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

The relationship between antibody response to Salmonella enteritidis vaccine and internal organ burden of S. enteritidis is not fully understood. The genetic relationship, therefore, between postchallenge S. enteritidis burden and antibody response to S. enteritidis vaccine was determined in broiler breeder chicks. Sibling chicks from a broiler breeder male line were either inoculated with a pathogenic S. enteritidis or vaccinated with a commercial S. enteritidis vaccine. Spleen, liver, cecal wall, and cecal content samples from S. enteritidis-challenged chicks (n = 120) were cultured for enumeration of bacteria. Unchallenged chicks (n = 314) were vaccinated at 11 days of age, and serum samples were taken at 10 days postvaccination. Antibody response to vaccination and number of S. enteritidis in cecal content cultures were negatively correlated (-0.772), demonstrating that genetic potential for greater antibody response to S. enteritidis vaccine is associated with lesser S. enteritidis bacterial burden in cecal content of broiler breeder chicks. The findings suggest that genetic selection for vaccine antibody responsiveness can lower bacterial burden in the gut lumenal content and, thus, potentially reduce contamination of poultry products at processing.
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PMID:Salmonella enterica serovar enteritidis burden in broiler breeder chicks genetically associated with vaccine antibody response. 1192 46

In rabbits, complete thymectomy before the age of 5 days produced immunologic deficiency in the adult animals, as indicated by reduced antibody production to bovine serum albumin and bacteriophage T(2). Homotransplantation immunity was unaffected, however. In an inbred strain of mice, complete neonatal thymectomy resulted in complete inability of the 60-day-old animals to form antibody to bacteriophage T(2). Inbred mice, completely thymectomized at birth, had a deficient homograft response, indicated by acceptance of skin homografts from strains differing in both the weaker and stronger (H-2) histocompatibility antigens. Tumor transplants (mammary adenocarcinoma) were also successful across the H-2 genetic barrier in mice thymectomized at birth. Neonatal thymectomy also eliminated the Eichwald-Silmser phenomenon, rendering female mice capable of accepting isografts of male skin. Transplantation immunity in mice was also affected by later thymectomy, at 30 days of age, in certain strain combinations involving weak histocompatibility differences. Spleen and lymph node cells from mice thymectomized at birth or at 6 days of age, and sacrificed 2 months later, did not produce a graft versus host reaction in appropriate F(1) hybrid recipients, indicating that such cells are immunologically inactive. Neonatal thymectomy of F(1) hybrid mice, and in one strain combination thymectomy at 40 days of age, produced animals with inordinate susceptibility to runt disease (homologous disease) following injection of parent strain spleen cells 35 days (neonatal surgery) and 10 days (surgery at 40 days) later. Mice thymectomized at birth also showed growth failure and were short-lived. Studies of newborn mice indicated that they have true lymphocytes only in the thymus, and lack such cells in the spleen, lymph nodes, and gut. In normal mice, adult lymphoid structure develops gradually, beginning during the 1st week of life and continuing for the next month. In contrast, mice thymectomized at birth do not develop mature lymphoid structure: the lymph nodes and spleens tend to be small and poorly organized, and show a quantitative deficiency in lymphoid cells. It is our current working hypothesis that the thymus makes a major contribution toward the centrifugal distribution of lymphoid cells which, in turn, is essential to the full expression of immunologic capacity.
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PMID:The role of the thymus in development of immunologic capacity in rabbits and mice. 1394 53

This study was undertaken to evaluate tissue transglutaminase (TG2) expression in guinea pig tissues, using an antibody against the guinea pig liver TG2. The tests were performed by means of a few immunohistochemical methods in specimens from: gut, skin, the lungs, lymph nodes, the heart, the thymus, the spleen, skeletal muscles of control guinea pigs and from inflamed skeletal muscles and skin. TG2 expression was found in artery, vein and lymphatic vessel endothelia, in mesothelia of pleura, pericardium and peritoneum, and in smooth muscle cells. Spleen deserves a special attention, since this organ, especially rich in TG2, may be much more involved in celiac disease and in liver diseases than it has been accepted so far. The subject calls for further elucidation.
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PMID:Expression of tissue transglutaminase in blood and lymphatic vessel endothelia and in mesothelium. 1563 21

Although anti-CD20 immunotherapy effectively treats human lymphoma and autoimmune disease, the in vivo effect of immunotherapy on tissue B cells and their subsets is generally unknown. To address this, anti-mouse CD20 mAbs were used in a mouse model in which the extent and kinetics of tissue B cell depletion could be assessed in vivo. CD20 mAb treatment depleted most mature B cells within 2 days, with 95-98% of B cells in the bone marrow, blood, spleen, lymph nodes, and gut-associated lymphoid tissues depleted by day 7, including marginal zone and follicular B cells. The few spleen B cells remaining after CD20 mAb treatment included pre-B, immature, transitional, and some B1 B cells that expressed CD20 at low levels. By contrast, peritoneal cavity B cells expressed normal CD20 densities and were coated with CD20 mAb, but only 30-43% of B1 cells and 43-78% of B2 cells were depleted by day 7. Spleen B cells adoptively transferred into the peritoneal cavity were similarly resistant to mAb-induced depletion, while transferred B cells that had migrated to the spleen were depleted. However, peritoneal B1 and B2 cells were effectively depleted in mAb-treated wild-type and C3-deficient mice by thioglycolate-induced monocyte migration into this otherwise privileged niche. Inflammation-elicited effector cells did not promote peritoneal cavity B cell depletion in FcR-deficient mice treated with CD20 mAb. Thus, the majority of CD20(+) cells and B cell subsets within lymphoid tissues and the peritoneum could be depleted efficiently in vivo through Fc-dependent, but C-independent pathways during anti-CD20 immunotherapy.
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PMID:The peritoneal cavity provides a protective niche for B1 and conventional B lymphocytes during anti-CD20 immunotherapy in mice. 1577 4

The lymphoid tissues of the red-tailed phascogale (Phascogale calura) were examined using histological and immunohistochemical techniques. The distribution of immune cells in the tissue beds was documented using antibodies to surface markers CD3 and an MHC Class II antigen (equivalent to HLA DRII). Spleen, gut-associated lymphoid tissues (GALT), lung, bronchus-associated lymphoid tissue (BALT) and liver were examined. The spleen had defined areas of red and white pulp, with follicles containing tingible-bodied macrophages. Anti-CD3 and anti-HLA DRII antibodies revealed the presence of T cells in areas of white pulp and around the peri-arterial lymphatic sheaths. GALT and BALT were detected and appeared as scattered areas of lymphocytes in the tissues beds. This is the first study to report on the lymphoid tissues of this endangered species of marsupial and the first report of the capacity of anti-human antibodies to a surface MHC molecule to react with Dasyurid cells.
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PMID:The immune tissues of the endangered red-tailed phascogale (Phascogale calura). 1653 20

To establish control values for circulating cells and immune associated organs over the course of a self-limiting Cryptosporidium muris infection and rechallenge infection, mice were sacrificed at intervals starting before oral inoculation and ending after oocyst shedding had ceased. These values were used in other experiments to evaluate changes in these parameters induced by a single dose glucocorticoid immunosuppression model and in other immunosuppression studies. Flow cytometry counts of circulating T-lymphocytes and neutrophils, differential leukocyte counts, leukocyte morphology, spleen and thymus changes, and oocyst shedding were evaluated. Immediately after C. muris oocyst inoculation and up to the start of oocyst production (day 0 to day 7), the circulating blood profile showed a 50% drop in all leukocytes, including both large and small lymphocytes and CD3, CD4 and CD8 T-lymphocytes. There was an initial slight rise in circulating mature neutrophils after oocyst inoculation but numbers promptly dropped below normal and remaineded below normal. In the differential cell counts, monocytes with a fat, oval morphology increased by 60% at 24 h and remained high through oocyst shedding and beyond (day 8 through day 36). During oocyst shedding and continuing past the end of shedding, T-lymphocytes increased 100%. Monocytes with a flat, angular morphology increased in a similar manner. Immediately after oocyst inoculation the spleen contracted by 29%, but became 92% larger than its pre-inoculation size by day 14 when heavy oocyst shedding began. It remained enlarged through the end of oocyst shedding (day 29) and beyond (day 36). Spleen volume decreased and increased similar to changes in T-cell numbers. Throughout the C. muris infection the thymus remained largely unchanged. The transit of an oocyst bolus was followed from the stomach through the gut to the colon. No oocysts could be found in the stomach, caecum or feces of mice one half hour after oocyst inoculation. Likewise, an oral bolus of India ink passed from the stomach entirely into the colon after 3 h; therefore, no oocysts from the inoculum passed completely through the intestine and out into the feces. Recovered mice rechallenged with C. muris showed increased B-lymphocyte numbers; however, T-lymphocyte numbers remained level. The large lymphocytes increased after rechallenge, peaking on day 3, then decreased through day 10. B-cell numbers followed a pattern similar to the large lymphocytes. On day 10 of infection monocytes with a fat oval morphology rose sharply while B-cells fell in number. In both the initial infection and the rechallenge there was no unique blood profile which could definitely indicate a protozoal disease or identify a specific point during the course of the disease. There was no increase in the number of either small or large lymphocytes prior to increases in fat or flat monocytes.
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PMID:Characterization of a Cryptosporidium muris infection and reinfection in CF-1 mice. 1719 93

Foxp3(+)CD25(+)CD4(+) regulatory T cells are produced in the thymus (natural T regs) but can also differentiate from peripheral Foxp3(-)CD4(+) precursors (induced or adaptive T regs). We assessed antigen presenting cell (APC) requirements for the latter differentiation. With added transforming growth factor (TGF)-beta, both immature and mature populations of dendritic cells (DCs) induced antigen-specific Foxp3(+) T regs from Foxp3(-) precursors. Using endogenous TGF-beta, DCs from gut-associated mesenteric lymph nodes were capable of differentiating Foxp3(+)T regs. Spleen DCs were 100-fold more potent than DC-depleted APCs for the induction of T regs and required 10-fold lower doses of peptide antigen. Interleukin-2 (IL-2) was essential, but could be provided endogenously by T cells stimulated by DCs, but not other APCs. The required IL-2 was induced by DCs that expressed CD80/CD86 costimulatory molecules. The DC-induced Foxp3(+)T regs divided up to 6 times in 6 days and were comprised of CD62L and CD103 positive and negative forms. The induced Foxp3(+)T regs exerted suppression in vitro and blocked tumor immunity in vivo. These results indicate that DCs are specialized to differentiate functional peripheral Foxp3(+)T regs and help set the stage to use DCs to actively suppress the immune response in an antigen-specific manner.
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PMID:Dendritic cells are specialized accessory cells along with TGF- for the differentiation of Foxp3+ CD4+ regulatory T cells from peripheral Foxp3 precursors. 1769 44

Here we investigated the effect of lifelong supplementation of the diet with coconut fat (CO, rich in saturated fatty acids) or fish oil (FO, rich in n-3 polyunsaturated fatty acids) on tumor growth and lactate production from glucose in Walker 256 tumor cells, peritoneal macrophages, spleen, and gut-associated lymphocytes. Female Wistar rats were supplemented with CO or FO prior to mating and then throughout pregnancy and gestation and then the male offspring were supplemented from weaning until 90 days of age. Then they were inoculated subcutaneously with Walker 256 tumor cells. Tumor weight at 14 days in control rats (those fed standard chow) and CO supplemented was approximately 30 g. Supplementation of the diet with FO significantly reduced tumor growth by 76%. Lactate production (nmol h(-1) mg(-1) protein) from glucose by Walker 256 cells in the group fed regular chow (W) was 381.8 +/- 14.9. Supplementation with coconut fat (WCO) caused a significant reduction in lactate production by 1.6-fold and with fish oil (WFO) by 3.8-fold. Spleen lymphocytes obtained from W and WCO groups had markedly increased lactate production (553 +/- 70 and 635 +/- 150) when compared to non-tumor-bearing rats ( approximately 260 +/- 30). FO supplementation reduced significantly the lactate production (297 +/- 50). Gut-associated lymphocytes obtained from W and WCO groups increased lactate production markedly (280 +/- 31 and 276 +/- 25) when compared to non-tumor-bearing rats ( approximately 90 +/- 18). FO supplementation reduced significantly the lactate production (168 +/- 14). Lactate production by peritoneal macrophages was increased by tumor burden but there was no difference between the groups fed the various diets. Lifelong consumption of FO protects against tumor growth and modifies glucose metabolism in Walker tumor cells and lymphocytes but not in macrophages.
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PMID:Glucose metabolism by lymphocytes, macrophages, and tumor cells from Walker 256 tumor-bearing rats supplemented with fish oil for one generation. 1894 76

Autoimmunity and inflammation are controlled in part by regulatory B cells, including a recently identified IL-10-competent CD1d(high)CD5(+) B cell subset termed B10 cells that represents 1-3% of adult mouse spleen B cells. In this study, pathways that influence B10 cell generation and IL-10 production were identified and compared with previously described regulatory B cells. IL-10-competent B cells were predominantly CD1d(high)CD5(+) in adult spleen and were the prevalent source of IL-10, but not other cytokines. B10 cell development and/or maturation in vivo required Ag receptor diversity and intact signaling pathways, but not T cells, gut-associated flora, or environmental pathogens. Spleen B10 cell frequencies were significantly expanded in aged mice and mice predisposed to autoimmunity, but were significantly decreased in mouse strains that are susceptible to exogenous autoantigen-induced autoimmunity. LPS, PMA, plus ionomycin stimulation in vitro for 5 h induced B10 cells to express cytoplasmic IL-10. However, prolonged LPS or CD40 stimulation (48 h) induced additional adult spleen CD1d(high)CD5(+) B cells to express IL-10 following PMA plus ionomycin stimulation. Prolonged LPS or CD40 stimulation of newborn spleen and adult blood or lymph node CD1d(low) and/or CD5(-) B cells also induced cytoplasmic IL-10 competence in rare B cells, with CD40 ligation uniformly inducing CD5 expression. IL-10 secretion was induced by LPS signaling through MyD88-dependent pathways, but not following CD40 ligation. LPS stimulation also induced rapid B10 cell clonal expansion when compared with other spleen B cells. Thereby, both adaptive and innate signals regulate B10 cell development, maturation, CD5 expression, and competence for IL-10 production.
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PMID:The development and function of regulatory B cells expressing IL-10 (B10 cells) requires antigen receptor diversity and TLR signals. 1949 69

NDRG4 is a member of the NDRG family (N-myc downstream-regulated gene), which is highly expressed in brain and heart. Previous studies showed that Ndrg1-deficient mice exhibited a progressive demyelinating disorder of peripheral nerves and Ndrg4-deficient mice had spatial learning deficits and vulnerabilities to cerebral ischemia. Here, we report generation of Ndrg4 mutant alleles that exhibit several development defects different from those previously reported. Our homozygous mice showed growth retardation and postnatal lethality. Spleen and thymuses of Ndrg4(-/-) mice are considerably reduced in size from 3 weeks of age. Histological analysis revealed abnormal hyperkeratosis in the squamous foregut and abnormal loss of erythrocytes in the spleen of Ndrg4(-/-) mice. In addition, we observed an abnormal hind limb clasping phenotype upon tail suspension suggesting neurological abnormalities. Consistent to these abnormalities, Ndrg4 is expressed in smooth muscle cells of the stomach, macrophages of the spleen and neurons. Availability of the conditional allele for Ndrg4 should facilitate further detailed analyses of the potential roles of Ndrg4 in gut development, nervous system and immune system.
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PMID:Postnatal lethality and abnormal development of foregut and spleen in Ndrg4 mutant mice. 2680 54


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