Disease relevance of Il2

• 4. Intravenous administration of desArg9Leu8BK (10 nmol kg-1) or Hoe 140 (100 pmol kg-1) following IL-1 beta (1 mu), IL-2 (10 mu), or IL-8 (0.1 mu) reversed the subsequent hyperalgesia [1].
• The effect of IL-2 was also abolished after pretreatment with pertussis toxin (PTX, 5 mg/l), but not by genistein (100 microM) [2].
• Gfi-1 is a cellular proto-oncogene that was identified as a target of provirus integration in T-cell lymphoma lines selected for interleukin-2 (IL-2) independence in culture and in primary retrovirus-induced lymphomas [3].
• Considering that uncontrolled division of cells may result from either excessive growth stimulation or deficient growth inhibition, the regulation of pituitary cell growth by IL-2 and IL-6 together with their intrinsic pituitary production could be of potential importance in pituitary adenoma pathogenesis [4].
• Thus, TF5 and cytokines have opposite effects on adenoma cells because IL-2 and IL-6 stimulate GH3 cell proliferation [5].

Psychiatry related information on Il2

• The present investigation assessed the effects of several systemically administered cytokines (IL-1beta, IL-2 and IL-6) on reward processes by evaluating responding for rewarding intracranial self-stimulation (ICSS) from the lateral hypothalamus [6].
• During juvenile stages, neonatal interleukin-2 treatment increased exploratory locomotor activity, whereas other cytokine treatments did not [7].
• At the post-puberty stage, however, the interleukin-2-induced abnormal motor activity became undetectable, whereas interleukin-1 alpha-treated rats developed abnormalities in startle response, prepulse inhibition (PPI), and social interaction [7].
• Effects of intra-hippocampal injection of interleukin-2 on pain threshold and formaldehyde-induced substance P-like immunoreactivity in periaqueductal gray and spinal cord [8].

High impact information on Il2

• CD45R+ or RB+ CD4 T cells are potent in graft-versus-host reactions, and interleukin-2 related activities, whereas the CD45R0+ subset responds in vitro to recall antigens and provides help for antibody synthesis [9].
• Interleukin-2 augments natural killer cell activity [10].
• This enzyme dimerizes interleukin-2, and the product is cytotoxic to oligodendrocytes in vitro [11].
• In both transient transfections and T lymphocyte-specific in vitro transcription, the homeodomain-containing protein Oct-1 participated in the inducible regulation of transcription of the IL-2 gene [12].
• Interleukin-2 did not alter the growth of either type of glial cell [13].

Chemical compound and disease context of Il2

• While other proinflammatory cytokines (interleukin 1beta, IL-2, IL-6) did not interfere with the astrocytic glutamate response, incubation in CSF from septic meningitis patients (CSF-SM) also reduced the glutamate induced intracellular Ca2+ increase [14].
• At 3.5 h after IL-1 beta, IL-2, or IL-8, administration of des-Arg9,Leu8-BK or HOE-140 (iv) completely reversed the hyperalgesia [15].
• Increased PGE2 production does not appear to be responsible for the IL-2 alterations in colitis [16].
• The addition of indomethacin to LPMC cultures decreased PGE2 levels in all groups, whereas IL-2 activity increased only for the chronic and resolved colitis groups [16].
• IL-2 can cause vascular leakage and edema and for this reason we examined the antitumor activity of a combined treatment with IL-2 and melphalan in our well-established ILP in soft tissue sarcoma-bearing rats (BN175) [17].

Biological context of Il2

• IL-1 alpha slightly increased vascular permeability, whereas recombinant IL-2 and recombinant tumour necrosis factor alpha had no significant effects [18].
• There was no difference in IL-2 gene expression between control and experimental animals in either hemisphere [19].
• Then, IL-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha cDNA levels were measured post-mortem using semi-quantitative, competitive, reverse transcription polymerase chain reaction [20].
• It is concluded that the effects of IL-2 on contraction and the [Ca2+]i transient of ventricular myocytes are mediated via the cardiac kappa opioid receptor, and the postreceptor signal transduction pathway includes a PTX-sensitive G protein and phospholipase C [2].
• In GH3 cells, both IL-2 (1-100 U/ml) and IL-6 (10-500 U/ml) significantly stimulated [3H]thymidine incorporation and cell count [4].

Anatomical context of Il2

• Furthermore, OX62(+) VDCs from infected rats primed naïve CD4(+) T-cell proliferation and release of cytokines, including gamma interferon, IL-2, IL-6, and IL-10, in response to staphylococcal enterotoxin B stimulation in vitro [21].
• To dissect the immunosuppressive activity of AMF, the effect of AMF on cytokine production and interleukin 2 (IL-2) receptor expression of concanavalin A-stimulated lymphocytes were investigated [22].
• Effects of interleukin-6, interleukin-2, and tumor necrosis factor alpha on transferrin release from Sertoli cells in culture [23].
• Effect of maternal ethanol consumption on in vitro tumor necrosis factor, interleukin-6 and interleukin-2 production by rat milk and blood leukocytes [24].
• In this study, we show the effect of Substance P on the production of Tumor Necrosis Factor-alpha, Interleukin 1-beta, Interleukin 2, and Interleukin 6 by T-lymphocytes, macrophages and neutrophils [25].

Associations of Il2 with chemical compounds

• IL-2, IL-6 and IL-8 did not affect the production of nitrite, a stable metabolite of NO, by VSMC [26].
• RESULTS: Pretreatment of the rings with IL-6 (10 ng/ml) for 180 min caused a significant inhibition of their contraction in response to 10(-5) M phenylephrine, wile Il-2 (10 ng/ml) and IL-8 (100 ng/ml) showed no significant effect on the contraction [26].
• With T. spiralis antigen, Concanavalin A (Con A) or lipopolysaccharide stimulation, milk cells from both ethanol-treated and pair-fed groups were capable of producing tumor necrosis factor (TNF), interleukin (IL)-6 and IL-2 [24].
• Milk cells from the ethanol group produced a significantly higher amount of IL-2 upon Con A stimulation, as compared with that from the pair-fed group (16 +/- 4 units/10(6) cells vs. 4 +/- 1 units/10(6) cells, p < 0.05) [24].
• In vitro interleukin 2 (IL-2) production increased, and tumor necrosis factor alpha, IL-1beta, prostaglandin E2, and leukotriene B4 production decreased in the CLA20 group [27].

Physical interactions of Il2

• Sequence of rat interleukin 2 and anomalous binding of a mouse interleukin 2 cDNA probe to rat MHC class II-associated invariant chain mRNA [28].

Regulatory relationships of Il2

• Effect of interleukin 1alpha and interleukin 2 over glucose metabolism in isolated uterus of restricted diet rats. Influence of NO and COX-2 [29].
• Effects of luteinizing-hormone-releasing hormone, alpha-melanocyte-stimulating hormone, naloxone, dexamethasone and indomethacin on interleukin-2-induced corticotropin-releasing factor release [30].
• Interleukin-2-activated rat natural killer cells express inducible nitric oxide synthase that contributes to cytotoxic function and interferon-gamma production [31].
• CONCLUSION: Recipient intramuscular cotransfection of transforming growth factor beta1 and interleukin 10 suppressed interleukin 2 expression and provided a synergistic effect that reduced acute lung graft rejection [32].
• The failure of Thy-1 and Ly-6 to trigger interleukin-2 production in the absence of surface T-cell antigen receptor complex (TCR) expression has been interpreted to suggest that functional signalling via these phosphatidylinositol-linked alternative activation molecules is dependent on the TCR [33].

Other interactions of Il2

• In cultured rat VSMC, synthesis of cAMP was increased time-dependently by IL-6, while IL-2 and IL-8 failed to show any significant effects [26].
• CD5(-) CD4(-) CD86(-) CD80(-) CD134L(+) VDCs from infected, but not noninfected, rats spontaneously released large amounts of interleukin-12 (IL-12) and tumor necrosis factor alpha, whereas all VDC subsets released comparable levels of IL-10 and IL-2 cytokines [21].
• Interleukin-2 and interferon-gamma mRNA showed maximal expression on POD 12, while in autografts, a marked decrease was observed after POD 3 [34].
• However, under our experimental conditions, IL1 alpha, IL2 and MCSF mRNA were not observed [35].
• 2. Co-administration of IL-1 receptor antagonist (0.1 micrograms) with IL-1 beta (1 mu), IL-2 (10 mu) or IL-8 (0.1 mu) prevented the subsequent development of the hyperalgesia [1].

Analytical, diagnostic and therapeutic context of Il2

• In this study, we examined the effects and possible mechanisms of interleukin-2 (IL-2) on contraction and the [Ca2+]i transient of enzymatically isolated ventricular myocytes with spectrofluorometry and video tracking [2].
• Moreover, IL-2 expression is frequently suppressed in models of allograft tolerance [36].
• IL-2 and IFN-gamma transcripts were found in allogeneic grafts at 1, 3, 5, and 7 days after transplantation with a peak at day 5, but these cytokines were almost absent from syngeneic grafts [37].
• Graft survival and IL-2 biosynthesis by reverse transcriptase-polymerase chain reaction in spleen and graft biopsy specimens were assessed [36].
• Northern blot analysis demonstrated that the level of Tf mRNA in cultures of polygonal astrocytes increased 148% above the level observed in untreated controls following treatment with either IL-1 or TNF, whereas no change was observed following treatment with IL-2 [38].

References