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

The effect of related and unrelated compounds on the specific binding of dinitrophenyl-coupled bacteriophage (DNP-T4) to lymphoid cell receptors has been examined and compared with the effect on the neutralization of DNP-T4 by anti-DNP serum. Spleen cells and sera from Balb/c mice immunized with DNP-bovine serum albumin were used. The binding of DNP-T4 to the cells was inhibited by DNP-eAcp, di-DNP-Lys, DNP-Tyr, DNP-p(Ornith) and DNP-BSA (among the DNP-derivatives tested), TNP-BSA, ARS-p(Tyr) and TGA. In addition with the above named DNP and TNP compounds, the DNP-T4neutralization by antiserum was also prevented by DNP-derivatives with either L-cysteic acid, alanine, glutamine or poly-L-glutamic acid, while ARS-p(Tyr) and TGA were not effective. Plain carriers (BSA, HSA, poly-ornithine, polylysine and polyglutaminc acid) and cell-mitogens (ConA, LPS and PPD) had no significant inhibitory effect. The results obtained indicate the occurrence of differences between cell-bound receptors and circulating antibodies in what concerning their specific reaction with the dinitrophenyl determinant.
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PMID:Inhibition of specific binding of DNP (dinitrophenyl) determinant to lymphoid-cell receptors by related and unrelated compounds : quantitative studies in vitro. 6 Sep 7

Intraperitoneal treatment of mice with adjuvants affects the in vitro response of their lymphocytes toward class-specific mitogen. Spleen cells from animals injected with Corynebacterium parvum organisms showed in some cases an increase in their response to all mitogens, while in other experiments, a moderate decrease in the reaction to T-specific mitogens (concanavalin A and phytohemagglutinin) was found. Injection of lipopolysaccharide (LPS) and in particular Bordetella pertussis bacteria, brought about a marked reduction in the response of spleen cells to B mitogens (LPS and PPD) but had little or no effect on the reaction to the T mitogens. Intraperitoneal administration of B. pertussis caused a marked depletion of lymph nodes and a high level of lymphocytosis. Blood cells of the treated mice showed an increased response to T mitogens, whereas mesenterial lymph node cultures reacted higher than the controls to LPS and without stimulation. No change was noted in the responses of cells from the axillary lymph nodes of these pertussis-treated mice.
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PMID:Effects of in vivo administered B. pertussis and other adjuvants on the mitotic responses of lymphocytes in vitro. 19 Jan 70

While the virgin AFC-progenitors for an adoptive immune response in neonatal germ-free CBA mouse spleen are small, dense cells, the equivalent cells in the adult are a larger, lighter density population. The effects of injections of unrelated antigens on the physical properties of the AFC-progenitors in neonatal spleen were investigated to test the postulate that the physically distinct "virgin" AFC-progenitors in the adult arose by a process of non-specific activation. Spleen cells from 7-day-old germ-free CBA mice were separated by sedimentation at unit gravity or by density on continuous albumin gradients, and the fractions were tested for NIP-specific AFC-progenitor activity using an adoptive immune assay which gave a direct linear measure of B cell activity. If the donor neonatal animals were injected one day previously with POL or PPD, the NIP-specific AFC-progenitor activity shifted from the typical small, dense lymphocytes to larger, lighter cells. The physical properties of these stimulated AFC-progenitors resembled those of IgM AFC-progenitors in normal adult mice. These results experimentally confirm the theory that environmental stimuli induce a non-specific "activation" of a particular subset of "virgin" B cells.
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PMID:Antigen-initiated B lymphocyte differentiation: non-specific stimulation changes the physical properties of virgin AFC-progenitors in neonatal mouse spleen. 30 16

Spleen cells from autoimmune (10-mont-old) NZB/NZW (B/W) mice failed to generate appreciable numbers of antibody-forming cells (AFC) in vitro to TNP-substituted sheep erythrocytes in response to the polyclonal B cell activators (PBA), LPS and PPD, despite normal DNA synthetic responses to these agents and normal AFC responses to TNP-Ficoll. The failure to respond to PBA in old B/W mice was not due to suppressor T cells since anti-brain-associated-theta-treated spleen cells still failed to generate AFC in response to PBA. The defect was age-related since cells from young B/W mice generated vigorous AFC responses to PBA. It is suggested that the failure of the spleen cells of old B/W mice to generate AFC is a result of in vitro polyclonal B cell activation in the course of autoantibody formation.
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PMID:Abnormal polyclonal B cell activation in NZB/NZW F1 mice. 56 Nov 28

Spontaneous diminution of granuloma formation around schistosome eggs in chronic schistosomiasis mansoni has been demonstrated previously. In the present study these findings were confirmed by injecting schistosome eggs into the pulmonary microvasculature and removing the lungs 8 days later from mice infected for 4, 8, 12, 16, and 20 weeks; the mean area of inflammation around the eggs was then measured. At 4 weeks a primary reaction was seen, by 8 weeks a massive secondary reaction occurred, but by 12 weeks the lesion was considerably reduced in size, and at 20 weeks it was smaller than the primary reaction. Concomitant measurements of humoral hemagglutinins to soluble egg antigens (SEA) revealed no detectable antibodies at 4 and 6 weeks, relatively low levels at 8 weeks, and an exponential increase in hemagglutinins at 12 weeks and beyond. Immunodiffusion analysis revealed no precipitins at 8 weeks, 1 major band and 2 minor bands at 12 and 16 weeks, and 2 major bands and 1 minor band at 20 weeks. Spleen cells from 8-week-infected mice showed peak migration inhibitory factor (MIF) output at a concentration of 1 mug/ml of soluble egg antigens and suppression of lymphokine secretion at higher concentrations. At 12 and 16 weeks, exponentially lower antigen concentrations both stimulated and suppressed peak MIF output; at 20 weeks MIF was not detectable after stimulation over a wide range of antigen concentrations. Delayed footpad swelling to SEA reached its peak at 10 weeks and declined thereafter, but the response to PPD in tuberculin-sensitized schistosome infected mice remained constant over the period of time studied.
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PMID:Spontaneous modulation of granulomatous hypersensitivity in schistosomiasis mansoni. 80 13

Mycobacterium avium infection was substantially more severe in C57BL/6 (Bcgs) than in (C57BL/6 x DBA/2)F1 hybrid (Bcgr) mice both in terms of bacterial growth in the spleens and lungs and in host survival. Prior Mycobacterium bovis BCG vaccination resulted in increased resistance as well as enhanced tuberculin hypersensitivity to both PPD-S (Mycobacterium tuberculosis) and PPD-A (M. avium). Mice heavily infected with M. avium were used as T-cell donors in an adoptive transfer system. Substantial resistance was observed for both recipient hosts regardless of the genotype of the donor strain. Transfer of resistance was ablated by treatment of the immune spleen cells with anti-Thy 1.2 monoclonal antibody and complement or by cyclophosphamide treatment. Spleen cells which were monodepleted of L3T4+ or Lyt-2+ T cells did not lose their ability to transfer resistance against a subsequent challenge. However, when these cells were doubly deleted, all resistance was ablated in both the BCG-susceptible and -resistant mice. The recipient host expressed a detectable adoptive immune response although the donor had been unable to reduce the growth of the primary M. avium infection in vivo.
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PMID:T-cell immune responses in Mycobacterium avium-infected mice. 172 79

Thirty seven patients with sarcoidosis were examined using ultrasound (US) to determine the size of the spleen. A Spleen Index (SI) was employed to evaluate splenomegaly and the SI was calculated using long (a) and short (b) dimensions on the sectional splenotomogram (SI = a x b). In 21 (57%) of these patients the spleen was judged ultrasonographically to be enlarged (SI 30), but in only 3 was it palpable. The clinical records of patients with and without splenomegaly detected by US were compared. There were no differences between patients with or without splenomegaly in hematologic findings (peripheral blood and bone marrow) or blood chemistry; furthermore no patients with hypersplenism were seen. In immunological parameters, the serum immunosuppressive acid protein level was significantly (p less than 0.05) higher in patients with splenomegaly than in those without splenomegaly; however, there were no differences in serum angiotenins converting enzyme activity, serum lysozyme level, PPD skin test or bronchoalveolar lavage fluid analysis. The patients with splenomegaly had significantly higher evidence of increased uptake of 67-Gallium in lung fields and positive lung infiltrates in chest X-ray than those without splenomegaly (p less than 0.01, p less than 0.05). These data suggest that ultrasound is a promising diagnostic tool for the assessment of the size of the spleen and is useful to detect disease activity and extent of disease in sarcoidosis. Patients with sarcoidosis who had splenomegaly had more disseminated disease, especially pulmonary parenchymal disease, than did those without splenomegaly.
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PMID:[Ultrasonographic analysis of splenomegaly in patients with sarcoidosis]. 221 17

In this study, the distribution of immune spleen cells was investigated after adoptive transfer of immunity in inbred strain 2 guinea pigs. Spleen cells obtained from line 10 immune donor animals became specifically restimulated in vitro with 3 M KCl-extracted line 10 soluble proteins, but not with 3 M KCl-extracted line 1 or liver proteins. After 4 days culture in vitro, these specifically restimulated immune spleen cells retained their antitumor activity in vivo after adoptive transfer. The specifically restimulated immune spleen cells were radiolabeled with [3H]thymidine, 1 X 10(8) viable cells were adoptively transferred in tumor-bearing guinea pigs, and their distribution was investigated. As controls for the specific localization of the immune cells at the line 10 tumor, the presence of labeled cells was studied in the contralateral transplanted line 1 hepatoma as well as in cellular inflammatory reactions elicited by injection with incomplete Freund's adjuvant (IFA) and complete Freund's adjuvant (CFA). A significantly higher localization of the labeled immune spleen cells in the line 10 tumor and the first and second draining lymph nodes of the line 10 challenge site were found when compared to the influx of these cells in the line 1 tumor and the nontumor antigen-related inflammatory reactions. Because our immune donor animals were immunized with a mixture of line 10 cells and BCG, these animals are immune to both. Line 10 immune spleen cells were restimulated in vitro with PPD and were radiolabeled. These PPD-restimulated immune spleen cells showed no preferential localization at the line 10 tumor challenge site but, as expected, a tendency for localization at the CFA (H37Ra) injection site. Furthermore, PPD-reactive spleen cells from BCG-immunized guinea pigs showed a significantly higher accumulation at the CFA injection site compared to the IFA injection site and the line 10 and line 1 tumor challenge site. From the results, it is concluded that line 10 tumor-immune and BCG-immune spleen cells are two distinct cell populations, and that the existence of cross-reacting antigens between BCG and the line 10 hepatocarcinoma are of no importance for the rejection of the line 10 tumor by immune spleen cells.
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PMID:Selective localization of tumor-immune spleen cells at the tumor challenge site after adoptive transfer of line 10 tumor immunity in strain 2 guinea pigs. 257 26

T-cell lines were established from the lymph node cells of syngeneic Louvain (LOU) rats previously immunized with native chick type II collagen (CII) emulsified in incomplete Freund's adjuvant. The CII lines proliferated in vitro to type II collagen but not to type I collagen, ovalbumin (OV), or PPD. Control lines, developed from LOU rats immunized with OV emulsified in complete Freund's adjuvant, were OV specific because they did not respond to other antigens in vitro. CII line cells could adoptively transfer delayed-type hypersensitivity (DTH) but did not induce IgG antibody production to collagen. Moreover, the intravenous administration of 2 X 10(7) CII line cells prevented the subsequent induction of collagen arthritis following immunization and suppressed DTH to collagen without affecting antibody responses in the recipients. Spleen cells, but not sera, from these resistant rats decreased CII line reactivity in vitro. OV or irradiated CII lines had no effect on clinical or immunologic parameters in this model. These findings demonstrate protection from arthritis afforded by T-cell line transfer and suggest that the phenomenon results from down-regulation of the recipients' cellular immunity to collagen.
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PMID:Attenuation of collagen arthritis and modulation of delayed-type hypersensitivity by type II collagen reactive T-cell lines. 349 39

The existence of T cells specific for soluble antigens in association with unique F(1) or recombinant major histocompatibility complex (MHC) gene products was first postulated from studies on the proliferative response of whole T cell populations to the antigen poly(Glu(55)Lys(36)Phe(9))(n) (GLphi). In this paper we use the newly developed technology of T lymphocyte cloning to establish unequivocally the existence of such cells specific for GLphi and to generalize their existence by showing that F(1)- specific cells can be isolated from T cell populations primed to poly(Glu(60)Ala(30)Tyr(10))(n) (GAT) where such clones represent only a minor subpopulation of cells. Gl.4b-primed B10.A(5R) and GAT-primed (B10.A x B10)F(1) lymph node T cells were cloned in soft agar, and the colonies that developed were picked and expanded in liquid culture. The GLphi-specific T cells were then recloned under conditions of high-plating efficiency to ensure that the final colonies originated from single cells. T cells from such rigorously cloned populations responded to stimulation with GILphi but only in the presence of nonimmune, irradiated spleen cells bearing (B10.A x B10)F(1) or the syngeneic B 10.A(5R) recombinant MHC haplotype. Spleen cells from either the B10 or B 10.A parental strains failed to support a proliferative response, even when added together. (B10 x B10.D2)F(1) and (B10 x B10.RIII)F(1) spleen cells also supported a proliferative response but (B10 x B10.Q)F(1) and (B10 X B10.S)F(1) spleen cells did not. These results suggested that the T cell clones were specific for GL[phi} in association with the beta(AE)(b)-alpha(E) (k,d,r,) Ia molecule and that recognition required both gene products to be expressed in the same antigen-presenting cells. Support for this interpretation was obtained from inhibition experiments using the monoclonal antibody Y-17 specific for a determinant on the beta(AE)(b)-alphaE Ia molecule. Y-17 completely inhibited the proliferative response of a GLphi-specific clone but had no effect on the response of either a PPD-specific or GAT-specific clone, both of which required the beta(A)-alpha(A) Ia molecule as their restriction element. No evidence could be found for the involvement of suppressor T cells in this inhibition. We therefore conclude that the phenomenon of F(1)-restricted recognition by proliferating T cells results from the presence of antigen- specific clones that must recognize unique F(1) or recombinant Ia molecules on the surface of antigen-presenting cells in addition to antigen in order to be stimulated.
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PMID:Antigen-specific T cell clones restricted to unique F1 major histocompatibility complex determinants. Inhibition of proliferation with monoclonal anti-Ia antibody. 616 4


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