and B cells in the spleen of mice was studied using short-term homing experiments in cobra venom factor (CoF)-treated animals. The localization ratio of B and T cells in the spleen of CoF-treated mice decreased significantly compared to control recipients. No changes could be found in the relative distribution of resident T and B cells in the spleen or other lymphoid organs of CoF-treated animals and when their spleen or lymph node cells were transferred, the localization pattern was normal. When cells were incubated in serum prior to transfer a disturbed localization ratio in the spleen of untreated recipients was observed. This was due to a blockade of complement receptors as determined by the inability of the incubated cells to form EAC rosettes. No blockade of EAC rosettes and no changes in localization ratios upon transfer could be observed when the cells were incubated in functionally C3-depleted serum. The results suggest a role for the complement-receptor on B cells in the initial localization in the spleen, whereas no influence upon the selective localization in high endothelial venules-bearing organs was found.

Animals↗
PubMed1986

A comparison of baseline and cyclophosphamide-induced sister chromatid exchanges in bone marrow and spleen cells of mouse and Chinese hamster.

Baseline sister chromatid exchange (SCE) frequencies were investigated in bone marrow and spleen cells of mice and Chinese hamsters. No significant difference in SCE frequency was noted for bone marrow in both species and for bone marrow and spleen in mice on per cell and per pg DNA basis. However, a significant difference was noted between species in spleen and between cell types in Chinese hamsters. Also, statistically significant differences were noted between species for both cell types when the same data were expressed on per chromosome basis. SCE levels in cultured bone marrow and spleen cells after intraperitoneal administration of the antineoplastic drug cyclophosphamide (10 and 20 mg/kg) differed significantly in mice and Chinese hamsters on per cell, per pg DNA content, and per chromosome basis. The spleen cells were much more sensitive to the effects of cyclophosphamide than bone marrow cells in both species. The replicative indices did not differ significantly between treated and control animals in either bone marrow or spleen cells of both species. Since SCE frequency is a sensitive measure of DNA damage, and bone marrow and lymphocytes are the most widely used cell types in human and animal in vivo assays, the methodologies and results reported here may be useful for comparative mammalian cytogenetic studies.

Animals↗
PubMed1977

Effect of BNU treatment on leukaemogenesis in lethally irradiated AKR mice restored with bone-marrow and spleen cells.

The leukaemogenic effect of N-butyl-N-nitrosourea (BNU) was studied in normal and thymectomized AKR mice which were lethally irradiated and restored with either bone-marrow (BM) or spleen cells from (AKR X AKR/T1ALD)F1 donors. In some instances T1ALD thymic cells were added to the restorative inoculum. It was possible to determine the origin of the leukemic cells by the metacentric marker chromosomes of T1ALD. The T- or B-cell characteristics were further ascertained by the cytotoxicity test for theta antigen and the EAC rosette test. All leukaemias whether thymic (TLS) or extra-thymic (ETL), developed from donor bone-marrow or spleen cells and never from the injected thymic cells. In non-thymectomized animals BNU increased the percentage of TLS and shortened their latency. Most of TLS which occurred after BNU treatment of BM-restored mice were theta-negative whereas the majority of TLS which occurred in controls and in spleen-restored animals were theta-positive. This suggests that during their maturation process BM-derived T precursors transit through a theta-negative compartment. This compartment does not reach a similar size during the maturation process of the spleen-derived precursors. Adding thymic cells to the restorative inoculum enhanced leukaemogenesis and suppressed theta-negative TLS in BM-restored mice. Thymectomized mice, restored either by BM or spleen, had a low incidence of ETL which was not significantly increased by BNU treatment except in the case of mice restored with spleen cells. The leukaemic cells of one ETL were theta-positive whereas all the other leukaemias had no detectable T or B marker. The percentage of ETL was higher in thymectomized mice treated with BNU alone than in those previously subjected to irradiation and restoration. These results strongly suggest that a theta-negative T precursor could be involved in extra-thymic leukaemogenesis but the possible involvement of a B precursor cannot be rule out unless experiments are carried out with specific markers of T- and B-cell sub-classes.

Animals↗
PubMed1989

In vitro proliferative responses of spleen lymphocytes from rats bearing progressive or regressive tumors induced by cell variants of a syngeneic colon carcinoma.

From one colonic carcinoma chemically induced in the rat, 2 sublines of tumor cells have been cloned, one (PROb) inducing progressive tumors, the other (REGb) generating tumors that regress a few weeks after s.c. injection into syngeneic hosts. Our study was aimed at comparing cellular immunity between animals bearing PROb or REGb tumors. Spleen cells were first tested for in vitro proliferation in response to mitomycin-treated PROb or REGb cells. Only spleen cells from rats injected with REGb cells proliferated significantly when mixed with PROb or REGb cells. The proliferative response induced by REGb cells was considerably higher than the response to PROb cells. When spleen cells from rats bearing REGb tumors were cultured with a mixture of REGb and PROb cells at various PROb/REGb cell ratios, PROb cells significantly suppressed the strong proliferative response generated by the same number of REGb cells alone. REGb-immune spleen cells, after in vitro stimulation by PROb or REGb cells, were not cytotoxic for either cell variant. REGb-immune spleen cells did not differ in their content of T lymphocytes expressing CD4 or CD8 markers when they were stimulated by PROb or REGb cells in vitro, but REGb cells induced a larger number of activated lymphocytes expressing the IL-2 receptor. Our results indicate that, compared to REGb cells, PROb cells are poorer stimulators of proliferation of tumor-immune spleen cells, and that they are able to suppress the proliferative response induced by REGb cells.

Adenocarcinoma↗
PubMed1989

The accelerating role of Abelson murine leukemia virus in murine plasmacytoma development: in vitro infection of spleen cells generates donor-type tumors after transfer to pristane-treated BALB/c mice.

The role of Abelson murine leukemia virus (A-MuLV) in the accelerated development of murine plasmacytomas (PCs) (Potter et al., 1973: Science, 132, 592-594) was studied in a new experimental system. Spleen cells from pristane-treated or untreated BALB/c mice carrying Robertsonian 6;15 fusion chromosomes were infected in vitro with helper-free A-MuLV overnight and subsequently transplanted into the peritoneal cavity of pristane-treated or untreated BALB/c mice. Donor-derived PCs developed in 4 out of 76 pristane-treated recipients [latent periods: 38-82 (mean 51) days] that had received spleen cells from pristane-treated donors, and also in 2 out of 41 pristane-treated recipients that had received untreated donor-derived spleen cells (latent periods: 65 and 120 days). Three of the PCs in the former and both PCs in the latter group were tested for integration and expression of the v-abl gene, with positive results. This indicates that the spleen contains PC-precursor cells that can be activated by A-MuLV even before the impact of pristane. All 6 donor-origin PCs carried a translocation involving chromosome 15, band D2/3. Four of these corresponded to a typical 12;15 translocation, one was a variant 6;15 translocation and the 6th may represent a previously unidentified translocation between chromosome 15 and the lambda gene-carrying chromosome 16. No PCs developed among 29 pristane-untreated recipients that had received pristane-treated donor-derived spleen cells. In addition to PCs, monocytic tumors developed in 37 (26%) of all recipients. Their development was independent of pristane treatment of recipients but was particularly frequent in those who had received spleen cells from pristane-treated donors.

Abelson murine leukemia virus↗
PubMed1992

Some approaches to improve the therapeutic effectiveness of adoptive chemoimmunotherapy with spleen cells from melphalan-treated BALB/c mice bearing a large MOPC-315 tumor.

Spleen cells from BALB/c mice that are in the process of eradicating a large MOPC-315 tumor following low-dose L-PAM therapy (L-PAM TuB spleen cells) were previously shown to be capable of bringing about the complete regression of a large (15 to 20 mm) s.c. MOPC-315 tumor in a substantial percentage of T-cell-deficient (athymic nude) mice that had been treated with low-dose L-PAM (adoptive chemo-immunotherapy; ACIT). Here we show that aggressive depletion of CD4+T-cells by treatment both of spleen-cell donors and of recipients with anti-L3T4 monoclonal antibody (MAb) greatly improved the therapeutic effectiveness of L-PAM TuB spleen cells in ACIT. In the light of the apparent importance of cytotoxic T-lymphocytes (CTLs) for tumor eradication in low-dose L-PAM-treated MOPC-315-tumor bearers, it is interesting that treatment of L-PAM TuB spleen-cell donors with anti-L3T4 MAb was found to result in the generation of enhanced splenic anti-MOPC-315 cytotoxicity. Although most athymic nude mice in which the tumor had apparently completely regressed following ACIT remained tumor-free, approximately 1/3 of the mice relapsed. However, a substantial percentage of the relapsing mice were rescued by a low dose of L-PAM, which was not effective in causing tumor regression in athymic nude mice bearing a comparably large tumor if the mice had not been subjected previously to ACIT. Almost all athymic nude mice that had been "cured" of a large MOPC-315 tumor by ACIT but did not resist a subsequent MOPC-315 tumor challenge were rescued by low dose L-PAM. Thus, the therapeutic effectiveness of L-PAM TuB spleen cells in ACIT may be improved by aggressive depletion of CD4+ T-cells, suggesting that a low dose of L-PAM, which leads to the acquisition of potent splenic-tumor-eradicating immunity in BALB/c mice bearing a large MOPC-315 tumor, does not eliminate completely (or possibly not at all) the inhibitory activity of CD4+ T-cells. In addition, athymic nude mice that are not endowed with fully protective tumor-eradicating immunity following ACIT still have a substantial residual anti-tumor immune potential that can be exploited to bring about eradication of a large tumor burden following low-dose L-PAM therapy.

Animals↗
PubMed1993

In vivo and in vitro reactivity of rat spleen cells against regressor and progressor colon-cancer cell variants.

Previous reports demonstrated that progressor and regressor tumor-cell variants isolated from the same colon carcinoma chemically induced in a BD-IX rat differed in their capacity to induce an immune response. The present study was aimed at analyzing the characteristics of the responses to the regressor REGb and progressor PROb clones. Spleen cells from rats bearing early REGb tumors neutralized PROb cell tumorigenicity in a Winn-type local transfer assay, but responded occasionally to REGb and PROb cells in vitro. However, spleen cells from rats immunized by several injections of REGb and PROb cells strongly proliferated when cultured with PROb or REGb cells. This response was selective for the cell lines generated from the individual tumor at the origin of PROb and REGb lines, was dependent on CD4+ spleen cells, and was partially inhibited by an antibody against major histocompatibility complex class-II molecules. Although PROb cells shared tumor-rejection antigen(s) with REGb cells, splenocytes from PROb tumor-bearing rats did not neutralize PROb-cell tumorigenicity in vivo, nor did they proliferate when cultured with PROb or REGb cells in vitro. The unresponsiveness of spleen cells from PROb tumor-bearing rats was not due to the presence of immune suppressive cells, and a defect of antigen-presenting cells was shown to be unlikely. This unresponsiveness was limited to a lymphocyte subpopulation, since spleen cells from tumor-bearing rats responded normally to stimulation by PHA or allogeneic lymphocytes. These results strongly suggest that unresponsiveness of spleen cells from tumor-bearing rats is due to a tumor-specific anergy of the lymphocyte clones able to respond to tumor-associated antigens.

Adenocarcinoma↗
PubMed1989

Relationships between spleen and respiration in the newt.

Specimens of newt, Triturus cristatus carnifex (Laurenti), anesthetized by submersion in 0.2% chlorbutol in tap water for 15 min, and then placed out of water in a damp terrarium, show hypertrophy of the spleen that in 2 hr gradually increases from 0.31 +/- 0.12%with respect to body weight to 1.56 +/- 0.26% (means and standard deviation calculated for groups of six animals). Other anesthetics either do not produce hypnosis (Veronal), do not have a prolonged enough effect (ethyl ether, chloroform), or induce vasodilatation, which prevents hypertrophy (MS-222, urethane). The spleen hypertrophy, seen histologically to be due exclusively to blood congestion, is not caused by either a pharmacological effect of the chlorbutol or by the hypnotic state, as it does not appear in submerged anesthetized animals, unless the water is constantly stirred by a magnetic agitator, and can be reversed depending on the ventilation of the animal's skin. The spleen hoards blood when oxygenation is good (in air or stirred water) and releases this supply in the bloodstream when oxygenation is insufficient (in still water). The hypoxic "diffusion boundary layer," which, in still water, forms around the immobile newts, hampers respiratory exchange and stimulates the spleen contraction. This mechanism and its relationship to oxygenation has been demonstrated statistically in unanesthetized newts as well, in both air and water, despite the interference of two contrasting factors--lung respiration and spontaneous motor activity--absent in anesthesized animals. Congestion and decongestion of the spleen are the physiological mechanisms compensating for variations in the level of oxygenation, an alternative to the "capillary recruitment" described by Poczopko and Burggren and Moalli in may amphibians that appears to be absent in newts. The newt spleen, known to play a lesser role in erythropoiesis and destruction of aged erythrocytes than that traditionally assigned to it is thus of primary importance in respiration.

Anesthesia↗
PubMed1983

The intermediate circulation in the nonsinusal spleen of the cat, studied by scanning electron microscopy of microcorrosion casts.

Scanning electron microscopy of microcorrosion casts was used to visualize circulatory pathways of the intermediate circulation in nonsinusal spleen of cat. The marginal sinus (MS) around lymphatic nodules is a distinct vascular space which fills preferentially before the filling of the marginal zone (MZ) and surrounding red pulp occurs. The MS, which has a plentiful vascular supply, does not usually enclose the nodule completely. From the MS, flow occurs radially outwards into the MZ. Corrosion casts and histological sections both showed that a diversity of forms of the MZ exists: The thickness of MZ and the arrangement of its reticulum vary among nodules and between different areas of the same nodule, from a complete absence to a region of up to 50 microns in width. No direct arteriovenous connections were found (in contrast to dog spleen: Schmidt et al., '83b). Aside from capillary endings in the MS and MZ, all arterial capillaries terminate in the reticular spaces of the red pulp, i.e., the circulation appears to be entirely "open." From each capillary termination a great variety of flow pathways through the reticular meshwork to the pulp venules is available; some of these routes are quite long but others may involve distances as short as 15-25 microns. Evidence of flow into ellipsoid sheaths was abundant in casts from dilated spleens, but scarce in contracted spleens. In contrast to the extensive system of interconnected venous sinuses in dog spleen, the pulp venules found in cat spleen are nonanastomosing, shorter, and much smaller in caliber, and all receive flow freely from the reticular meshwork via open ends and fenestrations in their walls.

Animals↗
PubMed1983

Reactivity of subpopulations of mouse spleen cells to concanavalin A in vitro.

Subpopulations of spleen cells of mice bearing virus-induced mammary tumors were assessed for responsiveness to Concanavalin A (Con A) under in vitro xenogeneic and syngeneic culture conditions. When cultured with human A+ plasma (xenogeneic), spleen cells of normal, nontumor-bearing BALB/c mice exhibited a high degree of synthesis as compared to unstimulated cells in response to Con A. Spleen cells of mice inoculated with tumor exhibited response exceeding that of their normal counterparts by 59%. When normal BALB/c sera (syngeneic) was used as the supplement, no response of normal spleen cells was observed upon stimulation by Con A; however, spleen cells from tumour bearing individuals demonstrated heightened activity. Tumor-bearer spleen cell response to Con A of mice inoculated with 1 X 10(6) viable cells was biphasic. The peak of the first phase appeared as early as 10 days postinoculation and declined within 3 days after its appearance. The peak of the second phase appeared within 6 days following decline of the first and declined drastically within 3 days after its appearance. Coincidental with the onset of the second phase, the tumor became ulcerated, purulent, and necrotic. Both phases were predominantly T-cell mediated.

Animals↗
PubMed1986

Comparative in vivo and in vitro sister chromatid exchange studies in Chinese hamster bone marrow and spleen cells.

The sister chromatid exchange (SCE) assay in bone marrow and spleen cells of Chinese hamsters was used to evaluate the differences between in vivo and in vivo/in vitro (exposure of animals to chemical followed by culturing of cells) conditions. Cyclophosphamide, a mutagenic carcinogen, caused dose-related SCEs both in vivo and in vivo/in vitro. In the in vivo group, both bone marrow and spleen cells showed approximately a five-fold increase in SCEs over controls following 40 mg cyclophosphamide/kg treatment. The same dose, under in vivo/in vitro conditions, caused about three- and six-fold increases in SCEs over controls in bone marrow and spleen cells, respectively. While the extent of cyclophosphamide-induced SCEs (after subtraction of baseline level) in bone marrow is approximately the same under both conditions, the response was significantly higher in spleen cells in vivo/in vitro than in vivo. Under in vitro conditions, treatment of bone marrow and spleen primary cell cultures with a direct acting mutagen, trinitrofluorenone, caused significant dose-related increases in SCEs in both cell types in an equivalent manner. The replicative indices under these experimental conditions remained almost the same. Thus, this study indicates the potential usefulness of Chinese hamster bone marrow and spleen cells for in vivo and in vitro comparative studies with the same tissue to better assess the genotoxic hazard of chemicals.

Animals↗
PubMed1996

Effect of melatonin on NF-kappa-B DNA-binding activity in the rat spleen.

It was recently demonstrated that the pineal neurohormone melatonin is a hydroxyl radical scavenger and antioxidant, and that it plays an important role in the immune system. In studies reported herein, we have investigated the relationship of the melatonin level and the NF-kB DNA binding activity in the spleen of Sprague. Dawley rats. These in vivo results indicate that NF-kB DNA binding activity in the spleen is lower at night, when endogenous melatonin levels are elevated, than during the day, when endogenous melatonin levels are lower. Furthermore, exogenously administered melatonin (10 mg/kg) was shown to cause a significant decrease in NF-kB DNA binding activity in the spleen at 60 min after intraperitoneal injection (as compared with vehicle-treated rats). These new findings suggest that the normal night time rise which can be expected for melatonin may be associated with increased NF-kB DNA binding activity in the spleen. The melatonin, therefore, could potentially act to modulate spleen function and/or the immune system by regulating the NF-kB DNA binding activity in the spleen.

Animals↗
PubMed1999

Cytokine gene activation in synovial membrane, regional lymph nodes, and spleen during the course of rat adjuvant arthritis.

Cytokine gene activation was assessed during rat adjuvant arthritis (AA) in synovial membrane (SM), popliteal lymph node (popl-LN), and spleen, using semiquantitative, competitive RT-PCR. Changes in the popl-LN were considerably higher than in spleen or SM. In the preclinical phase (day 6), cytokine mRNA elevations occurred exclusively in the popl-LN and included IFN-gamma, IL-1beta, IL-5, IL-6, and IL-10. In the acute phase (days 13-16) all three organs became involved: (i) in the SM, significant elevations were limited to IL-1beta and IL-6, which, notably, correlated positively with the degree of arthritis; (ii) in the popl-LN, IFN-gamma, IL-1beta, IL-6, and IL-10 (but not IL-5) were still elevated, while IL-2 rose significantly; (iii) in the spleen, TNF-alpha peaked simultaneously with the arthritis score (day 16) and dramatically dropped thereafter. Upon transition into the chronic phase (day 20) the following phenomena were observed: (i) IL-1beta and IL-6 were still significantly increased in the SM; (ii) IFN-gamma, IL-1beta, IL-2, IL-6, and IL-10 were still elevated in the popl-LN; and (iii) there was a progressive rise of IL-5 mRNA in the spleen, positively correlated with the arthritis score. In conclusion, cytokines with pro- and anti-inflammatory functions overlap throughout disease, but in different organ-related patterns. Local (SM) and regional (popl-LN) IL-1beta and IL-6, elevated throughout the entire course of AA, may directly contribute to disease severity. While in AA spleen TNF-alpha appears to be a systemic marker of acute disease, spleen IL-5 may be involved in disease resolution.

Animals↗
PubMed2001

Identification of a CD8alpha(+) dendritic cell subpopulation in rat spleen and evaluation of its OX-62 expression.

Rat spleen DC and bone marrow-derived DC were isolated and characterized by morphology and flow cytometry. We found a CD8alpha(+) DC subpopulation representing 19-48% (27.4 +/- 12.0) of total spleen DC. The OX-62 expression on total spleen DC was 41-59% (51.8 +/- 7.5). Myeloid bone marrow-derived DC were negative for CD8alpha and OX-62. We demonstrated the coexpression of CD8alpha and OX-62 molecules, at least in a portion CD8alpha(+) spleen DC. Both CD8alpha(+) and CD8alpha(-) spleen DC subpopulations separated by MACS were able to induce an in vivo primary immune response to OVA. The immune response induced by the CD8alpha(-) DC subpopulation was higher (P < 0.05). We identified a CD8alpha(+) DC subpopulation in rat spleen less effective in inducing an immune response than CD8alpha(-) DC. Moreover, our results suggest the presence of DC subpopulations with different lineages in DC preparations based on OX-62 expression.

Animals↗
PubMed1993

SART stress effects on lymphocytes in the thymus and spleen of normal, adrenalectomized, and sympathectomized mice.

The effects of stress due to specific alteration of rhythm of temperature (SART) on lymphocyte subpopulations of the thymus and spleen were examined in C3H/He mice. Thymic and splenic involution were evident in SART-stressed mice, and lymphocyte subpopulations were significantly changed. In the thymus, CD4+ CD8+ and CD3- or CD3low lymphocytes were decreased by SART stress more than other lymphocytes, and CD4- and CD8-single-positive lymphocytes and B lymphocytes in the spleen were decreased equally. Immunoregulation via the adrenal glands and sympathetic nervous system was studied in chemically sympathectomized and adrenalectomized SART-stressed mice. Neither chemical sympathectomy nor adrenalectomy alone influenced the thymus or spleen in nonstressed mice, but chemical sympathectomy enhanced SART stress-induced thymic changes and further decreased the number of B lymphocytes in the spleen of SART-stressed mice; adrenalectomy blocked SART stress-induced thymic changes and increased the number of B lymphocytes in the spleen. These findings indicate that the genesis of thymic changes induced by SART stress is in the adrenal glands, and malfunction of sympathetic nerves and insufficient excretion of adrenal hormones could alter the balance of lymphocytes in the spleen during stress. It was also clear that thymic changes induced by SART stress could be immediately reversed to pretest conditions by alleviating the stress.

Adrenal Glands↗
PubMed2000

Mechanisms of suppression of experimental autoimmune encephalomyelitis by intravenous administration of myelin basic protein: role of regulatory spleen cells.

Experimental allergic encephalomyelitis (EAE) can be downregulated by intravenous (iv) administration of myelin basic protein (MBP). In this report we show that downregulation of EAE by two 500-microgram doses of MBP administered iv before immunization was associated with reduced encephalitogenicity of both spleen and lymph node cells (day 12 postimmunization) in adoptive transfer studies. However, efficient downregulation of EAE by two 500-microgram iv doses of MBP on days 10 and 11 after active immunization (at the time of disease onset) was associated with no significant change in the encephalitogenicity of lymph node cells, but a complete abrogation of the ability of spleen cells (both at day 12 postimmunization) to transfer EAE compared to controls. Furthermore, coculture of spleen cells from rats tolerized by iv MBP on days 10 and 11 after active immunization with MBP with MBP-reactive T cells resulted in a decreased ability of the spleen T cells to transfer EAE compared to effector cells in monoculture. In contrast, coculture of MBP-reactive T cells with spleen cells from rats tolerized by iv MBP on days 14 and 7 before active immunization resulted in increased disease in recipient rats. These results suggest that reversal of clinical EAE by iv injection of MBP at the time of disease onset is due at least in part to a T cell control mechanism located in the spleen and suggest the presence of splenocyte regulatory cells that can suppress the ability of encephalitogenic T cells to induce EAE.

Adoptive Transfer↗
PubMed2002

Efficient gene transfer into spleen cells of newborn mice by a replication-competent retroviral vector.

A murine leukemia virus-derived replication-competent retroviral vector with a translational cassette for the enhanced green fluorescence protein (EGFP) was previously found to function efficiently in cell culture (Jespersen et al., 1999, Gene 239, 227-235). We here report that infection of newborn NIH Swiss mice gives rise to EGFP expression in a majority of spleen cells within the first days after infection. Among the nonadherent spleen cells, B, T, and NK lymphocytes were found to be efficiently marked by EGFP by flow cytometry analysis, whereas the adherent spleen cells were negative in most animals. Analysis at time points up to 60 days after infection reveals a decline in EGFP-positive spleen cells over time. Viremia analysis and PCR analysis of spleen DNA indicate that viruses that have lost the translation cassette predominate at later stages. The results provide a model for efficient gene delivery to spleen cells in a time window of 1 to 2 weeks after infection of newborns. Although this type of vector will not in itself be applicable in the clinic, we envision that efficient in vivo gene delivery will be valuable by analysis of differentiation and proliferation of hematopoietic cells in animal models and by development and evaluation of effectors interfering with these processes.

Animals↗