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

Spleen cells from ageing (24--30-month-old) mice, manifesting low response to concanavalin A (Con A) and phytohemagglutinin (PHA), were separated by peanut agglutinin (PNA) into agglutinable (PNA+) and unagglutinable (PNA-) fractions. The PNA+ cells were found to suppress the response of young (2--3-month-old) mouse spleen cells to the mitogens Con A and PHA. On the other hand, PNA- cells of the ageing mice expressed a response to these mitogens, at levels higher than those of the unseparated cells. Re-mixing of the PNA- and PNA+ cells of the ageing mouse spleens at various proportions indicated that the PNA- cells are indeed suppressible by the PNA+ cells. Anti Thy-1.2 treatment to the PNA+ fraction suggested that this suppression was not exerted by T cells. It thus appears that at least part of the reduced lymphoid cell function in ageing is related to an effect of suppressor cells, interfering with the expression of available reactive cells.
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PMID:Immune reactivity during ageing. III. Removal of peanut-agglutinin binding cells from ageing mouse spleen cells leads to increased reactivity to mitogens. 645 86

Spleen cells from mice bearing large methylcholanthrene (MCA)-induced sarcomas were injected intravenously into mice challenged in the hind footpads with heavily-irradiated cells from the same or a different sarcoma. As measured by [3H]-thymidine incorporation on day 5 or 6, cellular proliferation in the draining popliteal lymph nodes of these mice was significantly depressed as compared to control animals receiving normal spleen cells or medium intravenously. The suppression was found to be mediated by a Qa-1-positive, Thy-1 positive cell. It was relatively resistant to cyclophosphamide treatment (100 mg/kg). Furthermore, it had both antigen-specific and non-specific components. The findings are discussed in relation to a suppressor activator cell-suppressor acceptor cell pathway in the immunoregulation of tumor immunity.
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PMID:Suppressor pathways in tumor immunity: a requirement for Qa-1 positive tumor-bearer spleen T cells in suppression of the afferent immune response to tumor antigens. 645 94

Spleen effector cells for IgG- and IgM-induced antibody-dependent cellular cytotoxicity (ADCC) were characterized with respect to density and cell surface markers by using sheep erythrocytes (SRBC) coated with hybridoma-derived monoclonal anti-SRBC IgG or anti-SRBC IgM antibodies as targets. While basically the same effector cells are cytolytic for IgG and IgM antibody-coated SRBC, they differ with respect to their relative killing capacity for IgG- versus IgM-coated target cells. On the basis of physical and biochemical properties three populations with cytolytic capacity could be separated: (I) A light fraction of large cells had high cytolytic potential for both IgG- and IgM-coated SRBC. The cells were negative for the Fc receptor for IgG (Fc gamma-R-) and the C3-receptor (C3-R-), they carried the receptor for Helix pomatia A agglutinin (HP-A+), and reactivity was strongly reduced after treatment with anti-Thy-1 and complement (C). (II) High activity was also observed with a medium-dense fraction, preferably lysing IgG antibody-coated cells. The cells were Fc gamma-R+, partly C3-R+, mostly HP-A-, and only a minor portion of the cells were Thy-1+. (III) A dense fraction, displaying on a per cell basis low cytolytic potential, was more active in IgM than IgG ADCC. The cells were Fc gamma-R+, HP-A+ and Thy-1+. All three effector cell populations were non-adherent, non-phagocytic, and surface immunoglobulin-negative (s-Ig-).
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PMID:Characterization of effector cells mediating IgG and IgM antibody-dependent cellular cytotoxicity. 660 20

Direct binding of 125I-labeled rabbit anti-NPb idiotype antibodies (RaId) was used to quantitate the expression by immune spleen and thymus cells of NPbId, the characteristic Id of the lambda 1-containing antibodies made by C57BL/6 (B6) mice to the (4-hydroxy-3-nitrophenyl)acetyl (NP) group. Direct binding of RaId by B and T cell preparations reached a maximum of 12 ng RaId per 10(8) cells at 7 days after immunization. Spleen T cell preparations maintained similar levels of binding after positive selection for Thy-1.2+ cells and overnight culture. RaId binding was also demonstrated for immune B6 thymus cells and for spleen and thymus cells of immune SJL mice, which have the appropriate heavy chain allotype for NPbId expression but have only barely detectable serum Id. However, the NPbId of T and B cell preparations were indistinguishable by (a) the susceptibility of RaId binding by the cells to inhibition by hapten or by antibodies to the variable regions of lambda light chains (anti-V lambda) and by (b) the ability of anti-V lambda and of monoclonal antibodies to the constant region of lambda 1 chains (anti-C lambda 1) to immunoprecipitate antigen (NP10-bovine serum albumin)-binding proteins from detergent extracts of isotopically labeled cells. The results strongly imply that virtually all of the NPbId of T cell preparations is due to conventional NPbId antibody that is tightly bound to T cells. The results do not, however, exclude the possibility that the T cell preparations contain a trace amount (less than or equal to 1 ng/10(8) cells) of unusual NPbId-like molecules that lack lambda chains.
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PMID:Quantitative of anti-NP (4-hydroxy-3-nitrophenyl)-acetyl idiotype expression on spleen and thymus cells. 660 7

Treatment of mice with ascitic fluid containing high titres of T24-31.7 monoclonal antibody (rat anti-mouse Thy-1) lead to a rapid loss of T cells from peripheral lymphoid organs. Spleen and lymph node tissue lost all detectable Thy-1+ and mitogen-responsive T cells within 72 hr. These tissues were completely T cell-depleted for more than a week before repopulation with T cells began. Lectin-induced splenic T cell cytoxicity in culture was lost within 72 hr after treatment of mice in vivo. In contrast, treatment of mice with T24-31.7 ascitic fluid was followed by an immediate increase in natural killer (NK) cell-mediated cytolytic activity. After 96 hr, NK activity began to decrease and did not reappear in the T cell-depleted spleens. While purified T24-31.7 antibody was responsible for T cell depletion in vivo, a non-immunoglobulin component of the ascitic fluid stimulated splenic NK cell activity. The presence of phytohaemagglutinin (PHA) on target cells in the lytic assay was shown to inhibit NK activity but enhance T cell-mediated cytotoxicity. The relationship of NK cells and cytotoxic T lymphocytes (CTL) to the T cell lineage is discussed.
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PMID:In vivo modulation of thymus-derived lymphocytes with monoclonal antibodies in mice. II. Separation of natural killer cells and cytotoxic T cells. 660 15

Studies have shown that there is an abnormality in the thymus of dystrophic mice with respect to age-dependent thymus weight changes and altered morphology (T. DeKretser and B. Livett, Nature (London) 263, 682, 1976). Recently, others have shown that natural killer (NK) cells can lyse cells of a large, immature, rapidly dividing cell subpopulation within the thymus of normal young (3 weeks of age) mice (M. Hansson, K. Karre, R. Kiessling, J. Roder, B. Anderson, and P. Hayry, J. Immunol. 123, 765, 1979). The NK susceptibility of dystrophic mouse thymocytes as targets was therefore studied. Spleen cells from normal (+/+) and dystrophic (dy2J/dy2J) male C57BL/6J mice 8-10 weeks old were passed over nylon wool and the nonadherent cells were incubated with 51Cr-labeled YAC-1 lymphoma target cells or thymocytes in a 51Cr-release assay. Spleen cells from dystrophic mice killed twofold more YAC-1 target cells than did spleen cells from normal mice. Thymocytes from 3- to 4-week-old dystrophic mice were three to four times more susceptible to NK lysis by dystrophic mouse spleen cells as compared with normal mouse spleen cells. Spleen cells from dystrophic mice had the same NK activity against dystrophic and normal mouse thymocytes as targets. Normal mouse spleen cells killed three- to fourfold more dystrophic mouse thymocytes than that of normal mouse thymocytes as targets. Target cell-binding studies revealed that conjugate-forming cells from nylon nonadherent dystrophic mouse spleen cells were found to be two- to fourfold greater than for normal mouse spleen cells using YAC-1 tumor cells as targets. The number of lymphocytes bound per YAC-1 target cell ranged from 2 to 5 for dystrophic mouse spleen cells as compared with 1 to 2 for the normal control group. Using both normal and dystrophic mouse thymocytes as targets, the conjugate-forming cells from dystrophic mouse spleen cells were also found to be twofold greater than in the normal control group. Cold target inhibition studies revealed that the natural killing of dystrophic mouse thymocytes was due to a YAC-1-reactive NK cell. Effector cell depletion studies using monoclonal anti-Thy-1.2 plus complement treatment and plastic petri dish adherence also revealed that the natural killing of dystrophic mouse thymocytes was not due to either T lymphocytes or macrophages. Taken together, these results show an increase in NK-sensitive thymocyte targets in dystrophic mice, in combination with an increase in splenic NK activity.
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PMID:Enhanced natural killer (NK) cell activity and NK-sensitive thymic cells in murine muscular dystrophy. 665 89

89Sr-treated mice injected with concanavalin A (Con A) 24 h prior to infection with Listeria monocytogenes (LM) could not enhance the clearance of LM from the spleen. Adoptive transfer of normal syngeneic spleen cells together with Con A rendered these animals more resistant. Spleen cells of 89Sr-treated or age-matched control mice were stimulated with con A for 24 h, and supernatant fluids were assessed for macrophage-activating factor (MAF), i.e. the ability to activate resident peritoneal macrophages to kill LM intracellularly in vitro. A defective MAF production by spleen cells was observed in 89Sr-treated, 2 week-old, and athymic nude mice. Also, treatment of spleen cells with anti-Thy-1.2 antiserum plus complement inhibited MAF production. Synergism between spleen cells from 89Sr-treated and nude mice did not occur. The cells required for MAF production were relatively resistant to gamma irradiation. Nylon wool filtration did not modify the ability of spleen cells to make MAF. 89Sr-treated mice possess macrophages responsive to MAF derived from normal spleen cells. The data suggest that the failure of 89Sr-treated mice to develop an anti-LM response observed in thi system could be due to a defective capacity to produce protective humoral factors and/or cells in response to Con A.
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PMID:Concanavalin A-induced resistance to Listeria monocytogenes and activation of macrophages: defect in mice treated with 89Sr. 679 74

Mice injected with inactivated (UV light-irradiated) influenza virus produce specific antibody, become sensitized for a delayed-type hypersensitivity reaction, but do not generate specific cytotoxic T (Tc) cells. If injected 4-5 days later with infectious virus, the formation of Tc cells is suppressed by > 90%. If A strain viruses are used, the suppression observed is cross-reactive within A strain viruses but does not extend to B/LEE or to Sendai virus. Serum from mice injected with UV-irradiated virus contains antibodies which on adoptive transfer can inhibit Tc cell formation when infectious homologous virus is used to challenge the recipients. Spleen cells from the same mice, upon adoptive transfer, also inhibit (50-70%) Tc cell formation if transferred within 24 h of injection of infectious virus, and the specificity pattern observed is cross-reactive within A strains. The activity of the cells mediating suppression is destroyed by monospecific anti-Thy-1.2 antibody and complement. The immune cells require I region sharing between donor and recipient mice for their suppressor activity to be effective. (There is also a partial requirement for K, D region sharing, but the possible rejection of transferred cells is not excluded.) Dilution assays in which clonal expansion of Tc precursors is used to estimate their frequency and the presence of T helper (Th) cells indicate that suppressed mice possess Tc precursors and primed cells which, upon restimulation, act as Th cells. Furthermore, injection of irradiated Th cells with inactivated virus does not significantly reduce the ensuing suppression.
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PMID:Selective suppression of the cytotoxic T cell response to influenza virus in mice. 697 Jan 26

The expression of T cell-associated surface markers by lymphoid cells from congenitally athymic (nude) mice has been quantitatively investigated using flow microfluorometry. Spleen and lymph nodes from old (greater than 6 mo) nude mice on either a C57BL/6 or BALB/c genetic background were found to contain significant numbers (5 to 13% in spleen and 15 to 24% in lymph nodes) of cells expressing Thy-1 antigen. The proportion of Thy-1 positive cells in nude spleen was dramatically increased (to 22 to 67%) after passage of the cells over nylon wool columns. In contrast to older animals, young (1- to 2-mo-old) nude mice had undetectable levels (less than 1%) of Thy-1 bearing cells in spleen and reduced levels (6%) in lymph nodes. After passage of their spleen cells over nylon wool, some Thy-1 positive cells (10%) were detectable in 2-mo-old nude mice but none were detectable at 1 mo. In addition to Thy-1, we were able to detect the T cell alloantigens Lyt-1 and Lyt-2 on nylon wool-passed spleen cells from older C57BL/6 or BALB/c nu/nu mice. In general, the proportion of Lyt-1 bearing cells in nude lymphoid populations was similar to the proportion of Thy-1 positive cells. A smaller fraction of nude cells (corresponding to 35 to 59% of the total Thy-1 positive cells) were found to express Lyt-2. Analysis of the forward light scatter distributions of nude lymphoid cells bearing either Thy-1, Lyt-1, or Lyt-2 antigens further demonstrated that an overlapping population of relatively large-size cells expressed these surface markers. These data strongly imply that at least 2 subsets of T cells (i.e., Lyt-1+2- and Lyt-1+2+) develop in older nude mice in the apparent absence of thymic influence.
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PMID:Age-associated increase in expression of the T cell surface markers Thy-1, Lyt-1, and Lyt-2 in congenitally athymic (nu/nu) mice: analysis by flow microfluorometry. 697 Feb 23

The mitogenic property of supernatants from M. arthritidis cultures (MAS) is shown to be nonsedimentable, nondialyzable, labile to 56 degrees C for 1 hr, and active against spleen cells from both normal and germfree mice. Both viable M. arthritidis and MAS were active for T lymphocytes because anti-Thy-1 antiserum and C eliminated responsiveness. Spleen cells enriched for T lymphocytes by passage over nylon columns lost responsiveness unless supplemented with a radioresistant adherent cell population that was shown to bear Ia antigens. Evidence is also presented that the genetic control of T lymphocyte responses to the mycoplasma mitogen was exercised at the level of the Ia-bearing adherent cells. Thus adherent cells from positive responder mouse strains, but not those from nonresponder mouse strains, restored the responses of T cells from F1 hybrids between responder and nonresponder strains.
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PMID:Stimulation of mouse lymphocytes by a mitogen derived from Mycoplasma arthritidis. II. Cellular requirements for T cell transformation mediated by a soluble Mycoplasma mitogen. 697 80


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