Bibliografías temáticas / IL-5 / Artículos de revistas

Artículos de revistas sobre el tema "IL-5"

Siga este enlace para ver otros tipos de publicaciones sobre el tema: IL-5.
Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 28 de enero de 2023

Crea una cita precisa en los estilos APA, MLA, Chicago, Harvard y otros

Elija tipo de fuente:

Consulte los 50 mejores artículos de revistas para su investigación sobre el tema "IL-5".

Junto a cada fuente en la lista de referencias hay un botón "Agregar a la bibliografía". Pulsa este botón, y generaremos automáticamente la referencia bibliográfica para la obra elegida en el estilo de cita que necesites: APA, MLA, Harvard, Vancouver, Chicago, etc.

También puede descargar el texto completo de la publicación académica en formato pdf y leer en línea su resumen siempre que esté disponible en los metadatos.

Explore artículos de revistas sobre una amplia variedad de disciplinas y organice su bibliografía correctamente.

1

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

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
2

TAKATSU, Kiyoshi. "Interleukin-5, IL-5". Journal of Japan Atherosclerosis Society 23, n.º 10 (1996): 599–603. http://dx.doi.org/10.5551/jat1973.23.10_599.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
3

Malhi, Gin S. "DSM-5: Il buono, il cattivo, il brutto". Australian & New Zealand Journal of Psychiatry 47, n.º 7 (28 de junio de 2013): 595–98. http://dx.doi.org/10.1177/0004867413496363.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
4

NAKANISHI, KENJI. "Interleukin cascade of IL-4,IL-5 and IL-2." Japanese Journal of Clinical Immunology 13, n.º 5 (1990): 438–40. http://dx.doi.org/10.2177/jsci.13.438.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
5

Stein, Miguel L., Joyce M. Villanueva, Bridget K. Buckmeier, Yoshiyuki Yamada, Alexandra H. Filipovich, Amal H. Assa'ad y 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, n.º 6 (junio de 2008): 1473–83. http://dx.doi.org/10.1016/j.jaci.2008.02.033.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
6

Warren, H. S., B. F. Kinnear, J. H. Phillips y 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, n.º 10 (15 de mayo de 1995): 5144–52. http://dx.doi.org/10.4049/jimmunol.154.10.5144.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
7

Esnault, Stephane, Mats W. Johansson y Sameer K. Mathur. "Eosinophils, beyond IL-5". Cells 10, n.º 10 (1 de octubre de 2021): 2615. http://dx.doi.org/10.3390/cells10102615.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
8

Takatsu, Kiyoshi y Hiroshi Nakajima. "IL-5 and eosinophilia". Current Opinion in Immunology 20, n.º 3 (junio de 2008): 288–94. http://dx.doi.org/10.1016/j.coi.2008.04.001.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
9

Chung, K. F. "IL-5 in asthma". Thorax 57, n.º 8 (1 de agosto de 2002): 751. http://dx.doi.org/10.1136/thorax.57.8.751.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
10

Matthaei, Klaus I., Paul S. Foster y 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 (diciembre de 1997): 63–68. http://dx.doi.org/10.1590/s0074-02761997000800010.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
11

KOPF, MANFRED, GRAHAM LE GROS, ANTHONY J. COYLE, MARIE KOSCO-VTLBOIS, FRANK BROMBACHER y Georges Kohler. "Immune Responses of IL-4, IL-5, IL-6 Deficient Mice". Immunological Reviews 148, n.º 1 (diciembre de 1995): 45–69. http://dx.doi.org/10.1111/j.1600-065x.1995.tb00093.x.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
12

Takatsu, Kiyoshi. "Interleukin 5 (IL-5) and Its Receptor". Microbiology and Immunology 35, n.º 8 (agosto de 1991): 593–606. http://dx.doi.org/10.1111/j.1348-0421.1991.tb01591.x.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
13

STEIN, M., A. MUNITZ y M. ROTHENBERG. "Increased High Molecular Weight IL-5 Complex After Anti-IL-5 (Mepolizumab) Therapy". Journal of Allergy and Clinical Immunology 121, n.º 2 (febrero de 2008): S118. http://dx.doi.org/10.1016/j.jaci.2007.12.468.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
14

Dickason, R. R., M. M. Huston y D. P. Huston. "Delineation of IL-5 domains predicted to engage the IL-5 receptor complex." Journal of Immunology 156, n.º 3 (1 de febrero de 1996): 1030–37. http://dx.doi.org/10.4049/jimmunol.156.3.1030.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
15

Ohbo, Kazuyuki, Hironobu Asoa, Kouro Taku, Nakamura Masataka, Yuji Klkuchi, Satoshl Takaki y 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, n.º 6 (1996): 951–60. http://dx.doi.org/10.1093/intimm/8.6.951.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
16

Yamaguchi, Y., T. Suda, H. Shiozaki, Y. Miura, Y. Hitoshi, A. Tominaga, K. Takatsu y 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, n.º 3 (1 de agosto de 1990): 873–77. http://dx.doi.org/10.4049/jimmunol.145.3.873.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
17

TAKATSU, SEISHI. "IL-5 and its receptor." Japanese Journal of Clinical Immunology 13, n.º 5 (1990): 441–43. http://dx.doi.org/10.2177/jsci.13.441.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
18

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

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
19

BAGLEY, C., A. LOPEZ y M. VADAS. "New frontiers for IL-5". Journal of Allergy and Clinical Immunology 99, n.º 6 (junio de 1997): 725–28. http://dx.doi.org/10.1016/s0091-6749(97)80002-4.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
20

Leung, Donald Y. M., Harold S. Nelson, Stanley J. Szefler y William W. Busse. "Anti–IL-5 for hypereosinophilia". Journal of Allergy and Clinical Immunology 113, n.º 1 (enero de 2004): 2. http://dx.doi.org/10.1016/j.jaci.2003.11.004.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
21

Ameri, Abdol A. "Weiterer IL-5-Antikörper verfügbar". MMW - Fortschritte der Medizin 159, n.º 1 (enero de 2017): 67. http://dx.doi.org/10.1007/s15006-017-9167-7.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
22

Gregory, Bernard, Antje Kirchem, Simon Phipps, Phillipe Gevaert, Carol Pridgeon, Sara M. Rankin y 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, n.º 11 (1 de junio de 2003): 5359–66. http://dx.doi.org/10.4049/jimmunol.170.11.5359.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
23

Webb, Dianne C., Andrew N. J. McKenzie, Aulikki M. L. Koskinen, Ming Yang, Joërg Mattes y Paul S. Foster. "Integrated Signals Between IL-13, IL-4, and IL-5 Regulate Airways Hyperreactivity". Journal of Immunology 165, n.º 1 (1 de julio de 2000): 108–13. http://dx.doi.org/10.4049/jimmunol.165.1.108.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
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, n.º 6 (diciembre de 2001): 985–95. http://dx.doi.org/10.1016/s1074-7613(01)00243-6.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
25

Tominaga, A., T. Takahashi, Y. Kikuchi, S. Mita, S. Naomi, N. Harada, N. Yamaguchi y 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, n.º 4 (15 de febrero de 1990): 1345–52. http://dx.doi.org/10.4049/jimmunol.144.4.1345.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
26

Zhu, W., N. Liu, Y. Zhao, H. Jia, B. Cui y 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, n.º 10 (22 de marzo de 2010): 751–55. http://dx.doi.org/10.1007/bf03346682.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
27

H, Ha, Spicer T, He Xy, Chen J, Boyd R, Tran G, Hodgkinson Sj y Hall BM. "IL-4 AND IL-5 THERAPY INHIBITS HEYMANN NEPHRITIS (HN)". Nephrology 7, n.º 1 (febrero de 2002): A113. http://dx.doi.org/10.1046/j.1440-1797.2002.00007-1-113.x.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
28

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

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
29

Solinger, Alan M. "IL-1-5 Blocking IL-1β in type 2 diabetes". Cytokine 52, n.º 1-2 (octubre de 2010): 10. http://dx.doi.org/10.1016/j.cyto.2010.07.043.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
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, n.º 8 (noviembre de 2022): A64. http://dx.doi.org/10.1016/j.fander.2022.09.062.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
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 (noviembre de 2020): 605–14. http://dx.doi.org/10.2147/jaa.s270298.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
32

Reiman, Rachael M., Robert W. Thompson, Carl G. Feng, Danielle Hari, Rachel Knight, Allen W. Cheever, Helene F. Rosenberg y Thomas A. Wynn. "Interleukin-5 (IL-5) Augments the Progression of Liver Fibrosis by Regulating IL-13 Activity". Infection and Immunity 74, n.º 3 (marzo de 2006): 1471–79. http://dx.doi.org/10.1128/iai.74.3.1471-1479.2006.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
33

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

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
34

Namkung, J. H., J. E. Lee, E. Kim, H. J. Cho, S. Kim, E. S. Shin, E. Y. Cho y J. M. Yang. "IL-5 and IL-5 receptor alpha polymorphisms are associated with atopic dermatitis in Koreans". Allergy 62, n.º 8 (agosto de 2007): 934–42. http://dx.doi.org/10.1111/j.1398-9995.2007.01445.x.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
35

TAKATSU, Kiyoshi. "Structure and Function of IL-5 Receptor". YAKUGAKU ZASSHI 115, n.º 8 (1995): 570–83. http://dx.doi.org/10.1248/yakushi1947.115.8_570.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
36

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

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
37

Hatzistilianou, M. "Serum TNF-α, IL-1β, IL-4 and IL-5 levels in bronchial asthma". Immunology Letters 56, n.º 1-3 (mayo de 1997): 155. http://dx.doi.org/10.1016/s0165-2478(97)87457-3.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
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 y Donald W. Nicholson. "Epitope-labeled Soluble Human Interleukin-5 (IL-5) Receptors". Journal of Biological Chemistry 270, n.º 49 (8 de diciembre de 1995): 29236–43. http://dx.doi.org/10.1074/jbc.270.49.29236.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
39

MORI, A., O. KAMINUMA, T. MIKAMI, S. INOUE, Y. OKUMURA, K. AKIYAMA y 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, n.º 5 (mayo de 1999): S429—S436. http://dx.doi.org/10.1016/s0091-6749(99)70158-2.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
40

Randall, T. D., F. E. Lund, J. W. Brewer, C. Aldridge, R. Wall y R. B. Corley. "Interleukin-5 (IL-5) and IL-6 define two molecularly distinct pathways of B-cell differentiation". Molecular and Cellular Biology 13, n.º 7 (julio de 1993): 3929–36. http://dx.doi.org/10.1128/mcb.13.7.3929-3936.1993.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
41

Randall, T. D., F. E. Lund, J. W. Brewer, C. Aldridge, R. Wall y R. B. Corley. "Interleukin-5 (IL-5) and IL-6 define two molecularly distinct pathways of B-cell differentiation." Molecular and Cellular Biology 13, n.º 7 (julio de 1993): 3929–36. http://dx.doi.org/10.1128/mcb.13.7.3929.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
42

Johnson, Teresa R. y 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, n.º 10 (1 de octubre de 1999): 8485–95. http://dx.doi.org/10.1128/jvi.73.10.8485-8495.1999.

Texto completo
Resumen
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.
Los estilos APA, Harvard, Vancouver, ISO, etc.
43

Uings, Iain y Murray McKinnon. "Development of IL-5 Receptor Antagonists". Current Pharmaceutical Design 8, n.º 20 (1 de septiembre de 2002): 1837–44. http://dx.doi.org/10.2174/1381612023393800.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
44

Khan, S. "Anti-IL-5 therapy and DRESS". Canadian Medical Association Journal 182, n.º 9 (14 de junio de 2010): 941. http://dx.doi.org/10.1503/cmaj.110-2054.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
45

Lakatta, Edward G. "IL-5 The heart of survival". Journal of Molecular and Cellular Cardiology 34, n.º 10 (octubre de 2002): A6. http://dx.doi.org/10.1016/s0022-2828(02)90255-5.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
46

Einecke, Dirk. "Anti-IgE oder Anti-IL 5?" MMW - Fortschritte der Medizin 159, n.º 15 (septiembre de 2017): 70. http://dx.doi.org/10.1007/s15006-017-0015-6.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
47

SUTTON, S., A. ASSAAD y M. ROTHENBERG. "Anti-IL-5 and hypereosinophilic syndromes". Clinical Immunology 115, n.º 1 (abril de 2005): 51–60. http://dx.doi.org/10.1016/j.clim.2005.02.006.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
48

Ott, Christina. "IL-5-Rezeptor-Antikörper ergänzt Therapieoptionen". MMW - Fortschritte der Medizin 160, n.º 4 (marzo de 2018): 58. http://dx.doi.org/10.1007/s15006-018-0251-4.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
49

Zahn, Stefan, Paul Godillot, Akihiko Yoshimura y Irwin Chaiken. "IL-5-INDUCED JAB–JAK2 INTERACTION". Cytokine 12, n.º 9 (septiembre de 2000): 1299–306. http://dx.doi.org/10.1006/cyto.2000.0718.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
50

Russell, Richard y Christopher E. Brightling. "Anti-IL-5 for Severe Asthma". Chest 150, n.º 4 (octubre de 2016): 766–68. http://dx.doi.org/10.1016/j.chest.2016.06.013.

Texto completo
Los estilos APA, Harvard, Vancouver, ISO, etc.
También puede estar interesado en las bibliografías sobre el tema "IL-5" para otros tipos de fuentes:
Tesis Libros
Ofrecemos descuentos en todos los planes premium para autores cuyas obras están incluidas en selecciones literarias temáticas. ¡Contáctenos para obtener un código promocional único!

Pasar a la bibliografía