Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although mixed forms of Castleman's disease (CD) may occur, two classically recognized forms are the angiofollicular (hyaline vascular [V]) variant and the plasma cell (P) variant. The two forms of CD differ greatly in their clinical and histopathologic manifestations. Plasma cell CD is characterized by the presence of hyperplastic germinal centers (GCs) and sheets of plasma cells in the interfollicular areas. In this study we demonstrated an abundant expression of interleukin-6 (IL-6) in most GC B cells and in the numerous immunoblastoid B cells in the mantle zone and interfollicular areas in CD-P. Patients with CD-P also have an elevated serum IL-6 level. The increased IL-6 production is responsible for the marked plasma cell infiltration in lymph nodes and bone marrow as well as for the elevated gammaglobulin level in serum. In contrast, CD-V is distinguished by the presence of atrophic GCs, which often are populated by cytologically atypical follicular dendritic reticulum (FDR) cells, as well as by sheets of T-zone plasmacytoid histiocytes and increased numbers of capillaries in the interfollicular areas. In contrast to the findings in CD-P, we did not observe significant expression of IL-6 in GC cells or in immunoblastoid cells in CD-V; this may account for the paucity of plasma cells in this form of CD. The reason for the atypical changes in FDR cells as well as the increases in T-zone plasmacytoid histiocytes and capillaries seen in CD-V are not known inasmuch as no cytokines, such as IL-1, IL-4, IL-6, IL-7, IL-8, IL-9, tumor necrosis factor-alpha, granulocyte-macrophage colony-stimulating factor, or granulocyte colony-stimulating factor, were detectable in tissues. It is possible that in CD-V the atypical change in FDR cells could lead to a disturbance of B-lymphocyte/FDR cell interaction and subsequently to poor development of GCs. The study clearly indicates that the histopathologic and clinical features of CD vary greatly depending on the capacity of activated B cells to produce IL-6. However, lack of IL-6 secretion by GC cells alone cannot explain the histopathologic alterations in CD-V.
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PMID:Expression of interleukin-6 in Castleman's disease. 837 54

POEMS syndrome is a plasma cell dyscrasia that presents with numerous complications, one of which is rarely pulmonary hypertension. Here we present a case of POEMS syndrome with pulmonary hypertension who improved with steroids and six rounds of plasmapheresis done over 1 month, and we document the baseline immune mediator status and the changes associated with the therapeutic intervention. Serum levels of soluble immune mediators such as interleukin (IL)-5, IL-8, IL-10, and eotaxin were normal at baseline and throughout therapy, whereas those of tumor necrosis factor (TNF)-alpha, soluble TNF-receptor type I (sTNF-RI), IL-6, interferon (IFN)-gamma, IL-2, and sIL-2R, which were abnormally high at baseline normalized with steroids and plasmapheresis. Serum levels of sIL-6R, which were abnormally low at baseline, increased to normal after therapy. The latter results pinpoint not only potential mediators of the systemic manifestations of POEMS syndrome with pulmonary hypertension but also relevant markers in patient follow-up. In this respect, IL-6 has been involved in the pathogenesis of multiple myeloma and Castleman's disease, and the interplay between abnormally high levels of IL-6 and abnormally low levels of its soluble receptor, deficiencies that corrected with therapy in this patient, appears to be particularly relevant to the pathogenic manifestations of POEMS syndrome with pulmonary hypertension. These findings are discussed in the context of our current knowledge of the pathogenesis of pulmonary hypertension and of potential new therapeutic modalities for POEMS syndrome with pulmonary hypertension.
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PMID:Soluble immune mediators in POEMS syndrome with pulmonary hypertension: case report and review of the literature. 1065 28