Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spleen rosette forming cells (RFC) from adult thymectomized mice have a low sensitivity to inhibition by anitheta serum (AOS) and azathioprine (AZ) in comparison with normal spleen or thymus RFC. Thymus extracts and normal mouse serum (but not spleen extracts or thymectomized mouse serum) correct this abnormality after a 30 min in vitro incubation with spleen cells. We report here the existence of a serum factor produced in allogeneic reactions with the same activity on rosettes as thymic factor (TF). This 'allogeneic' factor (AF) is detectable in mice undergoing a graft versus host reaction (GVHR), rejecting skin allografts or allogeneic cells or responding to thymus-dependent antigens such as heterologous red blood cells or BSA. The T-cell origin of AF is indicated by AF presence in nude mice submitted to the same allogeneic stimuli as listed above and in normal mice injected with PVP or LPS. AF is distinct from the thymic factor as shown by differences in electric charge. Moreover, in contrast with TF there is no specific high molecular weight inhibitor of AF. Preliminary biochemical studies indicate that AF is probably a peptide of low molecular weight (greater than 5000 daltons). Its target cell is probably a T-cell precursor.
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PMID:Demonstration and characterization of a serum factor produced by activated T cells. 2 86

Spleen cell suspensions from mice undergoing a secondary response to sheep erythrocytes (SRBC) contained about one tenth as many specific antigen-binding, rosette-forming cells (RFC) when they had been washed at 37 degrees C instead of 4 degrees C before rosetting. This difference was correlated with the presence of IgG anti-SRBC antibody in the serum, and the 37 degrees C washings of immunised spleen cells could passively allergise non-immune spleen cells at 4 degrees C for specific rosette formation which was inhibitable by anti-mouse F(ab)2 serum. The RFC from actively immunised mice were lymphocytes and not macrophages by morphological and cytochemical criteria. It is suggested that the 37 degrees C-labile RFC are lymphocytes to which IgG antibodies bind in the cold. These data indicate that in the use of antigen-binding cell assays to monitor immunological responses, it is necessary to wash lymphocytes at 37 degrees C before testing.
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PMID:Temperature dependence of antigen-specific rosette formation by lymphocytes from immunised mice. 6 52

Murine lymphocytes from spleen, lymph node, and thymus were examined for IgM complex receptors. Lymphocytes from all three organs were found to bind SRBC sensitized with IgM from various sources including: primary anti-SRBC serum, murine and rabbit anti-Escherichia coli LPS sera, and a murine IgM myeloma (MOPC 104E). Rosette formation by lymphocytes with IgM-sensitized SRBC was inhibited by soluble antigen-IgM complexes but not by IgM or antigen alone. Rosette formation was also inhibited by human IgM (Fc)5mu but not by Fab mu. Antiserum and complement treatment of the cells and subsequent recovery of the viable cells by trypsinization, filtration, and washing revealed the IgM rosette-forming cell (RFC) in the thymus to be a T cell. Spleen on the other hand was found to contain both B and T cells capable of binding IgM sensitized SRBC. Removal of both B and T cells from spleen cell suspensions eliminated all IgM RFC. The IgM complex receptor was found to be trypsin insensitive. Anti-Ig column fractionation enriched IgM RFC in spleen and lymph node suspensions passed through the columns, whereas cells bearing surface Ig, IgG complex receptors, and C3 receptors were retained in the columns.
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PMID:IgM complex receptors on subpopulations of murine lymphocytes. 108 66

Spleen cells from unprimed mice or those primed with horse red blood cells (HRBC) were depleted of rosette-forming cells (RFC) with HRBC by the Ficoll-Hypaque density sedimentation, and the cells were examined in the adoptive transfer system whether they could raise IgM or IgG antibody-forming cells (AFC) after an immunization with HRBC. When spleen cells were pooled from unprimed mice, the response to HRBC of those depleted of RFC with HRBC (HRBC-RFC) was decreased to about a half in both IgM and IgG AFC. On the other hand, when spleen cells were from mice primed with HRBC, the response to HRBC of those depleted of HRBC-RFC was decreased dramatically to 1/20 of that of original cells in IgG AFC, but it was decreased to about a half in IgM AFC. In the time course of the response to HRBC of RFC-depleted spleen cells from mice primed with HRBC, an early IgG response was abolished but the late one was as high as that of untreated spleen cells. These results suggest that the depletion of RFC is most effective on the depletion of direct precursors of the secondary IgG AFC.
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PMID:Antigen specific receptors on murine B cell lineage. 2. Different effect of rosette-forming cell depletion on IgM and IgG antibody forming cell precursors in primary and secondary response. 616 Feb 71

Lipopolysaccharide (LPS) was administered into sheep red blood cells (SRBC)-primed mice, and the effect of LPS on SRBC-specific memory cells was investigated. Spleen cells from SRBC-primed mice which were injected with LPS exhibited much lower in vitro secondary plaque-forming cells (PFC) responses to SRBC than those from untreated SRBC-primed mice. The in vitro anti-SRBC response of the spleen cells to LPS was also reduced. The combination experiments of B cells and T cells from SRBC-primed mice which were injected with or without LPS demonstrated that the reduction of immune responses to SRBC after administration of LPS was caused by the defect of SRBC-specific B memory cells, but not T memory cells. B cell type rosette-forming cells (RFC) for SRBC markedly decreased after injection of LPS, while PFC as antibody-forming cells did not increase subsequently. Therefore, the reduction of RFC was not due to their differentiation into PFC. The lymphoid follicles in the spleens from mice injected with LPS were stained positively by in situ nick end labeling specific for fragmented DNA. A large percentage of Ig+ spleen cells from SRBC-primed mice which were injected with LPS was also stained positively. The injection of glucocorticoids into SRBC-primed mice induced similar reduction of B memory cells. It was suggested that LPS might induce apoptosis of B memory cells and regulate B cell memory in antigen-nonspecific manner.
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PMID:Lipopolysaccharide induces apoptotic cell death of B memory cells and regulates B cell memory in antigen-nonspecific manner. 887 Nov 9