Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 58-year-old man developed polyneuropathy, organomegaly, gynecomastia, skin pigmentation, and multiple myeloma (IgG-lambda type). Although transient clinical improvement was obtained with prednisolone and cyclophosphamide, his general condition deteriorated progressively, and he died 3 years after onset. Lymph nodes showed angiofollicular hyperplasia, and the sural nerve revealed segmental demyelination. At autopsy, the glomeruli were enlarged and showed mild mesangial cell proliferation with segmental mesangiolysis and proliferation of endothelial cells forming abnormal vessels. The massive volume of ascites contained a high level of interleukin-6 (IL-6). IL-6, a multifunctional cytokine, may be the pathogenic factor which induces the various clinical symptoms and pathological features of Crow-Fukase (POEMS) syndrome.
 ...
PMID:An autopsy case of Crow-Fukase (POEMS) syndrome with a high level of IL-6 in the ascites. Special reference to glomerular lesions. 147 60

The distribution of CD3+ T lymphocytes and the expression of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF alpha) by macrophages in canine lymph nodes with mineral-associated lymph-adenopathy, granulomatous lymphadenitis or reactive hyperplasia was examined immunohistochemically. In areas of preserved lymph node architecture, CD3+ T lymphocytes were located in the paracortex, with scattered cells in the follicular mantle and germinal centre, and small aggregates in the medullary cords. T cells were prominent within areas of diffuse granulomatous inflammation and formed a peripheral rim around microgranulomas. TNF alpha expression was demonstrated in macrophages from seven of 11 dogs with mineral-associated lymphadenopathy, one of five dogs with granulomatous lymphadenitis and three of five with reactive hyperplasia. Positive macrophage staining for IL-1 beta and IL-6 was seen in two lymph nodes with reactive hyperplasia. Lymph nodes from control (clinically normal) dogs showed no evidence of cytokine expression. Neutrophils expressing IL-1 beta were observed within the medullary sinuses of two lymph nodes with mineral-associated lymphadenopathy and one with reactive hyperplasia, and in the inflammatory infiltrate in one lymph node with granulomatous lymph-adenitis. The sensitivity of immunohistochemical examination as a means of detecting cytokines in abnormal tissue is discussed.
 ...
PMID:Expression of interleukin-1 beta, interleukin-6 and tumour necrosis factor alpha by macrophages in canine lymph nodes with mineral-associated lymphadenopathy, granulomatous lymphadenitis or reactive hyperplasia. 872 78

Castleman's disease is a rare B cell lymphoproliferative disorder related to excess interleukin-6 (IL-6)-like activity. Kaposi's sarcoma-associated herpesvirus (KSHV or HHV8), which encodes a functional cytokine (vIL-6), has been found in some patients with Castleman's disease. Lymph nodes from 14 HIV-seronegative Castleman's disease patients were compared to hyperplastic lymph nodes from 25 HIV-seronegative patients as well as Kaposi's sarcoma lesions from 48 patients for KSHV infection and vIL-6, human IL-6, and Epstein-Barr virus EBER expression. While all Kaposi's sarcoma tissues examined were polymerase chain reaction-positive and all control lymph nodes were polymerase chain reaction-negative for KSHV, none had detectable vIL-6 expression. Six of 14 (43%) Castleman's tissues were positive for KSHV by polymerase chain reaction and all 6 had evidence of vIL-6 expression by immunohistochemistry. vIL-6-positive Castleman's disease patients generally had the multicentric plasma cell variant form of the disease and had a rapidly fatal clinical course frequently associated with autoimmune hemolytic anemia and gammopathy. In contrast, 7 (88%) of the 8 vIL-6-negative Castleman's disease patients had localized disease and have remained disease-free after therapy. KSHV vIL-6 expression appears to be limited to hematopoietic cells and is not present in Kaposi's sarcoma spindle cells. These data suggest that Castleman's disease is a syndrome of multiple etiologies involving aberrant IL-6 activity from either endogenous or viral sources.
 ...
PMID:Expression of a virus-derived cytokine, KSHV vIL-6, in HIV-seronegative Castleman's disease. 940 1

Lymph nodes from 44 patients with Castleman disease (CD) without risk factors for HIV infection were analyzed with polymerase chain reaction (PCR), in situ hybridization (ISH), and immunohistochemical analysis for human herpesvirus 8 (HHV-8) and viral interleukin-6 (vIL-6). PCR detected HHV-8 genome in 2 of 4 cases; ISH detected it in 9 of 16 cases. HHV-8 vIL-6 peptides were detected in 2 of 44 cases. vIL-6- and ISH-positive cells were found in large transformed and small lymphocytes of the follicular mantle, respectively. Of 9 cases of plasma cell (PC) CD that demonstrated HHV-8 genome by PCR or ISH, 1 expressed vIL-6. Clonal populations of PCs in CD by immunohistochemical analysis or immunoelectrophoresis of serum and urine were associated with neuropathy. HHV-8 vIL-6 detection was associated with poor survival and lack of HHV-8 IL-6, with low risk for subsequent lymphoma. Although HHV-8 genome was detected in a considerable number of patients with PC CD, vIL-6 expression was infrequent. Expression of HHV-8 vIL-6 in CD may indicate poor prognosis in patients at risk for lymphoma who may prospectively require more aggressive treatment. The lack of vIL-6 expression in CD with HHV-8 genome suggests that human IL-6 rather than vIL-6 may be the principal pathogenic cytokine.
 ...
PMID:Analysis of the human herpesvirus 8 (HHV-8) genome and HHV-8 vIL-6 expression in archival cases of castleman disease at low risk for HIV infection. 1186 23

Viral interleukin-6 (vIL-6) is a product of Kaposi's sarcoma-associated herpesvirus (KSHV) expressed in latently infected cells and to a higher degree during viral replication. A distinctive feature of vIL-6 is the ability to directly bind and activate gp130 signaling in the absence of other receptor subunits. Secretion of vIL-6 is generally poor, but vIL-6 can activate gp130 from inside the cell. Due to the wide cell distribution of gp130, vIL-6 has the potential to induce a wide range of biological effects. Expression of vIL-6 is variable in KSHV-associated Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), multicentric Castleman's disease (MCD), and in a newly described MCD-like systemic inflammatory syndrome observed in human immunodeficiency virus-positive patients. PEL effusions usually contain vIL-6 at high concentrations; since vIL-6 induces vascular endothelial growth factor, vIL-6 likely contributes to vascular permeability and formation of PEL effusions. Lymph nodes affected with MCD contain vIL-6-positive cells, and vIL-6 levels rise in conjunction with flares of the disease and likely contribute to symptoms of inflammation. The development of vIL-6 inhibitors is a potentially important advance in the treatment of KSHV-associated malignancies where vIL-6 is expressed.
 ...
PMID:Viral interleukin-6: role in Kaposi's sarcoma-associated herpesvirus: associated malignancies. 2176 54