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Journal articles on the topic 'IL-5'

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Published: 4 June 2021
Last updated: 28 January 2023

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1

Kotsimbos, ATC, and Q. Hamid. "IL-5 and IL-5 receptor in asthma." Memórias do Instituto Oswaldo Cruz 92, suppl 2 (December 1997): 75–91. http://dx.doi.org/10.1590/s0074-02761997000800012.

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2

TAKATSU, Kiyoshi. "Interleukin-5, IL-5." Journal of Japan Atherosclerosis Society 23, no. 10 (1996): 599–603. http://dx.doi.org/10.5551/jat1973.23.10_599.

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3

Malhi, Gin S. "DSM-5: Il buono, il cattivo, il brutto." Australian & New Zealand Journal of Psychiatry 47, no. 7 (June 28, 2013): 595–98. http://dx.doi.org/10.1177/0004867413496363.

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4

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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5

Stein, Miguel L., Joyce M. Villanueva, Bridget K. Buckmeier, Yoshiyuki Yamada, Alexandra H. Filipovich, Amal H. Assa'ad, and Marc E. Rothenberg. "Anti–IL-5 (mepolizumab) therapy reduces eosinophil activation ex vivo and increases IL-5 and IL-5 receptor levels." Journal of Allergy and Clinical Immunology 121, no. 6 (June 2008): 1473–83. http://dx.doi.org/10.1016/j.jaci.2008.02.033.

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6

Warren, H. S., B. F. Kinnear, J. H. Phillips, and L. L. Lanier. "Production of IL-5 by human NK cells and regulation of IL-5 secretion by IL-4, IL-10, and IL-12." Journal of Immunology 154, no. 10 (May 15, 1995): 5144–52. http://dx.doi.org/10.4049/jimmunol.154.10.5144.

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Abstract Human NK cells produce IFN-gamma, TNF-alpha, and granulocyte macrophage-CSF when stimulated with susceptible target cells or through the CD16 and CD94 cell surface molecules. This study reports that NK cells also produce IL-5, a cytokine typically produced by Th2 cells, which mediates mobilization and differentiation of eosinophils. Polyclonal NK cell populations and NK cell clones produce IL-5 when stimulated to proliferate with gamma-irradiated MM-170 melanoma cells or JY B-lymphoblastoid cells and rIL-2. IL-5 is produced in cultures generated from freshly isolated NK cells (primary cultures) and when quiescent NK cells from primary cultures are restimulated to proliferate (secondary cultures). Production of IL-5 is on average 8.8-fold greater in secondary cultures compared with primary cultures (n > 18), suggesting that the ability of NK cells to produce IL-5 matures during primary stimulation. IL-5 secretion, particularly in primary cultures, is augmented by IL-4 and is inhibited by IL-12 and IL-10. By contrast, IL-4 and IL-12 have the reverse effects on IFN-gamma secretion. Cultured NK cells that no longer secrete cytokines can be restimulated to do so with either phorbol 12, 13 dibutyrate and ionomycin or with susceptible target cells in the presence of rIL-2. IL-5 production in these cultures occurs only when NK cells are in an exponential growth phase, whereas IFN-gamma, TNF-alpha, and granulocyte macrophage-CSF are produced also by stimulation of quiescent cells, although to a lesser extent. Furthermore, cytokine production is unrelated to the cytolytic activity of NK cells. In conclusion, proliferating human NK cells have the potential to produce IL-5 with secretion regulated by IL-4, IL-10, and IL-12.
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7

Esnault, Stephane, Mats W. Johansson, and Sameer K. Mathur. "Eosinophils, beyond IL-5." Cells 10, no. 10 (October 1, 2021): 2615. http://dx.doi.org/10.3390/cells10102615.

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8

Takatsu, Kiyoshi, and Hiroshi Nakajima. "IL-5 and eosinophilia." Current Opinion in Immunology 20, no. 3 (June 2008): 288–94. http://dx.doi.org/10.1016/j.coi.2008.04.001.

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9

Chung, K. F. "IL-5 in asthma." Thorax 57, no. 8 (August 1, 2002): 751. http://dx.doi.org/10.1136/thorax.57.8.751.

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10

Matthaei, Klaus I., Paul S. Foster, and Ian G. Young. "The role of interleukin-5 (IL-5 ) in vivo: studies with IL-5 deficient mice." Memórias do Instituto Oswaldo Cruz 92, suppl 2 (December 1997): 63–68. http://dx.doi.org/10.1590/s0074-02761997000800010.

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11

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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12

Takatsu, Kiyoshi. "Interleukin 5 (IL-5) and Its Receptor." Microbiology and Immunology 35, no. 8 (August 1991): 593–606. http://dx.doi.org/10.1111/j.1348-0421.1991.tb01591.x.

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13

STEIN, M., A. MUNITZ, and M. ROTHENBERG. "Increased High Molecular Weight IL-5 Complex After Anti-IL-5 (Mepolizumab) Therapy." Journal of Allergy and Clinical Immunology 121, no. 2 (February 2008): S118. http://dx.doi.org/10.1016/j.jaci.2007.12.468.

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14

Dickason, R. R., M. M. Huston, and D. P. Huston. "Delineation of IL-5 domains predicted to engage the IL-5 receptor complex." Journal of Immunology 156, no. 3 (February 1, 1996): 1030–37. http://dx.doi.org/10.4049/jimmunol.156.3.1030.

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Abstract IL-5 is an interdigitating homodimeric glycoprotein and a member of the helical bundle family of cytokines. IL-5 is a potent activator of eosinophils and a specific promoter of their differentiation. This activity has implicated IL-5 in the pathogenesis of asthma and allergic disease. A detailed understanding of IL-5 structure and function is required to develop immunomodulators of IL-5-mediated inflammatory responses. We generated a panel of neutralizing anti-IL-5 mAbs which were used to map functional domains on IL-5. In addition, the nucleotide sequences for human IL-5, murine IL-5, rat IL-5, and eight human/murine IL-5 chimeras were engineered and expressed in COS-7 cells. These recombinant cytokines and mAbs were used in TF-1 bioassays to identify five functional epitopes on the tertiary structure of IL-5. Residues responsible for the species-specific activity of human IL-5 were identified with the murine BCL1 bioassay. One set of epitopes cluster around the helix A-loop 2 region, which is predicted to engage the IL-5 receptor beta-chain. The second set of epitopes as well as the species specificity domain cluster around the loop 3-helix D region, which is predicted to engage the IL-5 receptor alpha-chain. Together, these analyses target the A/D helical face of IL-5 as the region involved in receptor engagement.
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15

Ohbo, Kazuyuki, Hironobu Asoa, Kouro Taku, Nakamura Masataka, Yuji Klkuchi, Satoshl Takaki, and Katsulku Hirokawa. "Demonstration of a cross-talk between IL-2 and IL-5 in Phosphorylation of IL-2 and IL-5 receptor β chains." International Immunology 8, no. 6 (1996): 951–60. http://dx.doi.org/10.1093/intimm/8.6.951.

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16

Yamaguchi, Y., T. Suda, H. Shiozaki, Y. Miura, Y. Hitoshi, A. Tominaga, K. Takatsu, and T. Kasahara. "Role of IL-5 in IL-2-induced eosinophilia. In vivo and in vitro expression of IL-5 mRNA by IL-2." Journal of Immunology 145, no. 3 (August 1, 1990): 873–77. http://dx.doi.org/10.4049/jimmunol.145.3.873.

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Abstract We recently demonstrated in vivo that IL-5 was an important mediator of eosinophilia in mice with parasite infections. In this study, we examined whether or not IL-5 was actually responsible for the eosinophilia induced by injection of human rIL-2. Mice administered hIL-2 developed eosinophilia during the course of the series of injections. This eosinophilia could be suppressed by a single injection of mAb against murine IL-5. The number of eosinophilic precursors increased more in the spleen cells of the IL-2-treated mice in comparison to the control mice, although in bone marrow precursors showed little change. Similarly, the number of granulocytic precursors increased markedly in the spleen cells of IL-2-treated mice. In vitro polymerase chain reaction amplification of cDNA subfragments corresponding to IL-5 mRNA (reverse transcription-polymerase chain reaction), followed by Southern blot analysis, revealed enhancement of IL-5 mRNA expression in spleen cells 3 days after starting the human IL-2 injections. We also observed enhanced murine IL-5 mRNA expression in spleen cells stimulated with IL-2 in vitro. The level of murine IL-5 mRNA expression by IL-2-stimulated spleen cells from normal mice increased at 24 h, reached a plateau after 48 h, and decreased again within 72 h of starting culture. These results indicate that the eosinophilia induced by IL-2 in vivo is presumably mediated by IL-5 released from IL-2-stimulated lymphocytes.
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17

TAKATSU, SEISHI. "IL-5 and its receptor." Japanese Journal of Clinical Immunology 13, no. 5 (1990): 441–43. http://dx.doi.org/10.2177/jsci.13.441.

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18

Narendra, Dharani K., and Nicola A. Hanania. "Targeting IL-5 in COPD." International Journal of Chronic Obstructive Pulmonary Disease Volume 14 (May 2019): 1045–51. http://dx.doi.org/10.2147/copd.s155306.

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19

BAGLEY, C., A. LOPEZ, and M. VADAS. "New frontiers for IL-5." Journal of Allergy and Clinical Immunology 99, no. 6 (June 1997): 725–28. http://dx.doi.org/10.1016/s0091-6749(97)80002-4.

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20

Leung, Donald Y. M., Harold S. Nelson, Stanley J. Szefler, and William W. Busse. "Anti–IL-5 for hypereosinophilia." Journal of Allergy and Clinical Immunology 113, no. 1 (January 2004): 2. http://dx.doi.org/10.1016/j.jaci.2003.11.004.

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21

Ameri, Abdol A. "Weiterer IL-5-Antikörper verfügbar." MMW - Fortschritte der Medizin 159, no. 1 (January 2017): 67. http://dx.doi.org/10.1007/s15006-017-9167-7.

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22

Gregory, Bernard, Antje Kirchem, Simon Phipps, Phillipe Gevaert, Carol Pridgeon, Sara M. Rankin, and Douglas S. Robinson. "Differential Regulation of Human Eosinophil IL-3, IL-5, and GM-CSF Receptor α-Chain Expression by Cytokines: IL-3, IL-5, and GM-CSF Down-Regulate IL-5 Receptor α Expression with Loss of IL-5 Responsiveness, but Up-Regulate IL-3 Receptor α Expression." Journal of Immunology 170, no. 11 (June 1, 2003): 5359–66. http://dx.doi.org/10.4049/jimmunol.170.11.5359.

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23

Webb, Dianne C., Andrew N. J. McKenzie, Aulikki M. L. Koskinen, Ming Yang, Joërg Mattes, and Paul S. Foster. "Integrated Signals Between IL-13, IL-4, and IL-5 Regulate Airways Hyperreactivity." Journal of Immunology 165, no. 1 (July 1, 2000): 108–13. http://dx.doi.org/10.4049/jimmunol.165.1.108.

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24

Fort, Madeline M., Jeanne Cheung, David Yen, Joana Li, Sandra M. Zurawski, Sylvia Lo, Satish Menon, et al. "IL-25 Induces IL-4, IL-5, and IL-13 and Th2-Associated Pathologies In Vivo." Immunity 15, no. 6 (December 2001): 985–95. http://dx.doi.org/10.1016/s1074-7613(01)00243-6.

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25

Tominaga, A., T. Takahashi, Y. Kikuchi, S. Mita, S. Naomi, N. Harada, N. Yamaguchi, and K. Takatsu. "Role of carbohydrate moiety of IL-5. Effect of tunicamycin on the glycosylation of IL-5 and the biologic activity of deglycosylated IL-5." Journal of Immunology 144, no. 4 (February 15, 1990): 1345–52. http://dx.doi.org/10.4049/jimmunol.144.4.1345.

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Abstract IL-5 is a T cell-derived lymphokine that induces B cell growth and differentiation in murine systems. In this study, we examined the role of carbohydrate moiety of IL-5 in the expression of biological function. IL-5 polypeptides translated in Xenopus oocytes were heterogeneous in terms of isoelectric point (pI 4.7 to 8.0) and m.w. (45,000 to 60,000 under nonreducing conditions) and yielded m.w. of 25,000 to 30,000 under reducing conditions. Treatment of rIL-5 with N-glycanase under reducing conditions yielded an IL-5 monomer of m.w. 12,000 to 14,000. Furthermore, deglycosylated rIL-5 that had been translated in the presence of tunicamycin showed very limited heterogeneity by two-dimensional gel electrophoresis (first dimension, nonequilibrium pH gradient electrophoresis; second dimension, SDS-PAGE). The m.w. was 27,000 to 28,000 under non-reducing conditions and migrated to m.w. 13,000 to 14,000 under reducing conditions. These results indicate that IL-5 is a glycoprotein carrying the N-glycosidically-linked carbohydrates. Treatment of IL-5 with sialidase caused the decrease in the heterogeneity in isoelectric point of IL-5. Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions. Scatchard plot analysis of equilibrium binding of 35S-labeled rIL-5 to T88-M cells revealed that the dissociation constants (Kd) of glycosylated rIL-5 and deglycosylated rIL-5 were 127 pM and 110 pM, respectively. IL-5 activities determined by both B cell growth and differentiation assays were not affected by deglycosylation. These results indicate that N-linked glycoside moiety of IL-5 molecules may not play an essential role in the expression of its activity.
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26

Zhu, W., N. Liu, Y. Zhao, H. Jia, B. Cui, and G. Ning. "Association analysis of polymorphisms in IL-3, IL-4, IL-5, IL-9, and IL-13 with Graves’ disease." Journal of Endocrinological Investigation 33, no. 10 (March 22, 2010): 751–55. http://dx.doi.org/10.1007/bf03346682.

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27

H, Ha, Spicer T, He Xy, Chen J, Boyd R, Tran G, Hodgkinson Sj, and Hall BM. "IL-4 AND IL-5 THERAPY INHIBITS HEYMANN NEPHRITIS (HN)." Nephrology 7, no. 1 (February 2002): A113. http://dx.doi.org/10.1046/j.1440-1797.2002.00007-1-113.x.

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28

Hashiguchi, Masaaki, Yuji Kashiwakura, Yumiko Kanno, Hidefumi Kojima, and Tetsuji Kobata. "IL-21 and IL-5 coordinately induce surface IgA+ cells." Immunology Letters 224 (August 2020): 21–27. http://dx.doi.org/10.1016/j.imlet.2020.05.004.

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29

Solinger, Alan M. "IL-1-5 Blocking IL-1β in type 2 diabetes." Cytokine 52, no. 1-2 (October 2010): 10. http://dx.doi.org/10.1016/j.cyto.2010.07.043.

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30

Bourdenet, V., G. Devouassoux, B. Antoine, C. Bernier, O. Carpentier, C. Chenivesse, A. Du Thanh, et al. "Eczéma paradoxal sous biothérapie ciblant l’axe IL-5/IL-5R." Annales de Dermatologie et de Vénéréologie - FMC 2, no. 8 (November 2022): A64. http://dx.doi.org/10.1016/j.fander.2022.09.062.

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31

Drick, Nora, Katrin Milger, Benjamin Seeliger, Jan Fuge, Stephanie Korn, Roland Buhl, Maren Schuhmann, et al. "Switch from IL-5 to IL-5-Receptor α Antibody Treatment in Severe Eosinophilic Asthma." Journal of Asthma and Allergy Volume 13 (November 2020): 605–14. http://dx.doi.org/10.2147/jaa.s270298.

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32

Reiman, Rachael M., Robert W. Thompson, Carl G. Feng, Danielle Hari, Rachel Knight, Allen W. Cheever, Helene F. Rosenberg, and Thomas A. Wynn. "Interleukin-5 (IL-5) Augments the Progression of Liver Fibrosis by Regulating IL-13 Activity." Infection and Immunity 74, no. 3 (March 2006): 1471–79. http://dx.doi.org/10.1128/iai.74.3.1471-1479.2006.

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ABSTRACT Eosinophils are frequently found in increased numbers in a variety of chronic fibrotic diseases; however, their role in the development of hepatic fibrosis has not been dissected in vivo. Here, we used interleukin-5 (IL-5) knockout (KO) mice to determine whether eosinophils contribute to the progressive liver fibrosis that develops in response to chronic Schistosoma mansoni infection. Although infection intensities were similar in C57BL/6 and IL-5 KO mice, the average size of granulomas was significantly smaller in both acutely and chronically infected IL-5 KO mice. Their granulomas were also completely devoid of eosinophils. In addition, the knockout mice displayed over a 40% reduction in hepatic fibrosis by week 16 postinfection. The reduced fibrosis was associated with increased production of the antifibrotic cytokine gamma interferon. Moreover, although IL-13 production did not decrease consistently in the absence of IL-5, IL-13-triggered responses were substantially reduced in the granulomatous tissues. This was confirmed by analyzing the expression of several genes associated with alternative macrophage activation, including arginase 1, Fizz-1, and YM-1. Importantly, all of these IL-13-regulated genes have been linked with the mechanisms of wound healing and fibrosis. In addition to IL-5 polarizing the antigen-specific CD4+ Th2 cell response, we found that granuloma eosinophils were themselves a significant source of IL-13. Thus, by producing profibrotic mediators and polarizing the Th2 response, these findings illustrate both direct and indirect roles for eosinophils and IL-5 in the pathogenesis of schistosomiasis-induced liver fibrosis. Thus, inhibiting the activity of IL-5 or eosinophils may prove effective for a variety of chronic fibrotic diseases.
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33

Hall, B., K. Plain, M. Nomura, N. Verma, G. Tran, R. Boyd, C. Robinson, and S. Hodgkinson. "ALLOGRAFT TOLERANCE MEDIATING CD4+T CELLS DEPEND UPON INTERLEUKIN-5 (IL-5), NOT IL-4." Transplantation 86, Supplement (July 2008): 136. http://dx.doi.org/10.1097/01.tp.0000332495.28926.ce.

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34

Namkung, J. H., J. E. Lee, E. Kim, H. J. Cho, S. Kim, E. S. Shin, E. Y. Cho, and J. M. Yang. "IL-5 and IL-5 receptor alpha polymorphisms are associated with atopic dermatitis in Koreans." Allergy 62, no. 8 (August 2007): 934–42. http://dx.doi.org/10.1111/j.1398-9995.2007.01445.x.

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35

TAKATSU, Kiyoshi. "Structure and Function of IL-5 Receptor." YAKUGAKU ZASSHI 115, no. 8 (1995): 570–83. http://dx.doi.org/10.1248/yakushi1947.115.8_570.

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36

Hatzistilianou, M., C. Aggouridaki, B. Tsotsou, A. Thymi, G. Koulouses, and A. Stogias. "Serum TNF-α, IL-1β, IL-4 and IL-5 levels in bronchial asthma." Immunology Letters 56 (May 1997): 155. http://dx.doi.org/10.1016/s0165-2478(97)85619-2.

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37

Hatzistilianou, M. "Serum TNF-α, IL-1β, IL-4 and IL-5 levels in bronchial asthma." Immunology Letters 56, no. 1-3 (May 1997): 155. http://dx.doi.org/10.1016/s0165-2478(97)87457-3.

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38

Brown, Pamela M., Philip Tagari, Kevin R. Rowan, Violeta L. Yu, Gary P. O'Neill, C. Russell Middaugh, Gautam Sanyal, Anthony W. Ford-Hutchinson, and Donald W. Nicholson. "Epitope-labeled Soluble Human Interleukin-5 (IL-5) Receptors." Journal of Biological Chemistry 270, no. 49 (December 8, 1995): 29236–43. http://dx.doi.org/10.1074/jbc.270.49.29236.

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39

MORI, A., O. KAMINUMA, T. MIKAMI, S. INOUE, Y. OKUMURA, K. AKIYAMA, and H. OKUDAIRA. "Transcriptional control of the IL-5 gene by human helper T cells: IL-5 synthesis is regulated independently from IL-2 or IL-4 synthesis." Journal of Allergy and Clinical Immunology 103, no. 5 (May 1999): S429—S436. http://dx.doi.org/10.1016/s0091-6749(99)70158-2.

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40

Randall, T. D., F. E. Lund, J. W. Brewer, C. Aldridge, R. Wall, and R. B. Corley. "Interleukin-5 (IL-5) and IL-6 define two molecularly distinct pathways of B-cell differentiation." Molecular and Cellular Biology 13, no. 7 (July 1993): 3929–36. http://dx.doi.org/10.1128/mcb.13.7.3929-3936.1993.

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Interleukin-5 (IL-5) and IL-6 have both been reported to act as B-cell differentiation factors by stimulating activated B cells to secrete antibody. However, it has not been possible to directly compare the effects of these two lymphokines because of the lack of a suitable B-cell line capable of responding to both. We have identified a clonal, inducible B-cell lymphoma, CH12, that has this property. Both IL-5 and IL-6 can independently stimulate increases in steady-state levels of immunoglobulin and J-chain mRNA and proteins, and they both induce the differentiation of CH12 into high-rate antibody-secreting cells. Nevertheless, there are significant differences in the activities of these two lymphokines. First, while IL-6 acts only as a differentiation factor, IL-5 also augments the proliferation of CH12 cells. Second, the differentiation stimulated by IL-5 but not by IL-6 is partially inhibited by IL-4. Inhibition of IL-5-induced differentiation was not at the level of IL-5 receptor expression, since IL-4 did not inhibit IL-5-induced proliferation. Third, IL-5 but not IL-6 stimulated increased mouse mammary tumor proviral gene expression in CH12 cells. These results demonstrate that while both IL-5 and IL-6 may act as differentiation factors for B cells, they induce differentiation by using at least partially distinct molecular pathways. Our results also establish that B cells characteristic of a single stage of development can independently respond to IL-4, IL-5, and IL-6.
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41

Randall, T. D., F. E. Lund, J. W. Brewer, C. Aldridge, R. Wall, and R. B. Corley. "Interleukin-5 (IL-5) and IL-6 define two molecularly distinct pathways of B-cell differentiation." Molecular and Cellular Biology 13, no. 7 (July 1993): 3929–36. http://dx.doi.org/10.1128/mcb.13.7.3929.

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Interleukin-5 (IL-5) and IL-6 have both been reported to act as B-cell differentiation factors by stimulating activated B cells to secrete antibody. However, it has not been possible to directly compare the effects of these two lymphokines because of the lack of a suitable B-cell line capable of responding to both. We have identified a clonal, inducible B-cell lymphoma, CH12, that has this property. Both IL-5 and IL-6 can independently stimulate increases in steady-state levels of immunoglobulin and J-chain mRNA and proteins, and they both induce the differentiation of CH12 into high-rate antibody-secreting cells. Nevertheless, there are significant differences in the activities of these two lymphokines. First, while IL-6 acts only as a differentiation factor, IL-5 also augments the proliferation of CH12 cells. Second, the differentiation stimulated by IL-5 but not by IL-6 is partially inhibited by IL-4. Inhibition of IL-5-induced differentiation was not at the level of IL-5 receptor expression, since IL-4 did not inhibit IL-5-induced proliferation. Third, IL-5 but not IL-6 stimulated increased mouse mammary tumor proviral gene expression in CH12 cells. These results demonstrate that while both IL-5 and IL-6 may act as differentiation factors for B cells, they induce differentiation by using at least partially distinct molecular pathways. Our results also establish that B cells characteristic of a single stage of development can independently respond to IL-4, IL-5, and IL-6.
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42

Johnson, Teresa R., and Barney S. Graham. "Secreted Respiratory Syncytial Virus G Glycoprotein Induces Interleukin-5 (IL-5), IL-13, and Eosinophilia by an IL-4-Independent Mechanism." Journal of Virology 73, no. 10 (October 1, 1999): 8485–95. http://dx.doi.org/10.1128/jvi.73.10.8485-8495.1999.

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ABSTRACT The attachment glycoprotein G of respiratory syncytial virus (RSV) is produced as both membrane-anchored and secreted forms by infected cells. Immunization with secreted RSV G (Gs) or formalin-inactivated alumprecipitated RSV (FI-RSV) predisposes mice to immune responses involving a Th2 cell phenotype which results in more severe illness and pathology, decreased viral clearance, and increased pulmonary eosinophilia upon subsequent RSV challenge. These responses are associated with increased interleukin-4 (IL-4) production in FI-RSV-primed mice, and the responses are IL-4 dependent. RNase protection assays demonstrated that similar levels of IL-4 mRNA were induced after RSV challenge in mice primed with vaccinia virus expressing Gs (vvGs) or a construct expressing only membrane-anchored G (vvGr). However, upon RSV challenge, vvGs-primed mice produced significantly greater levels of IL-5 and IL-13 mRNA and protein than vvGr-primed mice. Administration of neutralizing anti-IL-4 antibody 11.B11 during vaccinia virus priming did not alter the levels of vvGs-induced IL-5, IL-13, pulmonary eosinophilia, illness, or RSV titers upon RSV challenge, although immunoglobulin G (IgG) isotype profiles revealed that more IgG2a was produced. vvGs-priming of IL-4-deficient mice demonstrated that G-induced airway eosinophilia was not dependent on IL-4. In contrast, airway eosinophilia induced by FI-RSV priming was significantly reduced in IL-4-deficient mice. Thus we conclude that, in contrast to FI-RSV, the secreted form of RSV G can directly induce IL-5 and IL-13, producing pulmonary eosinophilia and enhanced illness in RSV-challenged mice by an IL-4-independent mechanism.
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43

Uings, Iain, and Murray McKinnon. "Development of IL-5 Receptor Antagonists." Current Pharmaceutical Design 8, no. 20 (September 1, 2002): 1837–44. http://dx.doi.org/10.2174/1381612023393800.

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44

Khan, S. "Anti-IL-5 therapy and DRESS." Canadian Medical Association Journal 182, no. 9 (June 14, 2010): 941. http://dx.doi.org/10.1503/cmaj.110-2054.

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45

Lakatta, Edward G. "IL-5 The heart of survival." Journal of Molecular and Cellular Cardiology 34, no. 10 (October 2002): A6. http://dx.doi.org/10.1016/s0022-2828(02)90255-5.

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46

Einecke, Dirk. "Anti-IgE oder Anti-IL 5?" MMW - Fortschritte der Medizin 159, no. 15 (September 2017): 70. http://dx.doi.org/10.1007/s15006-017-0015-6.

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47

SUTTON, S., A. ASSAAD, and M. ROTHENBERG. "Anti-IL-5 and hypereosinophilic syndromes." Clinical Immunology 115, no. 1 (April 2005): 51–60. http://dx.doi.org/10.1016/j.clim.2005.02.006.

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48

Ott, Christina. "IL-5-Rezeptor-Antikörper ergänzt Therapieoptionen." MMW - Fortschritte der Medizin 160, no. 4 (March 2018): 58. http://dx.doi.org/10.1007/s15006-018-0251-4.

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49

Zahn, Stefan, Paul Godillot, Akihiko Yoshimura, and Irwin Chaiken. "IL-5-INDUCED JAB–JAK2 INTERACTION." Cytokine 12, no. 9 (September 2000): 1299–306. http://dx.doi.org/10.1006/cyto.2000.0718.

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50

Russell, Richard, and Christopher E. Brightling. "Anti-IL-5 for Severe Asthma." Chest 150, no. 4 (October 2016): 766–68. http://dx.doi.org/10.1016/j.chest.2016.06.013.

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