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

The proliferative response of mouse B lymphocytes induced by Fc fragments was found to be dependent upon an adherent cell population. The adherent cell is esterase positive, irradiation resistant, and not susceptible to lysis by anti-thymus serum and complement. The mechanism(s) by which Fc fragments induce B-cell proliferation could be the result of the interaction of Fc with both B cells and adherent cells or with adherent cells which then release factors that trigger the B cells to proliferate. Spleen cells from the C3H/HeJ mouse were shown to be unable to respond to Fc fragments. The addition of adherent cells from either C3H/St or C3H/HeN mice to adherent cell depleted C3H/HeJ cells enabled them to respond to Fc, indicating the defect was in the adherent cell population.
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PMID:The requirement for adherent cells in the Fc fragment-induced proliferative response of murine spleen cells. 45 75

Spleen cells from germfree rats, conventionally reared rats, and gnotobiotic rats associated with two Pseudomonas species gave no positive blastogenic response when incubated with each of four lipopolysaccharide (LPS) preparations from Escherichia coli, with glycolipid extracted from Salmonella minnesota R595 or with S. minnesota R595 lipid A. However, spleen cell preparations from athymic mice demonstrated a positive blastogenic response when incubated with E. coli LPS. Removal of adherent cells from germfree and conventional-flora rat spleen cells did not increase the mitogenic activity of LPS for nonadherent cells (less than 0.5% esterase-positive cells). All rat spleen cell preparations gave positive blastogenic responses to phytohemagglutinin and concanavalin A. This study indicates that LPS may not be a mitogenic agent for rat spleen cells.
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PMID:The mitogenic activity of lipopolysaccharide for spleen cells from germfree, conventional, and gnotobiotic rats. 54 Feb 63

Mice CFW were infected per os with Trichinella pseudospiralis (150 larvae/mice). The mice were divided in two groups: nonstimulated and stimulated intraperitoneally with PHA-P at dose 10 mg/kg body weight. The animals were killed 7, 14, 21, 28, 42, 56, 70 and 150 day post infection (d.p.i.). Spleen et mesenteric lymph nodes were examined histopathologically (Hematoxylin-Eosin) and histochemically (nonspecific esterase reaction) for differentiation of T lymphocytes. The obtained results reveal that T. pseudospiralis infection caused weak mobilisation of mouse lymphatic system lasting only to 70 day of experiment. In the lymphatic organs of infected mice small number of T lymphocytes were observed mostly between 28 and 56 d.p.i. The intraperitoneally stimulation with PHA-P give rise to caused only little mobilisation of lymphatic tissue and small increase of T lymphocytes number. The obtained results were compared with analogic earlier experiments with T. spiralis infection.
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PMID:[Studies of the lymphatic system in mice infected with Trichinella pseudospiralis as well as infected and stimulated by Phytohaemagglutin (PHA-P)]. 129 55

A total of 102 children aged 5 to 14 years with virus hepatitis B were examined for the status of the mononuclear phagocytic system in accordance with the absolute monocyte count in the circulating blood, esterase and acid phosphatase activity in the monocytes, for function of organ macrophages of the liver and spleen using dynamic scintigraphy with TC-colloid and for macrophages of the skin by the "skin window" method. The rise of the absolute count and lowering of the functional and metabolic activity of blood monocytes were directly proportional to the gravity of virus hepatitis B. The changes persisted for a long time, namely up to 1.5 to 3 months since the disease onset. There was a progressive drop of the functional activity of Kupffer cells in the liver with a maximum decrease seen within 4 to 6 weeks since the disease onset, followed by returning to normal in cyclic disease and preservation of the changes in lingering and chronic virus hepatitis B. Spleen macrophages play an active compensatory role, maintaining normal "purifying" function of the mononuclear phagocytic system. That compensatory response tension appeared high in lingering and especially in chronic virus hepatitis and may serve as a criterion for process chronicity. The changes in the mononuclear phagocytic system observed in cyclic course of mild and medium-gravity virus hepatitis B may be regarded as normal adaptive reaction and do not require any drug correction. The latter one may only be indicated in patients with grave, lingering or chronic disease patterns associated with break down or depletion of the adaptive mechanisms of the system in question.
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PMID:[Functional-metabolic activity of the mononuclear phagocyte system of the blood, liver, spleen and skin in children with hepatitis B]. 225 75

Spleen cell blastogenesis to mitogens and antibody responses to sheep erythrocytes (sRBC) were tested in BALB/c mice with experimental E. cuniculi infections. Blastogenesis responses of spleen cells 1 week post-infection were significantly lower than normal to T-cell mitogens (Con A and PHA) and were unchanged in response to B-cell mitogens (LPS and PWM). After 2 weeks post-infection, the responses to T cell mitogens returned to normal. Mixing spleen cells from 1-week infected mice with cells from uninfected mice failed to reveal the presence of suppressor cells. Antibody responses to sRBC were significantly slower to develop in 1 week-infected mice compared with uninfected mice or mice infected 2 weeks earlier or at the same time as sRBC challenge. Infected mice displayed splenomegaly which was most pronounced 1 week post-infection and the differential spleen cell counts revealed the presence of lymphoblasts. Lymphohyperplasia appeared to cause the splenomegaly. No shifts in the proportion of Thy 1.2+ T cells, Ig+ B cells, or esterase-positive macrophages were detected. These results indicate that the immune system in BALB/c mice is depressed early during E. cuniculi infections.
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PMID:Modulated immune responsiveness associated with experimental Encephalitozoon cuniculi infection in BALB/c mice. 297 36

Spleen cells from BALB/c mice infected with 2 X 10(7) L. major promastigotes and developing progressive disease produced significantly lower levels of interleukin-2 (IL-2) in response to concanavalin A stimulation than did spleen cells from uninfected mice. In contrast, spleen cells from sublethally irradiated and infected mice, which were able to contain lesion development, produced significantly higher levels of IL-2. The increase in IL-2 production closely paralleled lesion regression. Mice protectively immunized by four intravenous injections with lethally irradiated promastigotes also produced enhanced levels of IL-2, which were sustained after challenge infection. In contrast, spleen cells from BALB/c mice given four s.c. injections of irradiated promastigotes produced high levels of IL-2 before but not after infection. These mice eventually produced levels of IL-2 indistinguishable from those of unimmunized mice with progressive disease. There is thus an inverse relation between disease progression and the ability of spleen cells to produce IL-2. Spleen cells from mice with uncontrolled disease not only produced lower levels of IL-2 but also impaired IL-2 production by normal spleen cells. The ability to inhibit IL-2 was abrogated by passing the cells through a Sephadex G-10 column, removal of plastic adherent cells, and removal of carbonyl iron-ingesting cells. Furthermore, Sephadex G-10 column-treated and plastic adherent, nonspecific esterase-positive spleen cells from mice with progressive disease were able to suppress IL-2 production by normal splenic T cells. The suppressive activity of the adherent cells was not affected by treatment with anti-Thy-1.2 antibody and complement. In contrast, adherent spleen cells from uninfected mice were devoid of such suppressor activity. The depressed IL-2 production by spleen cells from progressively infected mice could be restored to that of normal spleen cells by the addition of indomethacin to the culture. There was however, no correlation between IL-2 production and IL-1 activity in infected or immunized BALB/c mice. Thus, it appears that the suppression of IL-2 production is mediated by prostaglandins elaborated by macrophages from chronically infected mice.
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PMID:Suppression of interleukin-2 production by macrophages in genetically susceptible mice infected with Leishmania major. 349 Apr 40

Human monocytes, pulmonary alveolar macrophages (PAMs) and spleen macrophages were concentrated by immobilization on cold insoluble globulins. These cell preparations were 90 +/- 3%, 95 +/- 1% and 83 +/- 3% esterase rich, respectively, 87 +/- 4%, 95 +/- 3% and 66 +/- 11% phagocytic and 78 +/- 3%, 79 +/- 9% and 68 +/- 5% reactive with OKM1 monoclonal antibody. Spleen macrophages differed from the other two cell preparations in that significantly fewer reacted with 61D3 or 63D2 monoclonal antibodies. Monocytes and PAMs promoted the mixed leucocyte response by autologous lymphocytes when added at low concentrations, but suppressed this response at high concentrations. Spleen macrophages only promoted the mixed leucocyte reaction but were required in much higher numbers than either monocytes or PAMs for optimal promotion. Likewise, the added presence of monocytes or PAMs in high numbers suppressed Ig synthesis stimulated with pokeweed mitogen, while spleen macrophages were not suppressive in this system. This study shows that the distribution of macrophages that differ in their regulatory effects upon lymphocyte responses varies in different tissues. The human spleen is deficient in macrophage related suppression.
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PMID:A comparison of the regulatory effects of human monocytes, pulmonary alveolar macrophages (PAMs) and spleen macrophages upon lymphocyte responses. 622 57

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

Spleen cells from mice infected for 20 weeks with Schistosoma mansoni, exposed in vitro to soluble schistosomal egg antigens (SEA), treated with mitomycin C (Mc), and cocultured with syngeneic responder spleen cells increased the baseline proliferation of the otherwise unstimulated responder cells in cocultures. The role of macrophages in this "spontaneous" thymidine incorporation was studied directly by removal of macrophages on Sephadex G-10 columns. Removal of esterase-positive, Sephadex G-10-adherent cells (macrophages) greatly reduced the amount of SEA-induced, chronically infected spleen cell-mediated stimulation observed in cocultures. It also reduced an elevated background of spontaneous DNA synthesis seen with control cultures of spleen cells from infected animals. Depletion of T lymphocytes from chronic spleen cell populations by treatment with anti-Thy 1.2 serum and complement prior to exposure to SEA partially abrogated the augmentation effect. Comparison of these results with mitogen (concanavalin A)-induced spleen cell-mediated stimulation (which is elevated, rather than reduced, by macrophage removal) and with known alterations in splenic T- and B-lymphocyte ratios in chronic murine schistosomiasis suggests that antigen-stimulated, chronically infected splenic macrophage-dependent baseline augmentation may depend on specific T-lymphocyte-derived lymphokine induction. These results may reflect a general mechanism whereby animals harboring a persistent, chronic infection can respond quickly to a second or challenge infection or a flareup of the primary infection.
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PMID:Immunoregulation in experimental Schistosomiasis. III. Role of macrophages in soluble egg antigen-induced chronic spleen cell augmentation of baseline lymphocyte reactivity. 642 77

Rat spleen kallikrein was identified and purified by DEAE-cellulose and monoclonal antibody-affinity chromatography. The purified enzyme has Tos-Arg-OMe esterase activity and kinin-releasing activity from a purified low-molecular-weight kininogen substrate. In the direct radioimmunoassay for tissue kallikrein, the splenic enzyme displays parallelism with standard curves of rat urinary kallikrein. The pH profiles of the Tos-Arg-OMe esterase activities of spleen and urinary kallikrein were identical with optima at 9.0. Rat spleen kallikrein was inhibited strongly by aprotinin and affinity-purified kallikrein antibody and weakly by soybean trypsin inhibitor. The IC50 values were similar to those observed against rat urinary kallikrein. Neither the urinary nor the splenic enzyme was inhibited by lima bean trypsin inhibitor or preimmune serum immunoglobulins. Spleen kallikrein was labeled with [14C]diisopropylphosphorofluoridate and visualized by fluorography on a sodium dodecyl sulfate-polyacrylamide gel. The electrophoretic mobility of the splenic enzyme was indistinguishable from that of urinary kallikrein A with an estimated Mr of approx. 38 000. With Western blot analyses using a rabbit anti-kallikrein antibody followed by 125I-labeled protein A binding, the spleen and urinary kallikreins were again visualized at identical positions by autoradiography. The data show that there is a rat splenic tissue kallikrein which is indistinguishable from a renal kallikrein with respect to physicochemical properties, immunological character and susceptibility to inhibitors.
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PMID:Isolation of tissue kallikrein in rat spleen by monoclonal antibody-affinity chromatography. 656 77


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