Disease relevance of Il1

• Previous data indicated that several lines of murine sarcoma cells produced one or more activities that were able to regulate both Il-1 a and Il-1 b gene transcription in macrophages (MO) [1].
• Synovial fluids from patients with rheumatoid arthritis (13 cases), ankylosing spondylitis (six), psoriatic arthritis (two), osteoarthritis (three) and rubella arthritis (four) contain interleukin-1 (Il-1) activity as measured in the CH3/He mouse thymocyte assay [2].
• The PHT-induced Il-1 activity may be of importance in the development of gingival overgrowth [3].

High impact information on Il1

• B2m variants within the H3a-Il1 interval may represent one of these [4].
• After this time, the response of B cells depends no longer on the presence of Il-1 but on the presence of T cells or TRF [5].
• The presented data suggest that antigen-primed helper T cells (but not unprimed T cells) induce the release of Il-1 by macrophages, thereby also influencing the early phase of B cell differentiation [5].
• This is demonstrated in experiments in which Il-1 increases the number of B cells capable of responding to T cell help [5].
• Previous experiments indicated that repeated intraperitoneal injections of the Il-1 receptor antagonist (Il-1Ra), which inhibits binding of interleukin-1 (Il-1) to the type 1 Il-1 receptor (Il-1Rt1) blocks blastocyst implantation in superovulated mice [6].

Biological context of Il1

• Finally, the addition of murine Il-1 in vitro to cultures of burn-derived APCs, antigen, and T cell clone restored Th cell proliferation to control levels (from 38.3% to 92.8%) without nonspecifically enhancing similar cultures employing normal APCs [7].
• Concentrations of zinc which have been shown to restore antibody formation in cells from aged mice and to increase the production of Il-1 and Il-4 inhibited the production of Il-2 [8].
• The aim of the present study was to determine whether interleukin 1 alpha (Il-1), a cytokine known to have a stimulatory effect on collagenase production, also influences the phagocytosis and intracellular digestion of collagen fibrils by fibroblasts [9].
• When the effect of Il-1 on the major metabolic pathways of the adipocyte was investigated, lipolysis as measured by glycerol release from the cells was markedly enhanced after a 17 h incubation with the hormone, while no effect was observed on de novo fatty acid synthesis [10].

Anatomical context of Il1

• Blood monocytes produce two well-defined cytokines, tumor necrosis factor/cachectin (TNF) and Il-1, that have multiple immunologic and inflammatory functions [11].
• The present results suggest that Il-1 does not cause its effect on T lymphocytes via the same mechanism of protein kinase C activation that has been proposed for TPA [12].
• Il-1 showed only a very marginal growth inhibitory activity and the effects of its combination with DXR were essentially additive in all the cell lines, except in chemosensitive B16, where a slight synergism occurred [13].
• The results indicated that neither in calvarial nor in long bone periosteum the uptake and intracellular degradation of collagen by fibroblasts was influenced by Il-1 [9].
• Cultures of isolated B lymphocytes produced antibody to sheep red blood cells if the cells were provided with supplemental zinc and Il-1 [8].

Associations of Il1 with chemical compounds

• Il-1 required the simultaneous presence of ionomycin and TPA to have any demonstrable effect on T lymphocytes from spleen and on thymocytes [12].
• In addition, Il-1 increased the percentage of thymocytes resistant to hydrocortisone [14].
• The activity of Il-1 in the supernatant from macrophage cultures, stimulated with carbonyl iron powder, was calculated [14].
• That this activity is Il-1 was shown by: (i) the time course of thymocyte stimulation; (ii) failure of PHA blast cells to absorb out the activity; (iii) molecular weight of 15,000-20,000 daltons, and (iv) ability to stimulate prostaglandin E2 production from synovial cells [2].
• Furthermore, addition of the prostaglandin synthesis inhibitor indomethacin gave rise to increased Il-1 production, HLA-class II expression, and a stronger antigen-specific T-cell response to PPD [15].

Regulatory relationships of Il1

• Analysis of collagenase activity in the media demonstrated that under the influence of Il-1 collagenase release increased about 1.5- to 2-fold, most of the enzyme being in a latent form [9].

Other interactions of Il1

• These results indicate that IL-1 assays using LBRM33 1A5 and D10-G4.1 selectively detect Il-1, and are more specific assays for the detection of IL-1 in samples that may also contain IL-6 [16].
• The mechanism of inhibition is not due to production of soluble factors, consumption of available interleukin-1 (Il-1) or Il-2, but is dependent on cell-to-cell contact [17].
• Il-1 in vitro did not improve Th cell function in the absence of antigen [7].
• The media also proved to contain an inhibitor of collagenase, its production not being affected by Il-1 [9].

Analytical, diagnostic and therapeutic context of Il1

• A new method of determination of Il-1 activity, based on the inhibition of the autologous rosette formation by Il-1 is described [14].

References