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

The syngeneic mixed lymphocyte reaction (SMLR) is the proliferative response of T lymphocytes cultured with syngeneic non-T lymphocytes. The ontogenic development of the SMLR has been studied in BALB/c mice. The SMLR is not demonstrable in BALB/c mice less than 3 weeks old. The SMLR attains an adult level of activity at 4 weeks of age. Splenic T cells from mice less than 3 weeks old do not respond and splenic non-T cells do not stimulate an SMLR. T-cell preparations acquire the capacity to respond in the SMLR between 2 and 3 weeks of age and non-T cells acquire the capacity to stimulate in SMLR between 3 and 4 weeks old. Spleen cells from 1 week old mice suppress the adult SMLR. Suppressor activity was eliminated by depleting either Thy-1.2 positive cells or adherent cells. When suppressor activity was eliminated, spleen cells from 1 week old donors were capable of stimulating syngeneic T cells. Spleen cells from 1 week old nude BALB/c mice do not suppress the SMLR and stimulate syngeneic T cells normally. These results suggest that the impaired SMLR in very young mice is, at least in part, due to cell-mediated suppression of the SMLR.
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PMID:Studies on the syngeneic mixed lymphocyte reaction. I. The ontogeny of the syngeneic mixed lymphocyte reaction in mice. 621 53

We studied the surface markers of suppressor cells of the mixed leukocyte reaction (MLR) that are transiently present in the spleens of neonatal mice after birth and of adult mice after total lymphoid irradiation (TLI). Approximately 80% of the mononuclear cells in the spleen, within the first few days after birth or after TLI, express neither the Thy-1 antigen nor surface immunoglobulin (Ig). After 30 days, less than 20% of mononuclear cells bear this null phenotype. With the use of the panning technique, we showed that the suppressors of the MLR are confined to the null cell population. The null suppressor cells are not macrophages because they did not carry macrophage markers identified by the monoclonal antibodies anti-MAC-1 and F4/80. In addition, the suppressor cells did not stain for nonspecific esterase and did not adhere firmly to plastic or glass. Spleen cells from TLI-treated mice maintained their suppressive capacity after culture in vitro for 6 to 8 wk. The cultured suppressor cells did not develop mature T cell, B cell, or macrophage markers during this time interval. Thus, the suppressor cells did not appear to be precursors of the latter cells. There was no clear relationship between the suppressor activity of the spleens and natural killer (NK) activity; the kinetics of these activities in newborn spleen appear to be inversely related. The suppressor cells, however, are similar to NK cells in that both are found in the absence of antigenic challenge, lack antigen specificity, and bear the null surface phenotype. Thus, we have termed the former cells natural suppressor (NS) cells.
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PMID:Natural suppressor (NS) cells found in the spleen of neonatal mice and adult mice given total lymphoid irradiation (TLI) express the null surface phenotype. 622 75

Disseminated infection with Histoplasma capsulatum stimulates the production of a suppressor factor (SF-H) by spleen cells from C3H/HeJ mice and a helper factor (HF-H) by spleen cells from C57BL/6 mice. In the present study these disparate immunoregulatory factors were analyzed in detail with regard to: a) the surface phenotype of the cells that produce SF-H and HF-H; b) the role of accessory cells in the production of these factors; and c) the surface phenotype of the target cells activated by SF-H and HF-H. Treatment of spleen cells from Histoplasma-infected C3H/HeJ mice with anti-Thy-1.2 plus complement (C) or with anti-Ly-2 plus C or with anti-I-Jk antiserum plus C abolished production of SF-H. Conversely, generation of HF-H by spleen cells from C57BL/6 mice was abrogated by treatment with either anti-Thy-1.2 plus C or with anti-Ly-1 plus C. Thus, a Thy-1.2+, Ly-2+, I-J+ T cell releases SF-H, and a Thy-1.2+, Ly-1+ T cell secretes HF-H. Production of SF-H and HF-H by splenic T cells was reduced markedly by depletion of macrophages (M phi); readdition of 1% syngeneic, plastic-adherent splenocytes from normal or infected mice to M phi-depleted, splenic T cell cultures of either strain restored the capacity to generate immunoregulatory factors. Furthermore, adherent splenocytes from normal or infected mice liberated a factor or factors that enhanced production of both SF-H and HF-H. Kinetic studies demonstrated that activation of normal spleen cells required at least 48 hr of exposure to SF-H or HF-H. Both factors failed to activate splenocytes pretreated with anti-Thy-1.2 plus C. Spleen cells from C3H/HeJ mice depleted of Ly-1+, Ly-2+, or I-J+ cells and exposed to SF-H did not demonstrate suppressor activity, whereas Ly-1-depleted splenocytes from C57BL/6 mice exposed to HF-H failed to exert helper activity. Therefore, the target of SF-H is a Thy-1.2+, Ly-1+2+, I-J+ T cell, and the target of HF-H is a Thy-1.2+, Ly-1+ T cell.
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PMID:Cellular origins and target cells of immunoregulatory factors in mice with disseminated histoplasmosis. 623 Mar 99

Spleen organ cultures were prepared from lethally irradiated mice that had been injected with allogeneic bone marrow, with or without lymph node cells. These cultures were used in the analysis of graft-versus-host reactions (GVHR) in vitro. It was found that donor-derived T lymphocytes, which had been grown in an allogeneic spleen, prevented hemopoietic progenitor cells (colony-forming cells, CFC) of the recipient from differentiating in agar cultures. Furthermore, these lymphocytes were found to inhibit growth and differentiation of CFCs of the same donor. This graft-antigraft reactivity was not abolished by monoclonal anti-Thy-1 plus complement (C'), in contrast to the conventional GVHR. This indicates that the graft-versus-graft reaction depends on "de novo" generation of mature T lymphocyte effector cells from transplanted graft precursors.
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PMID:T lymphocyte-mediated graft--antigraft reactivity during graft-versus-host reaction in vitro. 623 Oct 67

YAC, a Moloney-virus-induced tumor of A-strain mice, is a nonimmunogenic tumor. Mice injected with the inactivated neoplastic cells and challenged with viable tumor cells did not survive longer than mice that received the challenge dose alone. The homogenate of this nonimmunogenic tumor was subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). After electrophoresis, the gel slices containing isolated molecular entities were injected into various groups of mice. The mice were challenged with low doses of viable tumor cells (10-30 cells) and their survival time was recorded. Small but significant numbers of mice injected with apparent 80-90 K SDS-PAGE-isolated molecular entity rejected the tumor or survived longer than the control groups of mice. Spleen cells from mice injected with 80-90 K molecular entity inhibited the YAC tumor cotransferred with them to naive recipients (Winn assay). Spleen cells from mice injected with monoclonal antibody against nonspecific T-cell helper factor and immunized with 80-90 K SDS-PAGE-isolated molecular entity failed to inhibit the tumor growth in naive recipients, indicating that helper T cells are involved in induction of the antitumor resistance. Nylon-wool-passed splenocytes from mice injected with 80-90 K inhibited tumor growth in some of the recipient mice. Spleen cells from these mice treated with anti-Thy-1 and complement also inhibited the tumor growth in some of the recipients, suggesting that the effector cells were both T and non-T cells. C57BL/6 mice immunized with apparent 20 K SDS-PAGE-isolated molecular entity of RBL5 tumor also induced in vivo resistance to the syngeneic viable RBL5 cells, but not to the syngeneic B16 melanoma cells, indicating the specificity of the protective effect. The practical and theoretical implications of these findings are discussed.
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PMID:The isolation of immunogenic molecular entities from immunogenic and nonimmunogenic tumor homogenates by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). 623 88

Resistance of SJL/J mice to intracranial inoculation with the JHM strain of mouse hepatitis, a coronavirus, is dependent upon the age of the animals at inoculation. Animals 12 weeks of age or older are resistant, whereas those 6 weeks or younger are uniformly susceptible to viral infection. Spleen cells or thioglycolate elicited peritoneal exudate cells can transfer resistance from 12-week-old to 6-week-old recipients. Removal of the adherent cells from either spleen or peritoneal cells ablated protection. Adherent cells from 12-week-old mice were protective even after depletion of Ia- and Thy-1-bearing cells. Antiviral antibody, thioglycolate injection into 6-week-old animals, and nylon wool-purified T cells were ineffective in mediating resistance. Adherent cells transferred 4 days before virus challenge, but not after challenge, were protective. Thus, there is an age-related change in SJL mice that protects from acute central nervous system disease, which may be due to maturation of a specialized adherent cell population.
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PMID:Resistance to fatal central nervous system disease by mouse hepatitis virus, strain JHM. II. Adherent cell-mediated protection. 624 28

The role of adherent phagocytic cells in an in vitro secondary cytotoxic response against Simian virus 40 (SV 40)-induced tumor-associated antigens was investigated. Spleen cells (responder cells), from mice primed with syngeneic SV 40-transformed cells, extensively depleted of macrophages by filtration through a Sephadex G-10 column followed by iron carbonyl treatment, had a markedly decreased capacity to generate in vitro secondary cytotoxic reactivity against syngeneic SV 40-transformed cells when cultured with the relevant stimulator cells. The secondary response was restored by the addition of adherent peritoneal cells from normal mice syngeneic to those immunized with the antigen. Within a certain dose range, small numbers of peritoneal cells completely reconstituted the response, whereas large numbers inhibited the reactivity. The restored cultures maintained specific cytotoxic reactivity against SV 40-induced tumor-associated antigens which was mediated by effector T cells as shown by sensitivity to anti-Thy-1.2 antiserum and complement. These results suggested a requirement for adherent phagocytic cells (accessory cells) in in vitro generation of a secondary, cytotoxic response to tumor-associated antigens.
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PMID:Macrophage requirement for in vitro generation of specific, secondary cell-mediated cytotoxicity against SV 40-induced tumor-associated antigens in mice. 625 Aug 54

Mouse spleen cells, either pretreated in vitro with 100 U/ml of OK-432-induced IFN gamma for 18 h or obtained from mice 24 or 48 h after i.v. injection of OK-432(100 micrograms/mouse), were examined for their anti-tumor effect by Winn's neutralization assay against Meth-A tumor cells in BALB/c mice. Spleen cells treated in vitro or obtained in vivo 24 h after i.v. injection clearly neutralized the growth of admixed Meth-A cells. Two booster injections of 200 U of IFN gamma near the tumor site accelerated this neutralizating effect. In order to determine the effector subpopulation, inhibitory spleen cells were treated with either anti-Thy-1 monoclonal antibody plus complement, anti-asialo GM1 serum plus complement or with adherence on plastic plates followed by Sephadex G-10 column treatment. The effector cell activity in Winn assay was lost only after the removal of macrophages through plastic plate adherence and Sephadex G-10 column treatment, but not after anti-Thy-1 or anti-asialo GM1 treatment, with either in vitro- or in vivo-treated spleen-cell populations. The growth of Meth-A cells was inhibited not only by these activated macrophages in Winn's assay, but also by adoptive transfer of OK-432-induced cytotoxic macrophages intralesionally 4 days after the implantation of 1 X 10(6) Meth-A cells. Our evidence suggests that the systemic action of OK-432 can be explained by the effect of induced IFNgamma, through the activation of macrophages.
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PMID:Activated macrophages are responsible for the tumor-inhibitory effect in mice receiving intravenous injection of OK-432. 642 Mar 51

Total lymphoid irradiation (TLI) was administered to mice as 17 fractions of 200 rads delivered to the major lymphoid organs. Spleen cells capable of suppressing the in vitro mixed leukocyte response (MLR) and in vivo graft-vs-host disease (GVHD) were found in mice after treatment with TLI. Suppression was not antigen specific and was markedly reduced by treatment of the spleen cells with anti-Thy-1.2 antiserum and complement. Suppressor activity declined with time after irradiation and disappeared within 30 to 40 days. The evidence suggests that the suppressor cells may prevent initial BM rejection and acute GVHD in allogeneic BM transplant recipients prepared with TLI.
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PMID:Suppression of the mixed leukocyte response and of graft-vs-host disease by spleen cells following total lymphoid irradiation (TLI). 645 Aug 2

Normal mice infected intravenously with 10(6) or 10(8) viable M. avium develop persistent infections of the lungs, liver and spleen. The liver and spleen counts remained relatively constant whereas those for the lung slowly increased until eventually some of the animals began to die as a result of the infection. None of the heavily infected mice developed delayed hypersensitivity (DTH) to the M. avium cytoplasmic protein antigen (CPA). Spleen cells harvested at increasing time periods after the M. avium infection were tested for their blastogenic responsiveness to PHA and M. avium CPA. The presence of suppressor T cells within the heavily infected spleens was demonstrated by means of cell-mixing experiments before and after treatment of the anergic spleen cells with anti-Thy-1.2 antiserum and complement. The specificity of the suppressor T cells was measured in terms of their ability to depress responsiveness to sheep erythrocytes and an allograft challenge. Initially, the suppressor T cell population affected all of the T cell-mediated responses but as the infection progressed, so the non-specific host responses tended to return gradually towards normal, whereas the specific M. avium CPA-mediated suppression persisted largely unchanged.
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PMID:The specificity of suppressor T cells induced by chronic Mycobacterium avium infection in mice. 645 15


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