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

Interleukin-6 (IL-6) is a pleiotropic cytokine previously known as B cell stimulatory factor (BSF-2), interferon-beta 2 (IFN-beta 2), 26-kDa protein, and hepatocyte stimulating factor (HSF). The name IL-6 was proposed when the nucleotide sequences of the cDNAs for these proteins had been determined and the molecules were found to be identical. IL-6 production can be induced by a wide variety of agents in a wide range of cells, although IL-6 gene expression seems to be regulated in a tissue and stimulus specific manner. At least 3 different signal pathways regulate IL-6 gene expression, emphasizing its multiply inducible nature. The currently known activities of IL-6 include regulatory functions in hematopoiesis, immune reactions and acute phase responses. IL-6 appears to be a key member of the IL family; however, it is still poorly understood how IL-6 interacts with other lymphokines within the network. The anti-viral activity of IL-6 seems to be negligible. Elevated IL-6 levels have been found in diseases like rheumatoid arthritis, multiple myeloma and systemic lupus erythematosus. The abnormal expression and dysregulation of IL-6 in certain disorders may be a typical feature of this cytokine, making it the first cytokine that may be directly related to pathogenesis.
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PMID:Interleukin-6: historical background, genetics and biological significance. 219 19

Paired serum and cerebrospinal fluid (CSF) specimens from 14 patients with systemic lupus erythematosus (SLE) and central nervous system (CNS) involvement were studied for interleukin-6 (IL-6) activity using the IL-6-dependent murine hybridoma, MH60.BSF2. We also studied 23 patients with noninflammatory neurologic diseases, and 9 SLE patients without CNS involvement. CSF IL-6 activity was elevated only in SLE patients with CNS involvement, although there was no significant difference in serum IL-6 activity among the 3 groups. CSF IL-6 activity was not correlated with either the CSF-serum albumin quotient (Q albumin; an indicator of blood-brain barrier function) or serum IL-6 activity in SLE patients with CNS involvement. The CSF IL-6 activity decreased significantly when CNS manifestations subsided after successful treatment. These results indicate that determination of CSF IL-6 activity may be useful in the evaluation of CNS disease activity in SLE. Moreover, the data confirm the presence of immune system activation within the CNS in patients with SLE-associated CNS disease.
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PMID:Elevated levels of interleukin-6 in cerebrospinal fluid from patients with systemic lupus erythematosus and central nervous system involvement. 234 20

One of the mediators responsible for the induction of the production of acute phase proteins by hepatocytes is interleukin-6 (IL-6), formally known as hybridoma growth factor (HGF). In a prospective study the biological significance of IL-6, but also the relationship with the acute phase response (C-reactive protein [CRP], alpha 1-antitrypsin and alpha 1-acid glycoprotein) during flare-ups in 12 systemic lupus erythematosus (SLE) patients was investigated. Only 2 SLE patients showed sustained elevated IL-6 levels, and in one of these patients a clear correlation was found between the increases in IL-6 and the acute phase response. In the other SLE patients hardly any response or change in the levels of IL-6, CRP, and/or alpha 1-antitrypsin was found. In contrast to the profiles of alpha 1-acid glycoprotein, in seven of the SLE patients a significant increase in the serum levels took place in the period preceding the exacerbation. This difference between the three acute phase proteins suggests that the regulatory mechanisms are different. Our results are in agreement with the findings that IL-6 might be responsible for the CRP response.
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PMID:Interleukin-6 (IL-6) and acute phase proteins in the disease course of patients with systemic lupus erythematosus. 247 Dec 49

To investigate the differential stages of B cell activation in patients with systemic lupus erythematosus (SLE), the effects of recombinant interleukin-4 (rIL-4) interleukin-6 (rIL-6), and low mol. wt BCGF (1-BCGF) on B cell proliferation and differentiation were evaluated. In a co-stimulatory assay with anti-IgM, proliferative response to rIL-4 and 1-BCGF showed no significant differences between SLE patients and healthy controls. In a restimulation assay, after pre-activation with anti-IgM for 3 days, proliferative response to rIL-4 and 1-BCGF was significantly decreased in SLE patients compared with normal healthy controls (P less than 0.01). With regard to rIL-6 induced B cell differentiation, SAC-pre-activated low density, large B cells from both SLE patients and healthy controls differentiated well, whereas high density B cells did not differentiate at all. Of particular interest, low density B cells from active patients directly differentiated into Ig secreting cells in response to rIL-6 without SAC activation. These data indicate that heterogeneity of B cell responsiveness to B cell-tropic interleukins resulted from the discrete stages of B cell activation in SLE.
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PMID:Heterogeneity of B cell responsiveness to interleukin 4, interleukin 6 and low molecular weight B cell growth factor in discrete stages of B cell activation in patients with systemic lupus erythematosus. 278 39

Recent knowledge of B-lymphocyte physiology has clarified the role of T cell-derived lymphokines in clonal proliferation and differentiation of B-cell responses. Lymphokine production was analyzed in 19 systemic lupus erythematosus (SLE) patients and sex- and age-matched controls in relation to clinical activity and steroid treatment. When in vitro production of interleukin-2 (IL-2) and B-cell growth factor (BCGF) was tested, both activities were found to be diminished in the group of patients (P less than 0.01), while B-cell differentiation factor (BCDF) activity was higher in this group with respect to normal controls (P less than 0.01). Interestingly enough, this in vitro BCDF synthesis was positively correlated with clinical activity regardless of low-dose steroid treatment. A correlation was also found between BCDF production and the levels of IgG (r = 0.64, P less than 0.01), anti-DNA antibodies (r = 0.52, P less than 0.05), and the IgG/IgM ratio (r = 0.7, P less than 0.01) in serum. Implications of these abnormal T-lymphocyte functions in SLE with respect to in vivo B-cell function are discussed.
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PMID:The B-cell activation pathway in human systemic lupus erythematosus: imbalanced in vitro production of lymphokines and association with serum analytical findings. 326 33

We examined the production of and the response to B-cell growth factor (BCGF) and B-cell differentiation factor (BCDF) in 21 patients with systemic lupus erythematosus (SLE) and 23 normal subjects. T cells, 2.5 X 10(6)/ml, were cultured for 24 or 72 h with 1% phytohaemagglutinin (PHA). After absorption of PHA by chicken erythrocytes (CRBC), they were used for BCGF and BCDF. In inactive SLE, BCGF activity was significantly lower than that in normal subjects. Active SLE contained two separate groups, one showing normal BCGF activity and the other showing lower activity than normal. In contrast, BCDF activity from initial culture in active SLE was elevated. The B-cell response both to BCGF and BCDF was elevated in active SLE without Staphylococcus aureus Cowan I antigen (SAC) preactivation. However, the B-cell response to SAC was markedly disturbed. Thus SLE B cells were shifted to the mature state in vivo. We also demonstrated pivotal abnormalities of monocytes in SLE B-cell growth and differentiation. These results may contribute to the understanding of the abnormalities of T-B interactions and the overproduction of antibody in SLE.
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PMID:Abnormal production of and response to B-cell growth factor and B-cell differentiation factor in patients with systemic lupus erythematosus. 387 63

Tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) play a main role in inducing acute phase protein production by hepatocytes. This study describes the serum levels of TNF alpha and IL-6 in relation to serum levels of C-reactive protein (CRP) and alpha 1-acid glycoprotein (alpha 1AG) in three systemic lupus erythematosus (SLE) patients. Disease courses of these patients were divided in a total of 19 clinical periods, according to the clinical symptoms and interleukin profiles. Significantly elevated TNF alpha levels were found in all but three of the defined periods, without being associated with disease activity. In only four of the defined periods elevated TNF alpha were observed combined with elevated IL-6 and CRP levels. Two of these periods coincided with minor symptoms of SLE, one with an exacerbation and the other one with a systemic infection while SLE activity was low. All other periods showed varying combinations of elevated TNF alpha and/or IL-6 levels being followed or not by elevated CRP levels. Significantly raised alpha 1AG levels were measured in all clinical periods. In most of the observed periods a dissociation was found between TNF alpha and IL-6 and also between the different cytokine (TNF alpha and IL-6) levels and acute phase protein (CRP and alpha 1AG) levels. These data could not be explained by differences in disease course or influences of medication. We conclude that more factors other than TNF alpha and IL-6 must play a role in the regulatory pathway of the acute phase response in SLE.(ABSTRACT TRUNCATED AT 250 WORDS)
Lupus 1993 Dec
PMID:Profiles of cytokines (TNF alpha and IL-6) and acute phase proteins (CRP and alpha 1AG) related to the disease course in patients with systemic lupus erythematosus. 751 Oct 20

As several possible prognostic and therapeutic applications of interleukin-6 are currently under trial, the available methods for its quantification in biological fluids should be evaluated. In this report, the 7TD1 hybridoma bioassay is compared to an enzyme immunoassay for the determination of interleukin-6 in serum and plasma of normal subjects and patients with cancer, sepsis, and systemic lupus erythematosus, as well as in malignant pleural effusions and culture supernatants. The results show a good correlation between the two methods in all cases. Mean values of the examined groups were statistically different between the assays only in the case of septic patients. This may be attributed either to the influence of other molecules on the assays or to the nonlinearity of the dose-response curves. Since immunoassays are easier to perform, it seems that they are more suitable for routine use, the bioassay being preferable in cases where increased sensitivity is required.
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PMID:Bioassay vs. immunoassay for quantification of interleukin-6 in biological fluids. 756 40

The process of autoantibody production in systemic lupus erythematosus is characterized by findings of both an antigen-driven response and polyclonal B-cell activation. Autoantibody production does not appear to be critically dependent on the presence of the CD5+ B cell subset. Increasing evidence supports a role for T helper cell type 2 cytokines, such as interleukin-4 and interleukin-6, in promoting and perpetuating B-cell hyperactivity and autoantibody formation.
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PMID:B-cell and T-cell function in systemic lupus erythematosus. 769 Nov 38

It has been proposed that interleukin-6 may play a role in the pathogenesis of autoimmune diseases like lupus erythematosus. We have therefore investigated the immunoreactivity of IL-6 in 32 skin biopsies of 23 patients suffering from chronic discoid lupus erythematosus (n = 16), subacute cutaneous lupus erythematosus (n = 5) and systemic lupus erythematosus (n = 5) as well as in uninvolved skin (n = 6) and in normal skin from healthy volunteers (n = 3). Increased immunohistochemical staining was detectable in 14 of 26 biopsies from lesional skin. The remaining biopsies from lesional, non-lesional and normal skin displayed only minimal or no reactivity, but 8 out of 12 lupus erythematosus patients had been pretreated with local or systemic antiinflammatory drugs. Irrespective of the LE subtype, immunolabelling was generally most intense in the basal layer of the epidermis, with additional intense suprabasal staining in sections from 2 of 5 SLE patients. Preferential production of IL-6 in the lower parts of the epidermis was confirmed by RNA in situ hybridization. No correlation was found between the deposition of immunoglobulins and complement at the dermo-epidermal junction and IL-6 expression in keratinocytes. These data suggest that IL-6 may be involved in LE although its exact role in the pathogenesis of the disease needs to be further elucidated.
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PMID:Interleukin-6 expression in the skin of patients with lupus erythematosus. 775 33


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