Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of a low protein (6%) diet on the immunologic function of NZB mice was investigated. The low protein intake was associated with decreased weight gain in both male and female NZB mice. The mice fed the low protein diet did not develop splenomegaly, which generally occurs by 7 to 10 months of age in NZB mice fed a normal amount of protein. Further, 7- to 10-month-old NZB mice fed the low protein(6%) diet, maintained: 1) more vigorous antibody production to sheep red blood cells; 2) greater capacity to produce graft-vs-host reactions, and 3) more vigorous cell-mediated "killer" cell immunity after immunization against DBA/2 mastocytoma cells than did NZB mice on a normal (22%) protein diet. The decrease of PHA and Con A response which normally occurs with aging in NZB mice was abrogated to some degree by protein restriction. However, response to LPS, which also declines with age in NZB mice, did not appear to be influenced by diet.
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PMID:Influence of protein restriction on immune functions in NZB mice. 0 5

Intravenous injection of LPS or allogeneic lymphocytes resulted in impaired maturation of B cells within the bursa of chick embryos. A gradual decline in the sensitivity of embryos towards both agents was reflected by a decrease in the number and size of bursal follicles following injection between 10 and 15 days of embryonation. The hypoplasia of these follicles in embryos injected with lymphocytes on the 10th day was a more sensitive measure of graft-versus-host reaction than splenomegaly. The relevance of results with this model to the aetiology of immunodeficiency diseases has been briefly discussed.
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PMID:Immunodeficiency in the chicken. III. Hypoplasia of bursal follicles following intravenous injection of embryos with lipopolysaccharide or allogeneic lymphocytes. 23 84

The spleen cell population of C3H/He mice injected with a single sublethal dose of cyclophosphamide (CY) was analysed. An initial atrophy was followed by a considerable hypertrophy and a progressive return to normal. During the phase of spleen atrophy, both B and T cell compartments were depleted. During regeneration, the percentage of Ig+ cells increased rapidly, and at the peak of splenomegaly, the percentage of Ig+ cells was high while no Thy1-2+ cells were detectable. The peculiar points of histology were disappearance of normal T and B compartments, substituted by a layer of lymphoid cells. During the phase of splenectomegaly, the in vitro reactivity of spleen cells to the mitogens PHA and LPS was drastically decreased. Furthermore, the spleen cell population from CY treated mice contained suppressor cells, capable of inhibiting the in vitro reactivity of normal lymphocytes to these mitogens and the multiplication of tumour cells in culture. These cells were adherent, Ig+, Thy1-2- cells. They developed in CY treated T deprived mice. After velocity sedimentation the suppressive activity was detected in the 6 mm/h fraction.
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PMID:[Suppressive cells induced by cyclophosphamide in the spleen of C3H mice]. 84 86

The number and distribution patterns of lymphocytes in the spleens and lymph nodes of Balb/c mice which express immunoglobulin surface receptors were studied in terms of the effects of a murine leukemia virus on the immune-response mechanism. Friend leukemia virus induces a prompt, marked depression of the immune response of mice to antigens such as sheep erythrocytes and E. coli LPS. A functioning T- and B-lymphocyte system is necessary for the response to the SRBC's whereas E. coli LPS, a T cell-independent antigen, stimulates B cells alone. Although the responses to both classes of antigen were markedly depressed in FLV-infected mice, the major defect appeared to be impairment of B-cell function, at least early in the course of infection. In order to examine in more detail the mechanism of interaction between FLV and lymphoid cells with Ig surface receptors, presumably B cells, immmunofluorescent analyses were performed with spleen, and lymph node cells from FLV-infected mice. Within a few days after infection there was a marked decrease in the percentage of spleen cells with Ig surface molecules, although the absolute number of these cells was either unchanged or increased due to marked splenomegaly caused by the virus. A marked decrease in the percentage of splenocytes with theta antigen, considered a marker for mature T cells, also was evident in infected mice. The number of spleen cells showing evidence of FLV infection (i.e., positive for FLV-associated antigens) increased rapidly during the first few days after infection, and within 2 to 2 1/2 weeks nearly all of the nucleated splenocytes were positive for the tumor antigen. In contrast to the results for spleen cells, there were increases rather than decreases in the percentages of Ig-positive and theta-positive cells in the lymph nodes after infection. The number of lymph-node cells that showed the presence of FLV antigen was much lower than in the spleen, and their appearance was also much slower as the leukemic process progressed. Despite these differences between spleen and lymph-node cells in terms of relative percentages of Ig- and theta-positive lymphocytes, relatively similar depressions were evident for the percentages of lymphoid cells that could redistribute their surface Ig receptors into polar caps when incubated with anti-Ig serum at 37 C. Marked impairment of the Ig-capping responses for both spleen and lymph-node cells paralleled the course of infection and development of immunosuppression. These observations indicate that murine leukemia virus infection can both alter the responsiveness of immunocompetent cells to T-dependent and independent antigens and depress the number and normal functional activity of these cells, as reflected by altered surface Ig receptors and antigens.
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PMID:Lymphocyte surface receptors and leukemia virus-induced immunosuppression. 109 86

We studied the effect of depleting NK1.1+ cells from an allograft of lymph node and spleen cells on the outcome of GVH disease in the parent----F1-hybrid combination C57BL/6----(C57BL/6xDBA/2)F1. Four treatment groups were established: group I mice were transplanted with an unmodified graft from normal donors; group II mice were transplanted with an NK1.1-depleted graft that had been harvested from normal donors; group III mice received grafts from donors that had been injected with Poly I:C (100 micrograms i.p.) 18 hr prior to harvesting (These grafts were incubated with complement, but no antibody.); group IV mice were transplanted with depleted grafts harvested from donors that had received Poly I:C. Recipients in each group were monitored for splenomegaly, mitogen responsiveness, NK and CTL activity, histopathology, weight loss, and mortality. Results showed that recipients in all four groups developed splenomegaly and unresponsiveness to LPS, PHA, and Con A by day 12. Augmented host-derived NK activity and graft-derived antihost CTL activity was also demonstrated. Group IV showed little or no weight loss, minimal histopathological changes and a marked reduction in mortality. Recipients in all other groups developed features characteristic of GVH disease and exhibited a steady decline in body weight beginning by day 12. Mortality generally began on day 18 and reached 75-90% by day 60. We postulate that anti-NK1.1 depletes cells from the graft are intimately connected with the effector mechanism in acute GVH disease.
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PMID:Prevention of acute lethal graft-versus-host disease in F1 hybrid mice by pretreatment of the graft with anti-NK-1.1 and complement. 163 23

Irradiated C57BL/6(B6) mice, when they were injected with spleen cells of C57BL/6J-lpr/lpr(B6-lpr) mice, developed splenomegaly at 2 weeks post-transfer, but afterward displaced by GVH-like disease. At 2 weeks the enlarged spleen in the chimeric mice, designated as [B6-lpr----B6] chimera, contained about 70% of the total cell population as CD8-positive T cells. Spleen cells from [B6-lpr----B6] chimeras were unresponsive to Con A and LPS stimulation and suppressed the mitogenic response of B6, B6-lpr, and C3H spleen cells to Con A. However, they had no cytotoxic activity towards Con A blasts of B6 and B6-lpr spleen cells. The suppressor activity found in the [B6-lpr----B6] spleen cells was removed by pretreatment of them with anti-Thy-1.2 or anti-CD8(Lyt2.2) plus complement. The present experiment showed that enormous proliferation of CD8-positive suppressor T cells was induced in the [B6-lpr----B6] chimeras. These cells were probably responsible for the GVH-like lymphoid atrophy observed in these [B6-lpr----B6] chimeras.
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PMID:Analysis of the mechanism of graft-versus-host-like disease in B6 mice with transferred B6-lpr spleen cells. 171 58

In previous studies we demonstrated that an induced asialo-GM1 positive (ASGM1+) cell of donor origin that exerts natural killer cell-like activity (NK activity+) plays a crucial role in the development of graft-versus-host (GVH)-associated tissue damage and severe immunosuppression. This study examined whether the ASGM1+ (NK activity+) GVH effector cells were activated by non-specific signals or whether these cells were triggered by specific alloantigens and displayed antigenic specificity. C57B1/6 (B6) donor mice were treated with either B6 x AF1 (B6AF1) lymphoid cells and anti-asialo GM1 antibodies (anti-ASGM1) to induce and eliminate specifically activated B6-anti-B6AF1 ASGM1+ (NK activity+) cells or with polyinosinic: polycytidylic acid (poly I:C), and anti-ASGM1 to eliminate non-specifically activated ASGM1+ (NK activity+) cells. Donor spleen and lymph node cells depleted of the specific allo-induced ASGM1+ NK reactive cells showed near normal numbers of L3T4+ and Lyt-2+ cells and retained T- and B-cell functions as measured by mitogen responses (to PHA, Con A and LPS), mixed lymphocyte responses (MLR) (to B6AF1) and the generation of cytotoxic T cells (CTL) (to B6AF1 blasts). Anti-ASGM1 treatment almost completely abrogated NK activity in all donor inocula. GVH reactions were induced by injecting treated donor cells into B6AF1, B6 x C3HejF1 (B6C3HF1) and B6 x SJLF1 (B6SJLF1) hybrids and monitored by splenomegaly, suppression of T-cell mitogen responses and the development of histopathological lesions in the thymus, liver and pancreas. Cells from donors depleted of non-specifically (poly I:C) induced ASGM1+ cells induced severe histological lesions, marked immunosuppression and splenomegaly in all three F1 hybrid combinations. When the donor cells were depleted of specifically induced (B6-anti-B6AF1) ASGM1+ cells and injected into the three F1 combinations they induced splenomegaly in all three but caused severe tissue injury and intense immunosuppression only in B6C3HF1 and B6SJLF1 mice and not in B6AF1 mice. Genetic analysis suggests that the H-2D (or a closely related) region of the H-2 complex plays an important role in the activation of the specific GVH effector cells. These results suggest that the cell(s) responsible for splenomegaly are different from the ones that cause severe GVH-associated tissue damage and immunosuppression although there may be cells and/or lymphokines common to both processes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Induction, specificity and elimination of asialo-GM1+ graft-versus-host effector cells of donor origin. 183 14

Injection of B10.D2 cells into irradiated H-2d compatible (DBA/2xB10.D2)F1 recipients provokes a lethal GVH that can be abrogated by donor preimmunization against host-specific DBA/2 non-H-2 antigens. To study the possible relationship between the observed protection and restoration of immune responsiveness, we compared spleen cellularity, selected T and B cell functions, and NK activity in GVH and protected mice during the 1st month after grafting. Normal and isografted mice served as controls. GVH was found to be characterized by an early stimulation phase associated with splenomegaly and increased percentages (but not numbers) of Lyt-2+ and L3T4+ cells, followed by profound aplasia and abrogation of IL-2 production. Response to a B cell mitogen (LPS) is depressed, and cells from GVH mice exert a strong suppressive effect on the LPS and PHA responsiveness of normal cells. Suppression appears to be mediated by a radioresistant, nylon nonadherent, asialo GM1 negative cell expressing a low level of Thy-1 antigen. In contrast, protection correlates with progressive restoration of spleen cellularity and LPS responsiveness, with decreased but clearly detectable IL-2 production, and transient nonspecific suppressor activity. The immune status of protected mice resembles that of isografted controls. No correlation was found between mortality (or protection) and either PHA responsiveness, which remained depressed in all grafted mice throughout the observation period, or NK activity, which was strongly depressed in both GVH and protected mice. In conclusion, protection correlates with the disappearance of nonspecific suppressor cells and the restoration of cellularity and certain nonspecific immune functions. Donor immunization against host-specific non-H-2 antigens, which protects against mortality, also protects against GVH-associated immune deficiency.
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PMID:Lethal graft-versus-host reaction against non-H-2 antigens. I. Prevention of GVH-associated immunodeficiency by preimmunizing the donor against host-specific non-H-2 antigens. 252 8

The activation of the protein kinase C (PKC) pathway plays an integral part in the proliferation of many cell types including lymphocytes. We report that the PKC inhibitor H-7 caused inhibition of three commonly studied blastogenic responses (Con A, LPS, and MLR) with the strongest suppression being detected in the MLR. In contrast, HA1004, a potent inhibitor of cyclic nucleotide-dependent protein kinases, did not alter the blastogenic response but occasionally caused augmentation. The phenothiazine compounds studied inhibited the Con A and, to a lesser extent, the LPS responses. One of the compounds, promethazine-HCl, was effective in vivo in inhibiting splenomegaly resulting from the induction of graft vs. host disease. Our studies support the involvement of PKC in lymphoid blastogenesis. They also suggest that agents that can inhibit PKC activity may be useful in inducing immunosuppression in vivo.
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PMID:The effects of protein kinase inhibitors on lymphocyte blastogenesis and GVHD-induced splenomegaly. 276 Apr 15

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


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