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)

Cellular and genetic analyses of interleukin-2 (IL-2) production and IL-2 receptor (IL-2R) expression were examined in a immunodeficient patient and his family members. Mononuclear cells (MNC) of the patient showed no proliferative response (stimulation index, less than 2) to T-cell mitogens (PHA and Con A) and were defective in IL-2 production and IL-2R expression (less than 1%), whereas productions of other lymphokines (B-cell differentiation factor and IFN-gamma) were not impaired significantly. His brother died of the same disease and his father also lacked in proliferative response and IL-2 production by PHA stimulation. In Southern blot analyses using DNA probes of IL-2 and IL-2R, patterns of the patient were the same as those of healthy volunteers, whereas the transcription of DNA coding for IL-2R to mRNA was lacking in the patient. These results suggest that inheritant defects of IL-2 production and IL-2R expression reside in this family and the defects are not linked to DNAs coding for IL-2 and IL-2R but to a transcriptional deficiency.
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PMID:Cellular and genetic analyses of IL-2 production and IL-2 receptor expression in a patient with familial T-cell-dominant immunodeficiency. 312 Dec 26

Interleukin-1 (IL-1) exhibits multiple biological properties on various tissues by modulating immunologic, inflammatory, metabolic, and neurologic functions. Considerable attention has focussed on the measurement of IL-1 activity. We reported a simple, sensitive, and specific bioassay for IL-1 using human melanoma A375 subclone which is highly sensitive for the cell growth inhibitory activity of IL-1. This bioassay method is allows detection of as low as 10pg of IL-1 beta/ml or 30pg of IL-1 alpha/ml. Since this A375 subclone cell dose not respond to prostaglandin E2 plant lectins, lipopolysaccharide, and cytokines such as interleukin-2, interleukin-6, tumor necrosis factor, interferon or colony-stimulating factor, it is an extremely useful and rapid method for the measurement of IL-1 activity in a variety of experimental and clinical conditions. The assay method was used in the presence of antisera to IL-1 beta to discriminate two species of IL-1, IL-1 alpha and IL-1 beta, produced in human peripheral mononuclear cells.
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PMID:A simple, sensitive bioassay for the detection of interleukin-1 using human melanoma A375 cell line. 326 84

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

A culture system that allows human blood monocytes to differentiate into macrophages in vitro was used to study B-cell stimulatory factor-2/interleukin-6 (interferon-beta 2/26 kd protein) expression in mononuclear phagocytes. Using B-cell stimulatory factor-2 (BSF-2) cDNA and a polyclonal, monospecific antibody directed against human BSF-2, we find that strong interleukin-6 (IL-6) expression is initiated in cultured monocytes on stimulation with endotoxin. Maximally induced monocytic BSF-2/IL-6 synthesis (1% to 2% of total proteins secreted by monocytes) is more than ten times stronger than in terminally differentiated macrophages (approximately 0.1% of total secretory proteins). BSF-2/IL-6 mRNA was detectable as early as one hour after stimulation with endotoxin, reaching maximum levels three hours after stimulus. Interleukin-1 (IL-1) was able to stimulate IL-6 synthesis in monocytes, but not in macrophages. Tumor necrosis factor, interferon-gamma and interleukin-2 (IL-2) had no effect on IL-6 synthesis in monocytes or macrophages. We found five molecular weight forms of BSF-2/IL-6 to be secreted by monocytes of 21.5 kd, 23.5 kd, 24 kd, 26 kd, and 28 kd apparent molecular weight. The 26 kd and 28 kd forms were found to represent N-glycosylated molecules, which were not detectable on treatment of the cells with the N-glycosylation inhibitor tunicamycin. The 21.5 kd, 23.5 kd, and 24 kd BSF-2/IL-6 forms were unaffected by tunicamycin treatment. We conclude from our data that cells of the mononuclear phagocyte lineage are one of the main sites of BSF-2/IL-6 (interferon-beta 2/26 kd protein/HSF) synthesis.
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PMID:Regulation of interleukin-6 expression in cultured human blood monocytes and monocyte-derived macrophages. 326 81

The induction of antibody secretion by B cells requires T-cell-derived factors1-5. Such factors have been described1,2,6-12 but the precise relationship among these various factors is not clear, and it has been difficult to demonstrate that these factors act directly on the B cell and do not exert their effect via T cells or macrophages. In this report we describe the direct induction of IgM synthesis and secretion in cloned lines of long-term tissue culture adapted neoplastic B cells (BCL1) by T-cell supernatants from phorbol-12-myristate 13-acetate (PMA)-induced EL-4 cells or concanavalin A (Con A)-induced 7.1.1a cells5,9. We have termed this activity BCDFmu (B-cell differentiation factor for IgM). The supernatants containing BCDFmu induce activated and neoplastic B cells to secrete IgM5 and the factor responsible is distinct from BCGF13, interleukin-2 (IL-2)5, the classical T-cell replacing factor (TRF) described by Schimpl and Wecker5, and immune interferon (IFN gamma)5.
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PMID:Lymphokine-induced IgM secretion by clones of neoplastic B cells. 660 74

Although previous studies have shown that simple laparotomy produces a depression in peritoneal macrophage (Mphi) antigen presentation capacity, it remains unknown whether the adverse effects of laparotomy are limited to peritoneal Mphi or whether such an insult also affects splenocyte immune function. To study this, mice were anesthetized and a 1-inch midline abdominal incision was made, followed by abdominal closure. At 2 and 24 hours after the surgical procedure, the animals were killed, splenocyte cultures established and stimulated for 48 hours with concanavalin A (2.5 micrograms/mL), while peritoneal macrophage cultures were stimulated with LPS (10 micrograms/mL). The proliferative capacity of the splenocytes, as well as their ability to release interleukin-2 and interleukin-3, was markedly decreased at 2 as well as 24 hours after laparotomy. Furthermore, the release of interleukin-6 by splenic and peritoneal macrophages from animals that underwent laparotomy were also significantly depressed at both 2 and 24 hours. These results support the concept that surgical stress in the form of midline laparotomy per se is sufficient to produce a significant impairment in cell-mediated immunity, thus setting the stage for increased incidence of postoperative complications.
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PMID:Effect of surgical trauma on splenocyte and peritoneal macrophage immune function. 747 48

Immunoregulatory cytokines have been implicated in the pathophysiology of graft dysfunction after heart transplantation (HTx). In 15 consecutive patients undergoing HTx we prospectively determined levels of interleukin-6 (IL-6), tumor-necrosis-factor-alpha (TNF-alpha), interleukin-2 (IL-2), and soluble-interleukin-2-receptor (sIL-2-R) at eight points in time during biopsy and right heart catheterization and within 12 hr of echocardiography during the first three months after HTx. Blood was taken from the pulmonary arterial line. IL-6-levels correlated positively with hemodynamic and echocardiographic parameters of pump dysfunction--namely, pulmonary capillary wedge pressure, pulmonary arterial pressure, right atrial pressure, heart rate--and negatively with isovolumic relaxation time and stroke volume independent of the degree of cellular rejection as classified by the ISHLT criteria. A similar pattern was found for TNF-alpha- and sIL-2-R, while IL-2 correlated negatively with left and right heart filling pressures and positively with fractional shortening. In the three patients who died of sepsis or multiorgan failure within the study period IL-6-, TNF-alpha, and sIL-2-R-levels were elevated and IL-2-levels were suppressed compared with the 12 patients with a stable clinical course. IL-6 and sIL-2-R correlated positively while IL-6 and IL-2 correlated negatively. In this pilot study, a cytokine pattern with elevated levels of IL-6, TNF-alpha, and sIL-2-R as well as suppressed levels of IL-2 in the early period after HTx corresponds to impaired hemodynamics independent of cellular rejection and may indicate an unfavorable prognosis. These cytokines may therefore be useful for monitoring and warrant further study.
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PMID:The relation of interleukin-6, tumor necrosis factor-alpha, IL-2, and IL-2 receptor levels to cellular rejection, allograft dysfunction, and clinical events early after cardiac transplantation. 748 19

The potential for 41.8 degrees C whole body hyperthermia (WBH) to enhance ionizing irradiation and cytotoxic chemotherapy without a commensurate increase in normal tissue toxicity is currently receiving renewed clinical interest. Additionally, WBH may have other biological sequela which may be clinically exploited. In this paper, data are summarized revealing the ability of WBH to induce elevated plasma levels of granulocyte-colony stimulating factor (G-CSF), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-alpha) within hours of WBH. Data regarding TNF-alpha shows induction in only a proportion of patients. No induction of C-reactive protein (CRP) or the following cytokines was observed: granulocyte macrophage-colony stimulating factor (GM-CSF), interferon-gamma (IFN-gamma), interleukin-1 alpha (IL-1 alpha), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-7 (IL-7), interleukin-11 (IL-11), interleukin-12 (IL-12), macrophage-colony stimulating factor (M-CSF), and macrophage inflammatory protein-1 alpha (MIP-1 alpha). Data regarding interleukin-3 (IL-3) and transforming growth factor-beta 1 (TGF-beta 1) were variable and inconclusive. The implications of these results to past and future clinical trials are discussed.
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PMID:Cytokine induction by 41.8 degrees C whole body hyperthermia. 749 63

The original descriptions of polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) in the medical literature date back to 1888 and 1890, respectively. Classification criteria for PMR and GCA are not standardized since most authors used subjective criteria based on their personal experience. Only one study has evaluated criteria for PMR and has found seven variables with high discriminant value. Criteria for GCA are less varied because a positive biopsy of the temporal artery is diagnostic. However, combinations of different clinical and laboratory features have been used for diagnosis when biopsy is negative or missing. Assessment of PMR/GCA is based on the serial determination of markers of acute phase such as ESR, CRP, or plasma viscosity. However, their value in predicting recurrence of the diseases is poor. New immunological factors including soluble interleukin-2 receptors, interleukin-6, serum soluble CD8, and serum soluble intercellular adhesion molecule-1 are presently under investigation.
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PMID:Polymyalgia rheumatica and giant cell arteritis. 749 36

The effect of recombinant human granulocyte colony-stimulating factor (rhG-CSF) on cytokine profile was evaluated in a case of severe congenital neutropenia. The plasma levels of cytokines were measured before and during rhG-CSF therapy. These included G-CSF, granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1 alpha, interleukin-1 beta, interleukin-2 (IL-2), interleukin-3 (IL-3), interleukin-4, interleukin-6 (IL-6), and tumor necrosis factor-alpha. Soluble interleukin-2 receptor (sIL-2R) was measured serially during rhG-CSF therapy. Lymphocyte subpopulations including CD2, CD3, CD4, CD8, CD19, CD20, and CD25 were also measured, rhG-CSF was administered once daily as a 30-min infusion. The patient was treated with increasing dose levels of 100, 200, 400, 800, and 1,600 micrograms/m2/day. The level of endogenous G-CSF was elevated to 334 pg/ml before treatment and GM-CSF, IL-2, IL-3, and IL-6 were slightly elevated. Clinically, he showed a moderate response to a high dose of rhG-CSF (1,600 micrograms/m2/day). Plasma levels of G-CSF markedly increased during therapy but plasma levels of other cytokines did not show significant changes during therapy and lymphocyte subpopulations did not significantly change. A drastic increase in sIL-2R expression was observed after rhG-CSF infusion and an increase in sIL-2R expression occurred even before a major increase in granulocyte counts. These results showed that a high dose rhG-CSF therapy may influence the cytokine network as judged by the increased sIL-2R expression.
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PMID:Cytokine profile during high-dose rhG-CSF therapy in severe congenital neutropenia. 750 1


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