Disease relevance of IL2

• After purification recombinant ovine IL-2 was functionally active as shown by its ability to support the proliferation of Con A-activated T cells and was capable of generating maedi visna virus-specific cytotoxic T cells from primed precursor cells [1].
• Since no side effects are observed, the IL2-IgG2b fusion protein may expand the therapeutic repertoire of reagents used for the treatment of allograft rejection and autoimmune diseases [2].
• T-cell-mediated cytotoxicity against autologous malignant melanoma: analysis with interleukin 2-dependent T-cell cultures [3].
• Inotropic and vasoactive drug treatment of interleukin 2 induced hypotension in sheep [4].
• This study examines the mechanism of respiratory failure related to IL-2, using sheep with chronic lung lymph fistulae [5].

High impact information on IL2

• Following T cell activation, the genes encoding IL-2 and the various chains of its receptor are transcriptionally induced [6].
• We have found that interleukin 2 stimulation of peripheral blood lymphocytes generates a cytotoxic activity against human monocytes [7].
• In the second stage, IL-2 directly triggered the responsive T cells to release B cell helper factors [8].
• Spleen cells thoroughly depleted of T cells required both IL-2 and this factor to produce antibody-secreting cells in response to sheep erythrocytes, although in the presence of IL-2 and a few T cells the requirement for the factor was less apparent [9].
• This fusion protein binds to IL-2 and Fc receptors and supports IL-2-dependent cell proliferation but does not mediate lysis of IL-2 receptor-positive cells in the presence of murine complement in vitro [2].

Chemical compound and disease context of IL2

• Mice were intranasally inoculated with Mycoplasma pulmonis (M. pul) and treated with IL-2, CYA, or minocycline (MINO) every day between Days 3 and 9 [10].
• Effects of interleukin-2 and cyclosporin A on pathologic features in Mycoplasma pneumonia [10].
• Steroid pretreatment reduces interleukin-2 toxicity in sheep [11].
• Each MC 1 microM suppressed phorbol 12-myristate 13-acetate (PMA) plus ionomycin-induced IL-2 mRNA expression in splenocytes and thymocytes, but not in EL-4 mouse thymoma cells [12].

Biological context of IL2

• Nevertheless, no significant differences in IL2 transcription between the genotypes could be detected [13].
• The obtained results argue against an impact of this polymorphism on the IL2 transcription and the genetic disease resistance in sheep [13].
• Functionally, they were able to provide "help" for antibody production, and they could be stimulated to produce moderate amounts of interleukin-2, while unable to proliferate in response to mitogens [14].
• In contrast, the non-IL-2-infused sheep (n = 3) recruitment of the lung vasculature by left atrial balloon inflation led to a rise in QL from 2.4 to 8.2 ml/30 min, whereas the L/P ratio declined from 0.62 to 0.25, suggesting that the protein-rich lymph flow after IL-2 administration reflected increased microvascular permeability [15].
• We studied the effect of the anticancer drug taxol on the cytotoxic mechanism of major histocompatibility complex nonrestricted lymphocytes and their activation with interleukin 2 [16].

Anatomical context of IL2

• However, in vivo the IL2-IgG2b fusion protein suppresses both cellular and humoral immune responses after immunization with sheep erythrocytes [2].
• The data suggests a sequential exit of T cell subsets from an antigen-stimulated lymph node and that the appearance of IL2-like activity and IL2-responsive cells in efferent lymph fluid are temporally distinct events [17].
• B cell helper factors. I. Requirement for both interleukin 2 and another 40,000 mol wt factor [9].
• Dendritic cells induce T lymphocytes to release B cell-stimulating factors by an interleukin 2-dependent mechanism [8].
• Thus, IL-2-activated T cells and NK cells form conjugates with and directly inhibit the growth of C. neoformans [18].

Associations of IL2 with chemical compounds

• For this purpose, transcription of IL2 mRNA was quantified by real-time polymerase chain reaction in unstimulated PBMC and in PBMC incubated for 4h in the presence of concanavalin A (ConA) or phorbol 12-myristate 13-acetate plus ionomycin (PMA/I) [13].
• Role of thromboxane in interleukin 2-induced lung injury in sheep [15].
• IL-2, 10(5) units/kg (n = 6), or its excipient control (n = 5) was given as an i.v. bolus over 2 min [15].
• Pretreatment with the Tx synthetase inhibitor OKY 046 (n = 7) lowered baseline plasma and lymph TxB2 levels to 22 and 52 pg/ml (P less than 0.05) and prevented the IL-2-induced increase in plasma and lung lymph TxB2 (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)[15]
• IL 2 mRNA could be superinduced several folds by addition of cycloheximide 3 hr after induction of J32 with mitogens [19].

Other interactions of IL2

• Interferon-gamma and interleukin-2 release by lymphocytes derived from the blood, mesenteric lymph nodes and intestines of normal sheep and those affected with paratuberculosis (Johne's disease) [20].
• Few B cells (lymphocytes with either immunoglobulin or Ia-like antigen on the cell surface), and few cells with receptors for transferrin and interleukin 2 were detected [21].

Analytical, diagnostic and therapeutic context of IL2

• cDNA cloning of ovine interleukin 2 by PCR [22].
• The molecular cloning of ovine interleukin 2 gene by the polymerase chain reaction [23].
• Fusion protein was detected in Western blot analysis with polyclonal antisera raised to recombinant bovine IL-2 [1].
• METHODS: We used the genetically engineered murine IL2-IgG2b fusion protein in a fully MHC-mismatched mouse keratoplasty model [24].
• These fractions also suppressed (p less than 0.001) IL-2-mediated blastogenesis of T-lymphocytes [25].

References