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)

Various organs--lung, trachea, liver, kidney, heart, adrenal gland, skin, spleen, thymus, lymph node, gut, thyroid, spinal cord and brain--were removed from 43 seals at dissections performed on the German North sea coast. The specimens were fixed in formalin and routinely processed for light microscopy. The major pathological findings were Lung: acute congestion with interstitial and intra-alveolar oedema; intra-alveolar haemorrhage; suppurative bronchitis and bronchopneumonia; larvae and adult forms of Parafilaroides gymnurus. Liver: acute congestion; granulomatous lesions and infiltrates of eosinophils; intravascular nematodes. Spleen: varying degrees of atrophy of the white pulp; haemosiderosis; acute congestion of the red pulp. Lymph nodes: varying degrees of atrophy of the lymphatic tissue; long-standing sinus histiocytosis with partial fibrotic obliteration of the lumina; parasitic infiltration, sometimes with the Splendore-Hoeppli phenomenon; germinal centre hyperplasia. Thymus: pronounced atrophy of the lymphatic tissue, particularly in the cortical areas. Thyroid: marked reduction in colloid content. The other organs studied were normal or showed only minor histopathological changes. The morphological findings do not allow definite conclusions to be made about the aetiology and pathogenesis of the illness and death of the seals. However, evidence has been published that the seals' illness is probably due to canine distemper virus. The atrophy of the lymphoreticular tissues is consistent with infection by this virus.
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PMID:Histopathological findings in harbour seals (Phoca vitulina) found dead on the German North sea coast. 236 46

To study the role of IL-4 in development of granulomatous experimental autoimmune thyroiditis (EAT), IL-4 gene-disrupted mice expressing the EAT-susceptible H-2k haplotype were generated and used for EAT induction. Spleen cells from mouse thyroglobulin (MTg) and LPS-primed IL-4(+/+) and IL-4(-/-) donors could induce severe granulomatous EAT when spleen cells were activated with MTg and anti-IL-2R mAb in the presence of IL-12. Thyroid lesions had extensive follicular cell proliferation, large numbers of histiocytes, polymorphonuclear leukocytes, and multinucleated giant cells, in addition to lymphocytes and other mononuclear cells. Expression of IFN-gamma gene mRNA and production of IFN-gamma by effector spleen cells stimulated with MTg and IL-12 were similar for both IL-4(+/+) and IL-4(-/-) mice. Although IL-4 was undetectable in IL-4(-/-) mice, expression of mRNA for IL-5, IL-10, and IL-13 and production of IL-5 by both MTg-activated spleen cells and anti-CD3-activated CD4+ T cells were comparable for cells from IL-4(+/+) and IL-4(-/-) mice, indicating that the absence of IL-4 did not prevent production of other Th2 cytokines. Production of MTg-specific IgG1 was very low or undetectable in IL-4(-/-) mice. IL-4 gene mRNA and MTg-specific IgG1 could be detected in IL-4(+/+) or IL-4(-/-) recipients only when they received effector cells from IL-4(+/+) donor mice, indicating that IL-4- and IgG1-secreting cells are of donor origin. These results demonstrate that IL-4 is not essential for development of granulomatous EAT.
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PMID:Induction of granulomatous experimental autoimmune thyroiditis in IL-4 gene-disrupted mice. 955 67