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Journal articles on the topic 'IL-4'

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Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Usha, Prof. "IL-4 and IL-6 in Bronchial Asthma Does IL-6 Plays More Important Role than IL-4? A Preliminary Study." Journal of Medical Science And clinical Research 05, no. 04 (April 18, 2017): 20446–50. http://dx.doi.org/10.18535/jmscr/v5i4.115.

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2

Kelly-Welch, A., E. M. Hanson, and A. D. Keegan. "Interleukin-4 (IL-4) Pathway." Science Signaling 2005, no. 293 (July 12, 2005): cm9. http://dx.doi.org/10.1126/stke.2932005cm9.

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3

Borish, Larry. "IL-4 and IL-13 Dual Antagonism." American Journal of Respiratory and Critical Care Medicine 181, no. 8 (April 15, 2010): 769–70. http://dx.doi.org/10.1164/rccm.201002-0147ed.

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4

Schindler, C., H. Kashleva, A. Pernis, R. Pine, and P. Rothman. "STF-IL-4: a novel IL-4-induced signal transducing factor." EMBO Journal 13, no. 6 (March 1994): 1350–56. http://dx.doi.org/10.1002/j.1460-2075.1994.tb06388.x.

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5

Gause, W. C., T. Takashi, J. D. Mountz, F. D. Finkelman, and A. D. Steinberg. "Activation of CD 4-, CD 8- thymocytes with IL 4 vs IL 1 + IL 2." Journal of Immunology 141, no. 7 (October 1, 1988): 2240–45. http://dx.doi.org/10.4049/jimmunol.141.7.2240.

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Abstract Thymocytes from C57BL/6 mice were highly purified to obtain the CD 4-, CD 8- subpopulation which constitutes only 5% of all thymocytes. Substantial proliferation was induced in vitro with either IL-1 + IL-2 or with IL-4 in the presence of PMA. IL-1 and IL-2 synergized in inducing proliferation of these purified CD 4-, CD 8- thymocytes whereas neither synergized with IL-4. In order to determine whether stimulation with IL-1 + IL-2 acted via IL-4 or vice versa, cultures were treated reciprocally with affinity-purified anti-IL-2 or anti-IL-4 antibodies. Cultures with IL-4 were inhibited by anti-IL-4 but were unaffected by anti-IL-2. The CD 4-, CD 8- thymocytes cultured with IL-1 + IL-2 + anti-IL-2 were inhibited to baseline IL-1 stimulation. At low concentrations of IL-1 (1 U/ml) and IL-2 (100 U/ml), anti-IL-4 had no effect, whereas at higher levels of IL-1 (2 U/ml IL-1), and 100 or 200 U/ml IL-2, anti-IL-4 significantly reduced DNA synthesis. This result suggests that at higher concentrations the combination of IL-1 + IL-2 can induce cells to produce IL-4 which then contributes to overall proliferation. When CD 4-, CD 8- thymocytes were cultured with the low doses of IL-1 + IL-2 for 72 h, 62% expressed cell surface T3 complex (vs 11% at initiation) and 27% were F23.1+ (vs 5% at initiation). In contrast, culture with IL-4 led to no increase in numbers of T3+ cells and none were F23.1+; however, there was coexpression of Thy1 and 6B2 on 20% of cells at the end of culture (vs 4% at initiation). Thus, IL-1 + IL-2 causes expansion of a CD 4-, CD 8- thymocyte population expressing the alpha, beta-T cell receptor, whereas IL-4 induces cells to express a phenotype present in small numbers in the periphery of normal mice and in larger numbers in mice bearing the lpr gene.

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6

NAKANISHI, KENJI. "Interleukin cascade of IL-4,IL-5 and IL-2." Japanese Journal of Clinical Immunology 13, no. 5 (1990): 438–40. http://dx.doi.org/10.2177/jsci.13.438.

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7

Atamas, S. P., J. Choi, V. V. Yurovsky, and B. White. "An alternative splice variant of human IL-4, IL-4 delta 2, inhibits IL-4-stimulated T cell proliferation." Journal of Immunology 156, no. 2 (January 15, 1996): 435–41. http://dx.doi.org/10.4049/jimmunol.156.2.435.

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Abstract Alternative splicing of mRNA can generate protein isoforms that are preferentially expressed in different tissues or during different states of cell differentiation or activation. Protein isoforms may have different functions. In this study, we cloned, expressed, and tested functional effects of a naturally occurring splice variant of human IL-4, called IL-4 delta 2. In IL-4 delta 2, the second exon of IL-4 is omitted by alternative splicing, with exons 1, 3, and 4 joined in an open reading frame. We found that IL-4 delta 2 RNA is expressed in the PBMC of all donors tested, usually in lower amounts than IL-4 RNA. In contrast, IL-4 delta 2 RNA is expressed in much higher levels than IL-4 RNA in thymocytes and bronchoalveolar lavage cells, suggesting tissue specificity of expression. IL-4 delta 2 cDNA was expressed in yeast. Recombinant human (rh) IL-4 delta 2 was partially purified and found to be glycosylated, with a protein core of 13 to 15 kDa. Unlike rhIL-4, rhIL-4 delta 2 did not act as a costimulator for T cell proliferation. However, rhIL-4 delta 2 inhibited the ability of rhIL-4 to act as a T cell costimulator. Inhibition was independent of glycosylation and was not mediated by toxicity. Iodinated IL-4 delta 2 was found to bind specifically to human PBMC and tumor lines known to express IL-4 receptors. Excess unlabeled IL-4 inhibited cellular binding of labeled IL-4 delta 2. Thus, rhIL-4 delta 2 is a naturally occurring splice variant of IL-4 that is preferentially expressed in the thymus and airways and inhibits function of complete IL-4. The balance between IL-4 and IL-4 delta 2 may be important in the regulation of IL-4 effects.

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8

Noben-Trauth, N., L. D. Shultz, F. Brombacher, J. F. Urban, H. Gu, and W. E. Paul. "An interleukin 4 (IL-4)-independent pathway for CD4+ T cell IL-4 production is revealed in IL-4 receptor-deficient mice." Proceedings of the National Academy of Sciences 94, no. 20 (September 30, 1997): 10838–43. http://dx.doi.org/10.1073/pnas.94.20.10838.

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9

Ho, S. N., R. T. Abraham, A. Nilson, B. S. Handwerger, and D. J. McKean. "Interleukin 1-mediated activation of interleukin 4 (IL 4)-producing T lymphocytes. Proliferation by IL 4-dependent and IL 4-independent mechanisms." Journal of Immunology 139, no. 5 (September 1, 1987): 1532–40. http://dx.doi.org/10.4049/jimmunol.139.5.1532.

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Abstract The role of IL 1 in the activation of IL 4-producing murine T cell clones was investigated by using a calcium ionophore (ionomycin) or a phorbol ester (12-O-tetradecanoylphorbol 13-acetate; TPA) as T cell receptor-independent costimuli. The use of these pharmacologic agents to investigate IL 1-mediated T cell activation revealed two distinct mechanisms of activation. IL 1 in combination with ionomycin (iono/rIL 1) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies. Furthermore, inhibition of this proliferative response with an anti-IL 4 monoclonal antibody or cyclosporine indicated that IL 4 functions as an autocrine growth factor. In contrast, IL 1 synergized with TPA (TPA/rIL 1) to induce proliferation in the absence of either IL 4 or IL 2 gene transcription or lymphokine secretion. The IL 4-independence of this activation mechanism was further supported by the failure of both anti-IL 4 antibodies and cyclosporine to inhibit the response. In addition, activation by TPA/rIL 1 caused no detectable alteration in cytoplasmic calcium levels. Both IL 4-dependent and IL 4-independent activation responses were associated with the expression of functional receptors for IL 2 as well as IL 4. Characterization of these activation responses suggests that the synergistic activity of IL 1 during T cell activation is multipotential. The nature of an IL 1-dependent T cell growth response, therefore, may vary depending on the balance of intracellular signals generated concurrently through the T cell receptor complex and other regulatory surface molecules.

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10

Reich, Adam, Justyna Szczęch, and Dominik Samotij. "Biologics for Itch: IL-4/IL-13, IL-31, IL-17, and IL-23 Antagonists." Current Dermatology Reports 6, no. 4 (October 17, 2017): 263–72. http://dx.doi.org/10.1007/s13671-017-0204-7.

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11

Vélez, C., D. Williamson, and M. Koncurat. "IL-1β, IL-2, IL-4 and IL-10 profile during porcine gestation." Placenta 51 (March 2017): 116. http://dx.doi.org/10.1016/j.placenta.2017.01.065.

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12

Rubin, J. T., A. Brumfield, and H. T. Lotze. "OIL-BASED DELIVERY OF IL-2, IL-4, IL-12, and IL-15." Journal of Immunotherapy 16, no. 3 (October 1994): 243. http://dx.doi.org/10.1097/00002371-199410000-00044.

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13

Guida, Pier Luigi. "Il nuovo PMBOK "4"." PROJECT MANAGER (IL), no. 2 (June 2010): 15–20. http://dx.doi.org/10.3280/pm2010-002006.

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14

Pan, Ping-Ying, and Paul Rothman. "IL-4 receptor mutations." Current Opinion in Immunology 11, no. 6 (December 1999): 615–20. http://dx.doi.org/10.1016/s0952-7915(99)00026-6.

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15

Strait, Richard T., Suzanne C. Morris, Kristi Smiley, Joseph F. Urban, and Fred D. Finkelman. "IL-4 Exacerbates Anaphylaxis." Journal of Immunology 170, no. 7 (April 1, 2003): 3835–42. http://dx.doi.org/10.4049/jimmunol.170.7.3835.

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16

Pearce, Edward J., Joao Pedras Vasconcelos, Laura Rosa Brunet, and Elizabeth A. Sabin. "IL-4 in Schistosomiasis." Experimental Parasitology 84, no. 2 (November 1996): 295–99. http://dx.doi.org/10.1006/expr.1996.0116.

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17

de Moraes-Pinto, M. I., G. S. Vince, B. F. Flanagan, C. A. Hart, and P. M. Johnson. "Il-4 and Il-4 receptors in human pregnancy tissues at term." Placenta 17, no. 5-6 (July 1996): A52. http://dx.doi.org/10.1016/s0143-4004(96)90268-4.

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18

Jeannin, Pascale, Yves Delneste, Jean-Pierre Aubry, Sybille Lecoanet-Henchoz, Jean-François Gauchat, Paul Life, and Jean-Yves Bonnefoy. "Thiols Decrease Human IL-4 Production and IL-4-lnduced Immunoglobulin Synthesis." International Archives of Allergy and Immunology 113, no. 1-3 (1997): 329–30. http://dx.doi.org/10.1159/000237591.

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19

Jung, Thomas, Kathrin Wagner, Christine Neumann, and Christoph H. Heusser. "Enhancement of human IL-4 activity by soluble IL-4 receptorsin vitro." European Journal of Immunology 29, no. 3 (March 1999): 864–71. http://dx.doi.org/10.1002/(sici)1521-4141(199903)29:03<864::aid-immu864>3.0.co;2-t.

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20

Jiang, Hong, Miera B. Harris, and Paul Rothman. "IL-4/IL-13 signaling beyond JAK/STAT." Journal of Allergy and Clinical Immunology 105, no. 6 (June 2000): 1063–70. http://dx.doi.org/10.1067/mai.2000.107604.

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21

Minton, Kirsty. "What 'drives' IL-4 versus IL-13 signalling?" Nature Reviews Immunology 8, no. 3 (March 2008): 167. http://dx.doi.org/10.1038/nri2283.

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22

Zurawski, S. M., F. Vega, E. L. Doyle, and G. Zurawski. "The receptors for IL-4 and IL-13." Cytokine 6, no. 5 (September 1994): 580. http://dx.doi.org/10.1016/1043-4666(94)90320-4.

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23

KOPF, MANFRED, GRAHAM LE GROS, ANTHONY J. COYLE, MARIE KOSCO-VTLBOIS, FRANK BROMBACHER, and Georges Kohler. "Immune Responses of IL-4, IL-5, IL-6 Deficient Mice." Immunological Reviews 148, no. 1 (December 1995): 45–69. http://dx.doi.org/10.1111/j.1600-065x.1995.tb00093.x.

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24

DAVID, MURIEL, JACQUES BERTOGLIO, and JOSIANE PIERRE. "TNF-α Potentiates IL-4/IL-13-Induced IL-13Rα2 Expression." Annals of the New York Academy of Sciences 973, no. 1 (November 2002): 207–9. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04633.x.

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25

Vélez, Carolina, Mariángeles Clauzure, Delia Williamson, Mirta A. Koncurat, Tomás A. Santa-Coloma, and Claudio Barbeito. "IL-1β, IL-2 and IL-4 concentration during porcine gestation." Theriogenology 128 (April 2019): 133–39. http://dx.doi.org/10.1016/j.theriogenology.2019.01.017.

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26

Baranova, N. I., B. A. Molotilov, L. A. Ashchina, and N. A. Shkurova. "Role of IL-1β, TNF-α, IL-10, IL-17, and IL-4 gene polymorphisms in the pathogenesis of chronic rhinosinusitis with nasal polyps." Russian Medical Inquiry 6, no. 2 (2022): 57–61. http://dx.doi.org/10.32364/2587-6821-2022-6-2-57-61.

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Background: chronic rhinosinusitis with nasal polyps (CRSwNP) is a multifactorial disease, those mechanisms are not fully understood. A significant role of cytokines, e.g., interleukin (IL)-1β, tumor necrosis factor (TNF) α, IL-10, IL-17А, IL-4, and their genes, in the pathogenesis and predisposition to CRSwNP and treatment efficacy is established. Aim: to investigate IL-1β (Т-31С), TNF-α (G-308A), IL-10 (G-1082A), IL-17(G-197A), and IL-4 (С-589Т) gene polymorphisms and their role in CRSwNP pathogenesis. Patients and Methods: this open-label, prospective, randomized study enrolled 100 patients with CRSwNP. The control group included 72 healthy volunteers. DNA was isolated from the whole venous blood. IL-1β (Т-31С), TNF-α (G-308A), IL-10 (G-1082A), IL-17 (G-197A), and IL-4 (С-589Т) gene polymorphisms were assessed by the real-time polymerase chain reaction (PCR). Results: the analysis of IL-4 (С-589Т) gene polymorphism has demonstrated that 589С/С genotype is more common in CRSwNP patients compared to the controls (р=0.021, odds ratio/OR=1.248 [0.449–3.465]). The analysis of IL-10 (G-1082A) gene polymorphism has demonstrated that 1082А/A genotype is more common in CRSwNP patients compared to the controls (p=0.043, OR=1.027 [0.374–2.830]). The analysis of IL-17 (G-197A) gene polymorphism has demonstrated that 197A/А genotype is more common in CRSwNP patients than in the controls (p=0.046, OR=7.250 [0.863–2.532]). The analysis of TNF-α (G-308A) gene polymorphism has demonstrated that 308 G/G genotype is more common in CRSwNP patients compared to the controls (p=0.045, OR=1.789 [0.892–4.776]). Conclusion: the most relevant predictors of the increased risk of CRSwNP are 589С/С genotype of IL-4 gene, 1082А/A genotype of IL-10 gene, 197A/А genotype of IL-17 gene, and 308 G/G genotype of TNF-α gene. The analysis of essential cytokine gene polymorphisms, i.e., IL- 1β (Т-31С), TNF-α (G-308A), IL-10 (G-1082A), IL-17 (G-197A), and IL-4 (С-589Т), allows assessing genetic predisposition to CRSwNP. This technique is an important tool for predicting treatment efficacy. KEYWORDS: chronic rhinosinusitis with nasal polyps, cytokines, genotype, gene polymorphism, pathogenic mechanisms. FOR CITATION: Baranova N.I., Molotilov B.A., Ashchina L.A., Shkurova N.A. Role of IL-1β, TNF-α, IL-10, IL-17, and IL-4 gene polymorphisms in the pathogenesis of chronic rhinosinusitis with nasal polyps. Russian Medical Inquiry. 2022;6(2):57–61 (in Russ.). DOI: 10.32364/2587-6821-2022-6-2-57-61.

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27

Le Gros, G., S. Z. Ben-Sasson, R. Seder, F. D. Finkelman, and W. E. Paul. "Generation of interleukin 4 (IL-4)-producing cells in vivo and in vitro: IL-2 and IL-4 are required for in vitro generation of IL-4-producing cells." Journal of Experimental Medicine 172, no. 3 (September 1, 1990): 921–29. http://dx.doi.org/10.1084/jem.172.3.921.

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T cell populations derived from naive mice produce very small amounts of interleukin 4 (IL-4) in response to stimulation on anti-CD3-coated dishes. IL-4 production by such cells is mainly found among large- and intermediate-sized T cells and is dependent upon IL-2. Injection of anti-IgD into mice, a stimulus that leads to striking increases in serum levels of IgG1 and IgE, causes a striking increase in the IL-4-producing capacity of T cells. This increase is first observed 4 d after injection of anti-IgD. IL-4 production by T cells from anti-IgD-injected donors is mainly found among large- and intermediate-sized T cells. Small, dense T cells are poor producers of IL-4. The capacity of T cells from anti-IgD-injected donors to produce IL-4 is enhanced by addition of IL-2 and is largely, but not completely, inhibited by neutralization of in situ produced IL-2. These results indicate that the control of IL-4 production in T cells from naive and anti-IgD-injected donors is similar. However, it is possible that a portion of the IL-4-producing activity of T cells from activated donors is IL-2 independent. Although small T cells from naive donors have a very limited capacity to produce IL-4 in response to stimulation with anti-CD3, even in the presence of added IL-2, they can give rise to IL-4-producing cells upon in vitro culture on plates coated with anti-CD3 if both IL-2 and IL-4 are added. This leads to the appearance of IL-4-producing cells within 2 d. When analyzed after 5 d of culture by harvesting and re-exposure to anti-CD3-coated culture wells and IL-2, these cells have increased their IL-4-producing capacity by approximately 100-fold. The development of IL-4-producing cells in response to anti-CD3, IL-2, and IL-4 is not inhibited by interferon gamma (IFN-gamma), nor does IFN-gamma diminish IL-4 production by these cells upon challenge with anti-CD3 plus IL-2.

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28

Ben-Sasson, S. Z., G. Le Gros, D. H. Conrad, F. D. Finkelman, and W. E. Paul. "IL-4 production by T cells from naive donors. IL-2 is required for IL-4 production." Journal of Immunology 145, no. 4 (August 15, 1990): 1127–36. http://dx.doi.org/10.4049/jimmunol.145.4.1127.

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Abstract Utilizing a sensitive and selective assay for IL-4, it was shown that lymph node T cells from naive mice could produce small amounts of this lymphokine in response to anti-CD3 antibodies adsorbed to culture dishes. The capacity of these cells to produce IL-4 in response to plate-bound anti-CD3 was substantially enhanced by the addition of IL-2 to the culture and was strikingly inhibited by monoclonal anti-IL-2 antibody. Thus, IL-2 appears to be essential for IL-4 production by anti-CD3 antibody-stimulated T cells from naive mice. The effect of IL-2 was not mediated either by preferential proliferation or survival of precursors of IL-4 producing cells, indicating that IL-2 regulates T cell production of IL-4. IL-4 producing capacity of T cells from naive mice was found mainly among CD4+ T cells. Large T cells produced much more IL-4, on a per cell basis, than did small T cells. In contrast, small T cells appeared to be equal or superior to large T cells in producing IL-2. The superiority of large T cells in IL-4-producing capacity was not accounted for by a lack of an accessory cell population from the small T cells as addition of large spleen cells depleted of both B and T cells did not enhance IL-4 production by small lymph node T cells. These results suggest that the bulk of IL-4 production by T cell populations, from normal mice, in response to anti-CD3 depends upon cells that are already activated and that IL-2 is required for such production.

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29

Furusu, A., M. Miyazaki, T. Koji, K. Abe, Y. Ozono, T. Harada, P. K. Nakane, K. Hara, and S. Kohno. "Involvement of IL-4 in human glomerulonephritis: an in situ hybridization study of IL-4 mRNA and IL-4 receptor mRNA." Journal of the American Society of Nephrology 8, no. 5 (May 1997): 730–41. http://dx.doi.org/10.1681/asn.v85730.

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Interleukin-4 (IL-4) has been recently implicated in the pathogenesis of glomerulonephritis. However, the expression of IL-4 and IL-4 receptor (IL-4R) in human kidney has not been fully determined. Nonradioactive in situ hybridization was used to examine the expression of IL-4 mRNA and IL-4R mRNA in tissues from normal kidneys and specimens from a variety of human kidney diseases. In normal glomeruli, a few mesangial cells and cells of the Bowman's capsule weakly expressed IL-4 and IL-4R mRNA, whereas in diseased glomeruli both mRNA types were strongly expressed in resident glomerular cells, including mesangial cells, glomerular epithelial cells, and cells of the Bowman's capsule. The relationship between the expression of these mRNA and the degree of glomerular injury was different in different types of glomerulonephritis. In IgA nephropathy and non-IgA mesangial proliferative glomerulonephritis, IL-4 expression correlated positively with the degree of mesangial hypercellularity and extracellular matrix expansion. However, IL-4R expression was relatively constant. In contrast, the expression of IL-4 and IL-4R mRNA correlated negatively with the degree of glomerular injury in lupus nephritis. Coexpression and discordant expression of these mRNA forms were observed in individual cells. In tubulointerstitium with severe lesions, IL-4 mRNA and IL-4R mRNA were observed in atrophic tubules and some of the infiltrating cells and fibroblasts. The interstitial expression of these mRNA forms was similar in IgA nephropathy, non-IGA mesangial proliferative glomerulonephritis, and lupus nephritis and correlated positively with the degree of tubulo-interstitial changes. These results suggest that an autocrine and/or paracrine pathway of IL-4 is present in human diseased kidneys and that IL-4 may be involved in tissue injury in glomerulonephritis.

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30

Konenkov, Konenkov V. I., Koroleva E. G. Koroleva, Orlov N. B. Orlov, Prokof’ev V. F. Prokof’ev, Shevchenko A. V. Shevchenko, Novikov A. M. Novikov, Dergacheva T. I. Dergacheva, and Ostanin A A. Ostanin A. "Anti-inflammatory activity of serum cytokines (IL-4, IL-10, IL-13) and the natural IL-1β receptor antagonist (IL-1Ra) in women with uterine myoma." Akusherstvo i ginekologiia 10_2018 (October 31, 2018): 80–85. http://dx.doi.org/10.18565/aig.2018.10.80-85.

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31

Ho, I.-Cheng, Mark H. Kaplan, Laurie Jackson-Grusby, Laurie H. Glimcher, and Michael J. Grusby. "Marking IL-4-producing cells by knock-in of the IL-4 gene." International Immunology 11, no. 2 (February 1999): 243–47. http://dx.doi.org/10.1093/intimm/11.2.243.

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32

Jeannin, P., Y. Delneste, S. Lecoanet-Henchoz, J. F. Gauchat, P. Life, D. Holmes, and J. Y. Bonnefoy. "Thiols decrease human interleukin (IL) 4 production and IL-4-induced immunoglobulin synthesis." Journal of Experimental Medicine 182, no. 6 (December 1, 1995): 1785–92. http://dx.doi.org/10.1084/jem.182.6.1785.

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N-Acetyl-L-cysteine (NAC) is an antioxidant precursor of intracellular glutathione (GSH), usually given in human as a mucolytic agent. In vitro, NAC and GSH have been shown to act on T cells by increasing interleukin (IL) 2 production, synthesis and turnover of IL-2 receptors, proliferation, cytotoxic properties, and resistance to apoptosis. We report here that NAC and GSH decrease in a dose-dependent manner human IL-4 production by stimulated peripheral blood T cells and by T helper (Th) 0- and Th2-like T cell clones. This effect was associated with a decrease in IL-4 messenger RNA transcription. In contrast, NAC and GSH had no effect on interferon gamma and increased IL-2 production and T cell proliferation. A functional consequence was the capacity of NAC and GSH to selectively decrease in a dose-dependent manner IL-4-induced immunoglobulin (Ig) E and IgG4 production by human peripheral blood mononuclear cells. Interestingly, NAC and GSH also acted directly on purified tonsillar B cells by decreasing the mature epsilon messenger RNA, hence decreasing IgE production. In contrast, IgA and IgM production were not affected. At the same time, B cell proliferation was increased in a dose-dependent manner. Not all antioxidants tested but only SH-bearing molecules mimicked these properties. Finally, when given orally to mice, NAC decreased both IgE and IgG1 antibody responses to ovalbumin. These results demonstrate that NAC, GSH, and other thiols may control the production of both the Th2-derived cytokine IL-4 and IL-4-induced Ig in vitro and in vivo.

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33

Nakashima, H., K. Miyake, Y. Inoue, S. Shimizu, M. Akahoshi, Y. Tanaka, T. Otsuka, and M. Harada. "Association between IL-4 genotype and IL-4 production in the Japanese population." Genes & Immunity 3, no. 2 (April 2002): 107–9. http://dx.doi.org/10.1038/sj.gene.6363830.

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34

Kubo, Masato, Masakatsu Yamashita, Ryo Abe, Tomio Tada, Ko Okumura, John T. Ransom, and Toshinori Nakayama. "CD28 Costimulation Accelerates IL-4 Receptor Sensitivity and IL-4-Mediated Th2 Differentiation." Journal of Immunology 163, no. 5 (September 1, 1999): 2432–42. http://dx.doi.org/10.4049/jimmunol.163.5.2432.

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Abstract The development of Th1 and Th2 cells is determined by the type of antigenic stimulation involved in the initial cell activation step. Evidence indicates that costimulatory signals, such as those delivered by CD28, play an important role in Th2 development, but little is known about how CD28 costimulation contributes to Th2 development. In this study, TCR cross-linking was insufficient for Th2 development, while the addition of CD28 costimulation drastically increased Th2 generation through the IL-4-mediated pathway. Th2 generation following CD28 costimulation was not simply explained by the enhancement of IL-4 production in naive T cells. To generate Th2 cells after TCR cross-linking only, it was necessary to add a 20- to 200-fold excess of IL-4 generated after TCR and CD28 stimulation. TCR cross-linking increased the expression level and binding property of the IL-4R, but enhanced the sensitivity to IL-4 only slightly. In contrast, as evidenced by the enhanced phosphorylation of Jak3, the IL-4Rα-chain, and STAT6 following IL-4 stimulation, CD28 costimulation increased IL-4R sensitivity without affecting its expression and binding property. This evidence of the enhancement of IL-4R sensitivity increases our understanding of how CD28 costimulation accelerates Th2 development.

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35

Park, Yong Jin, and He Ro Yoon. "Expression of IL-4, IL-6, GM-CSF and IFN-γ mRNAs in Nasal Polyps." Journal of Clinical Otolaryngology Head and Neck Surgery 10, no. 1 (May 1999): 53–60. http://dx.doi.org/10.35420/jcohns.1999.10.1.53.

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Dubin, Celina, Ester Del Duca, and Emma Guttman-Yassky. "The IL-4, IL-13 and IL-31 pathways in atopic dermatitis." Expert Review of Clinical Immunology 17, no. 8 (July 21, 2021): 835–52. http://dx.doi.org/10.1080/1744666x.2021.1940962.

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Klatka, Janusz, and Jacek Tabarkiewicz. "Dendritic Cells, IL-2, IL-4 and IL-12 in Laryngeal Cancer." Otolaryngology–Head and Neck Surgery 143, no. 2_suppl (August 2010): P214—P215. http://dx.doi.org/10.1016/j.otohns.2010.06.420.

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Cicuttini, F. M., K. A. Byron, D. Maher, A. M. Wootton, K. D. Muirden, and J. A. Hamilton. "Serum IL-4, IL-10 and IL-6 levels in inflammatory arthritis." Rheumatology International 14, no. 5 (January 1995): 201–6. http://dx.doi.org/10.1007/bf00262298.

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Huang, H., J. Hu-Li, H. Chen, S. Z. Ben-Sasson, and W. E. Paul. "IL-4 and IL-13 production in differentiated T helper type 2 cells is not IL-4 dependent." Journal of Immunology 159, no. 8 (October 15, 1997): 3731–38. http://dx.doi.org/10.4049/jimmunol.159.8.3731.

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Abstract CD4+ T cell differentiation into cells capable of producing IL-4 and IL-13 (Th2 cells) requires the presence of IL-4 and is STAT-6 dependent. Here we show that IL-4 is not required for IL-4 or IL-13 production by Th2 cells. Anti-IL-4 or anti-IL-4R Ab did not diminish IL-4 production by Th2 cells in response to TCR-mediated stimulation, nor did IL-4 enhance IL-4 production in response to stimulation of Th2 cells with limiting amounts of Ag. Th2 cells prepared from IL-4 knockout mice were capable of producing IL-13 mRNA in response to stimulation with immobilized anti-CD3. IL-4 did not increase IL-13 mRNA expression. Despite the failure of IL-4 to effect IL-4 production by primed Th2 cells, a STAT-6 binding element was demonstrated in the IL-4 promoter. The authenticity of this element was demonstrated by oligonucleotide competition, by supershifting with anti-STAT-6 Ab, and by IL-4-inducible effects on transcription of a reporter gene under the control of a multimerized element fused to an IL-4 minimal promoter. Nonetheless, an IL-4 promoter construct lacking the STAT-6 binding element was as effective as a construct containing this element in anti-CD3-induced reporter transcription. Thus, this element, if biologically active, must function at a step in T cell responsiveness distinct from the acute production of IL-4 by Th2 cells in response to Ag or anti-CD3.

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Perkins, Charles, Marsha Wills-Karp, and Fred D. Finkelman. "IL-4 induces IL-13–independent allergic airway inflammation." Journal of Allergy and Clinical Immunology 118, no. 2 (August 2006): 410–19. http://dx.doi.org/10.1016/j.jaci.2006.06.004.

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McCormick, Sarah M., and Nicola M. Heller. "Commentary: IL-4 and IL-13 receptors and signaling." Cytokine 75, no. 1 (September 2015): 38–50. http://dx.doi.org/10.1016/j.cyto.2015.05.023.

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Keegan, Achsah D. "IL-4 and IL-13: From “supe” to nuts." Cytokine 75, no. 1 (September 2015): 1–2. http://dx.doi.org/10.1016/j.cyto.2015.06.001.

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Krymskaya, V., G. Vass, R. Z. Syed, R. A. Panettieri, and A. Haczku. "IL-4 and IL-13 induce fibroblast-myofibroblast differentiation." Journal of Allergy and Clinical Immunology 115, no. 2 (February 2005): S120. http://dx.doi.org/10.1016/j.jaci.2004.12.493.

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Murata, Takashi, Nicholas I. Obiri, and Raj K. Puri. "Human ovarian-carcinoma cell lines express IL-4 and IL-13 receptors: Comparison between IL-4- and IL-13-induced signal transduction." International Journal of Cancer 70, no. 2 (January 17, 1997): 230–40. http://dx.doi.org/10.1002/(sici)1097-0215(19970117)70:2<230::aid-ijc15>3.0.co;2-m.

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Chasserio, Stephanie, Philippe Pailot, and Corinne Poroli. "4. L’entrepreneuriat est-il genré ?" Regards croisés sur l'économie 19, no. 2 (2016): 62. http://dx.doi.org/10.3917/rce.019.0062.

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Berndt, J. D. "The IL-4 Brown Out." Science Signaling 7, no. 331 (June 24, 2014): ec170-ec170. http://dx.doi.org/10.1126/scisignal.2005623.

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Marshall, Hilary. "Aspirin inhibits IL-4 production." Trends in Immunology 22, no. 5 (May 2001): 242. http://dx.doi.org/10.1016/s1471-4906(01)01949-4.

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Patton, Elisabeth A., Laura Rosa Brunet, Anne C. La Flamme, João Pedras-Vasconcelos, Manfred Kopf, and Edward J. Pearce. "Severe Schistosomiasis in the Absence of Interleukin-4 (IL-4) Is IL-12 Independent." Infection and Immunity 69, no. 1 (January 1, 2001): 589–92. http://dx.doi.org/10.1128/iai.69.1.589-592.2001.

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ABSTRACT An interleukin-4 (IL-4)-dependent Th2 response allows wild-type mice to survive infection with the parasite Schistosoma mansoni. In the absence of IL-4, infected mice mount a Th1-like proinflammatory response, develop severe disease, and succumb. Neither the Th1 response nor morbidity is IL-12 dependent in this system.

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Kong, Su-Kang, Byung Soo Kim, Tae Gi Uhm, Hun Soo Chang, Jong Sook Park, Sung Woo Park, Choon-Sik Park, and Il Yup Chung. "Aspirin induces IL-4 production: augmented IL-4 production in aspirin-exacerbated respiratory disease." Experimental & Molecular Medicine 48, no. 1 (January 2016): e202-e202. http://dx.doi.org/10.1038/emm.2015.96.

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Fanslow, W. C., K. N. Clifford, L. S. Park, A. S. Rubin, R. F. Voice, M. P. Beckmann, and M. B. Widmer. "Regulation of alloreactivity in vivo by IL-4 and the soluble IL-4 receptor." Journal of Immunology 147, no. 2 (July 15, 1991): 535–40. http://dx.doi.org/10.4049/jimmunol.147.2.535.

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Abstract Although numerous in vitro studies have demonstrated that cytokines are involved in the generation of alloreactive effector cells, the role of these regulatory substances in vivo is less well defined. We have recently cloned and expressed cDNAs encoding both membrane bound and soluble forms of the murine IL-4R. The effects of murine rIL-4 and a recombinant, soluble, extracellular portion of the murine IL-4R soluble(s) IL-4R on the generation of alloresponsiveness in vivo were evaluated by measuring the lymphoproliferative response to a localized injection of allogeneic cells and the survival of cardiac allografts. Administration of IL-4 to BALB/c mice resulted in a slight augmentation of the anti-C57BL/6 lymphoproliferative response compared to that occurring in control, mouse serum albumin-(MSA) treated mice. In contrast, the sIL-4R suppressed this response to allogeneic cells in a dose-dependent manner, with a dose of 50 micrograms/kg/day causing nearly complete inhibition of the response as compared to the response observed in controls. The inhibitory effect of sIL-4R was reversed by simultaneous administration of IL-4. A neutralizing antibody against IL-4 (11B11) and another against the IL-4R (M1) were also effective inhibitors of the response when given at 100- to 1000-fold higher concentrations than the amount of sIL-4R required to inhibit the response. In cardiac allograft experiments, BALB/c mice were engrafted with newborn C57BL/6 hearts in the ear pinnae and treated with sIL-4R (50 micrograms/kg) or MSA. Such allografts survived an average of 4 days longer in sIL-4R-treated mice than in MSA-treated controls. In conclusion, neutralization of IL-4 inhibits alloresponsiveness in vivo. These results confirm a regulatory role for this pleiotropic cytokine in allograft rejection and suggest a therapeutic value for IL-4 antagonists alone or in combination with other immunosuppressive regimens.

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