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Journal articles on the topic 'Interleukin-4'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 June 2025

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1

Wu, Albert Y., Sanjiv Sur, J. Andrew Grant, and Julia W. Tripple. "Interleukin-4/interleukin-13 versus interleukin-5." Current Opinion in Allergy and Clinical Immunology 19, no. 1 (2019): 30–37. http://dx.doi.org/10.1097/aci.0000000000000490.

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2

&NA;. "Interleukin-4." Reactions Weekly &NA;, no. 606 (1996): 9. http://dx.doi.org/10.2165/00128415-199606060-00029.

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3

&NA;. "Interleukin-4." Reactions Weekly &NA;, no. 468 (1993): 8. http://dx.doi.org/10.2165/00128415-199304680-00038.

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&NA;. "Interleukin 4." Reactions Weekly &NA;, no. 399 (1992): 8. http://dx.doi.org/10.2165/00128415-199203990-00030.

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&NA;. "Interleukin 4." Reactions Weekly &NA;, no. 492 (1994): 8. http://dx.doi.org/10.2165/00128415-199404920-00033.

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6

Isakson, Peter. "Interleukin 4." Advances in Neuroimmunology 2, no. 1 (1992): 55–65. http://dx.doi.org/10.1016/s0960-5428(06)80005-7.

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7

Arreaza, Guillermo A., Mark J. Cameron, and Terry L. Delovitch. "Interleukin-4." Clinical Immunotherapeutics 6, no. 4 (1996): 251–60. http://dx.doi.org/10.1007/bf03259087.

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8

Jansen, J. H., W. E. Fibbe, R. Willemze, and J. C. Kluin-Nelemans. "Interleukin-4." Blut 60, no. 5 (1990): 269–74. http://dx.doi.org/10.1007/bf01736226.

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9

Banchereau, Jacques. "Interleukin 4." International Journal of Radiation Applications and Instrumentation. Part B. Nuclear Medicine and Biology 17, no. 7 (1990): 619–23. http://dx.doi.org/10.1016/0883-2897(90)90074-b.

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10

BRINCKMANN, Roland, Max S. TOPP, Ildikó ZALÁN, et al. "Regulation of 15-lipoxygenase expression in lung epithelial cells by interleukin-4." Biochemical Journal 318, no. 1 (1996): 305–12. http://dx.doi.org/10.1042/bj3180305.

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We have studied the expression of the 15-lipoxygenase gene in various permanent mammalian cell lines in response to interleukins-4 and -13, and found that none of the cell lines tested expressed 5-, 12- or 15-lipoxygenase when cultured under standard conditions. However, when the lung carcinoma cell line A549 was maintained in the presence of either interleukin for 24 h or more, we observed a major induction of 15-lipoxygenase, as indicated by quantification of 15-lipoxygenase mRNA, by immunohistochemistry, by immunoblot analysis and by enzyme activity assays. This effect was 15-lipoxygenase-specific, since expression of 5- and 12-lipoxygenases remained undetectable. The time course of interleukin-4 treatment indicated maximal accumulation of both 15-lipoxygenase mRNA and functional protein after 48 h. Binding studies revealed that A549 cells express about 2100 high-affinity interleukin-4 binding sites per cell. The interleukin-4 mutant Y124D, which is capable of binding to the interleukin-4 receptor but is unable to trigger receptor activation, counteracted the effect of the wild-type cytokine. Other cell lines, including several epithelial cells and various monocytic cell lines expressing comparable numbers of interleukin-4 receptors, did not express 15-lipoxygenase when stimulated with interleukin-4. These data indicate that A549 cells selectively express 15-lipoxygenase when stimulated with interleukins-4 and -13. The activation of the interleukin-4/13 receptor(s) appears to be mandatory, but not sufficient, for 15-lipoxygenase gene expression.

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11

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

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12

Van Epps, Heather L. "Indecisive interleukin-4?" Journal of Experimental Medicine 201, no. 12 (2005): 1867. http://dx.doi.org/10.1084/jem20112iti3.

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13

Smith, Lorna J., Christina Redfield, Jonathan Boyd, et al. "Human interleukin 4." Journal of Molecular Biology 224, no. 4 (1992): 899–904. http://dx.doi.org/10.1016/0022-2836(92)90457-u.

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14

Vargiolu, M., T. Silvestri, E. Bonora, et al. "Interleukin-4/interleukin-4 receptor gene polymorphisms in hand osteoarthritis." Osteoarthritis and Cartilage 18, no. 6 (2010): 810–16. http://dx.doi.org/10.1016/j.joca.2010.02.005.

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15

Maroof, Asher, Michelle Penny, Rosetta Kingston, et al. "Interleukin-4 can induce interleukin-4 production in dendritic cells." Immunology 117, no. 2 (2006): 271–79. http://dx.doi.org/10.1111/j.1365-2567.2005.02305.x.

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16

Enzle, K., and G. Schulz. "Regulation of interleukin-4 activity by soluble interleukin-4 receptors." Journal of Clinical Laboratory Analysis 9, no. 6 (1995): 450–55. http://dx.doi.org/10.1002/jcla.1860090617.

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17

FLÓREZ, O., J. MARTÍN та C. I. GONZÁLEZ. "Interleukin 4, interleukin 4 receptor-α and interleukin 10 gene polymorphisms in Chagas disease". Parasite Immunology 33, № 9 (2011): 506–11. http://dx.doi.org/10.1111/j.1365-3024.2011.01314.x.

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18

Murray, Richard. "Physiologic roles of interleukin-2, interleukin-4, and interleukin-7." Current Opinion in Hematology 3, no. 3 (1996): 230–34. http://dx.doi.org/10.1097/00062752-199603030-00011.

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19

Song, Gwan Gyu, Sang-Cheol Bae, Jae-Hoon Kim, and Young Ho Lee. "Interleukin-4, interleukin-4 receptor, and interleukin-18 polymorphisms and rheumatoid arthritis: a meta-analysis." Immunological Investigations 42, no. 6 (2013): 455–69. http://dx.doi.org/10.3109/08820139.2013.804084.

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20

PARRY, R. G., K. M. GILLESPIE, A. PARNHAM, A. G. B. CLARK, and P. W. MATHIESON. "Interleukin-4 and interleukin-4 receptor polymorphisms in minimal change nephropathy." Clinical Science 96, no. 6 (1999): 665–68. http://dx.doi.org/10.1042/cs0960665.

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Minimal change nephropathy (MCN) is an important cause of nephrotic syndrome, especially in children, that is strongly associated with atopy and IgE production. The immunogenetics of MCN are poorly understood. Interleukin-4 (IL-4) is the critical cytokine involved in the development of atopy. Polymorphic regions in the genes encoding IL-4 itself and the IL-4 receptor have been demonstrated that may predispose to increased activity. We have analysed these polymorphisms in 149 patients with MCN and 73 controls to test the hypothesis that these loci are involved in genetic predisposition to MCN. In our populations there were no polymorphisms in the IL-4 promoter. We did confirm allelic variation in a dinucleotide repeat in the second intron of the IL-4 gene, but there was no significant difference between allele distributions in MCN and controls. Similarly, allele frequencies for the IL-4 receptor α chain polymorphism were similar in patients and controls. Genetic loci which are believed to influence IL-4 responsiveness and to predispose to atopy do not appear to be associated with susceptibility to MCN.

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21

PARRY, R. G., K. M. GILLESPIE, A. PARNHAM, A. G. B. CLARK, and P. W. MATHIESON. "Interleukin-4 and interleukin-4 receptor polymorphisms in minimal change nephropathy." Clinical Science 96, no. 6 (1999): 665. http://dx.doi.org/10.1042/cs19980391.

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22

Landi, Stefano, Fabio Bottari, Federica Gemignani, et al. "Interleukin-4 and interleukin-4 receptor polymorphisms and colorectal cancer risk." European Journal of Cancer 43, no. 4 (2007): 762–68. http://dx.doi.org/10.1016/j.ejca.2006.10.024.

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23

Dolzani, P., E. Olivotto, E. Assirelli, et al. "184 INTERLEUKIN-4/INTERLEUKIN-4 RECEPTOR SYSTEM ACTIVITY IN OSTEOARTHRITIC CHONDROCYTES." Osteoarthritis and Cartilage 16 (September 2008): S90. http://dx.doi.org/10.1016/s1063-4584(08)60230-7.

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24

Holter, Wolfgang. "Regulation of Interleukin 4 Production and of Interleukin 4-Producing Cells." International Archives of Allergy and Immunology 98, no. 4 (1992): 273–78. http://dx.doi.org/10.1159/000236198.

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25

Rowe, A., and C. B. Bunker. "Interleukin-4 and the interleukin-4 receptor in allergic contact dermatitis." Contact Dermatitis 38, no. 1 (1998): 36–39. http://dx.doi.org/10.1111/j.1600-0536.1998.tb05634.x.

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26

Galli Sanchez, Ana Paula, and Tatiane Ester Aidar Fernandes. "The Simultaneous Inhibition of IL‑4 and IL‑13 by Dupilumab." Journal of Clinical Research in Dermatology 8, no. 2 (2021): 1–4. http://dx.doi.org/10.15226/2378-1726/8/2/001138.

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Interleukins (IL) IL-4 and IL-13 are key players in diseases in which the Type 2 immune response is predominant, such as atopic dermatitis (AD), asthma, and chronic rhinosinusitis with nasal polyposis (CRSwNP), that are currently being treated with dupilumab. Dupilumab is a fully human IgG4 monoclonal antibody that targets the IL-4 receptor alpha chain (IL-4Rα), preventing both IL-4 and IL-13 mediated signaling. This mini-review summarizes the IL-4 receptor system as well as the mechanism of action of dupilumab. Keywords: IL-4; IL-13; dupilumab; Type 2 immunity Abbreviations AD: Atopic Dermatitis CRSwNP: Chronic Rhinosinusitis with Nasal Polyps DNA: Deoxyribonucleic Acid JAK: Janus Kinase IL: Interleukin IL-4R: Interleukin 4 Receptor IL-4Rα: Interleukin 4 Receptor alpha chain IL-13Rα1: Interleukin 13 Receptor alpha 1 chain IL-13Rα2:Interleukin 13 Receptor alpha 2 chain STAT: Signal Transducer and Activator of Transcription TGF-β: Transforming Growth Factor beta TNF: Tumor Necrosis Factor TYK2: Tyrosine Kinase 2 γc: Common gamma chain

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27

Kelly-Welch, A. E. "Interleukin-4 and Interleukin-13 Signaling Connections Maps." Science 300, no. 5625 (2003): 1527–28. http://dx.doi.org/10.1126/science.1085458.

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28

Galanakis, E., A. Makis, K. L. Bourantas, and Z. L. Papadopoulou. "Interleukin-3 and Interleukin-4 in Childhood Brucellosis." Infection 30, no. 1 (2002): 33–34. http://dx.doi.org/10.1007/s15010-002-2039-8.

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29

Ho, Steffan N., Robert T. Abraham, Steven Gillis, and David J. McKean. "Differential bioassay of interleukin 2 and interleukin 4." Journal of Immunological Methods 98, no. 1 (1987): 99–104. http://dx.doi.org/10.1016/0022-1759(87)90441-8.

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30

Yamasaki, Satoshi, and Atsushi Kawakami. "4. Interleukin-1 Inhibitor." Nihon Naika Gakkai Zasshi 100, no. 10 (2011): 2985–90. http://dx.doi.org/10.2169/naika.100.2985.

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31

Kaufman, Stefan H. E., Masashi Emoto, Gudrun Szalay, Johannes Barsig, and Inge E. A. Flesch. "Interleukin-4 and listeriosis." Immunological Reviews 158, no. 1 (1997): 95–105. http://dx.doi.org/10.1111/j.1600-065x.1997.tb00995.x.

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32

Ramı́rez, Francisco, Phil Stumbles, Mike Puklavec, and Don Mason. "Rat interleukin-4 assays." Journal of Immunological Methods 221, no. 1-2 (1998): 141–50. http://dx.doi.org/10.1016/s0022-1759(98)00176-8.

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33

Müller, W., K. Rajewsky, and R. Kühn. "Interleukin-4-deficient mice." Research in Immunology 144, no. 8 (1993): 637–38. http://dx.doi.org/10.1016/s0923-2494(05)80018-5.

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34

Steinke, John W. "Anti–interleukin-4 therapy." Immunology and Allergy Clinics of North America 24, no. 4 (2004): 599–614. http://dx.doi.org/10.1016/j.iac.2004.06.008.

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35

Paul, William E. "History of interleukin-4." Cytokine 75, no. 1 (2015): 3–7. http://dx.doi.org/10.1016/j.cyto.2015.01.038.

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36

Klein, W., A. Tromm, T. Griga, et al. "Interleukin-4 and interleukin-4 receptor gene polymorphisms in inflammatory bowel diseases." Genes & Immunity 2, no. 5 (2001): 287–89. http://dx.doi.org/10.1038/sj.gene.6363779.

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37

Lesan, Andrei, Milena Adina Man, Roxana Maria Nemes, et al. "Serum Interleukin 4 and 6 Levels Measured Using the ELISA Method in Patients with Acquired Bronchiectasis Compared to Healthy Subjects. An anti-inflammatory and pro-inflammatory relation." Revista de Chimie 70, no. 7 (2019): 2410–14. http://dx.doi.org/10.37358/rc.19.7.7351.

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Evaluation of the inflammatory response based on the Interleukin 4 and Interleukin 6 levels in patients with acquired bronchiectasis (non-cystic fibrosis) and healthy controls. The study was conducted on a group of 77 subjects, divided into 2 lots: the first lot consisting of 57 patients with acquired bronchiectasis objectified by Computed Tomography and 20 healthy individuals. The serum Interleukins 4 and 6 levels were measured using the ELISA biochemical spectrophotometry test. The results are significant from a statistical point of view, especially when it comes to the mean value of Interleukin 4 that was much higher in the control lot. Interleukin 4 is a proinflammatory cytokine and therefore we can draw the conclusion that to some extent bronchiectasis can be associated with an immunodeficiency disorder prior to the pathology itself or it can be caused by the pathology. Future research is open in this field for the analysis of interleukin levels in bronchioloalveolar lavage compared to serum levels.

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38

Najafi, Shamsolmoulouk, Mahsa Mohammadzadeh, Fateme Rajabi, et al. "Interleukin-4 and Interleukin-4 Receptor Alpha Gene Polymorphisms in Recurrent Aphthous Stomatitis." Immunological Investigations 47, no. 7 (2018): 680–88. http://dx.doi.org/10.1080/08820139.2018.1480033.

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39

Masood, Aetsam, Mahmood Kayani, and Sajida Batool. "Targetting Interleukins Involved in Glioblastoma – A New Pharmacological Approach." Journal of Life and Bio Sciences Research 1, no. 3 (2020): 82–88. http://dx.doi.org/10.38094/jlbsr1330.

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Brain tumor is unchecked growth of brain cells disrupting many of its important functions and, affecting molecular regulatory and signaling networks. Glioblastoma is one of the most deleterious tumors of human brain. Cytokines are secondary messenger molecules in many of the immunological and other biochemical reactions. With glioblastoma progression, various cytokines are secreted that either up-regulate or down-regulate many others with immunological function. Interleukins are a family of cytokines acting mainly as immune-regulatory proteins. They have been implicated in brain tumor initiation, progression and invasion. Due to their multiple and varied regulatory roles at every stage of tumor, they are now becoming an attractive target for study in glioblastoma. This mini review briefly summarizes the types and roles of major interleukins and their regulation and, effects in glioblastoma that have been studied so far. Immunotherapeutic aspects are particularly emphasized as the promising therapeutic targets to control brain tumors. Main types of interleukins which are implicated in brain tumors are discussed here which includes interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), and interleukin-12 (IL-12). Glioblastoma is one of the most invasive tumor and still lack effective control measures clinically. Conventional treatments like chemotherapy and radiation therapy are not only ineffective in controlling the spread of glioblastoma, but also have damaging and unwanted side effects on healthy cells. Immunotherapy by blocking and/or increasing the action of certain interleukins has proven to be effective control measure in laboratory investigations. Future work extending these findings to clinical and human trials is expected to provide effective treatment measures.

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40

SEWELL, WILLIAM A., and HONG-HUA MU. "Dissociation of production of interleukin-4 and interleukin-5." Immunology and Cell Biology 74, no. 3 (1996): 274–77. http://dx.doi.org/10.1038/icb.1996.48.

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41

Callard, R. E., D. J. Matthews, and L. M. Hibbert. "Interleukin 4 and interleukin 13: same response, different receptors." Biochemical Society Transactions 25, no. 2 (1997): 451–55. http://dx.doi.org/10.1042/bst0250451.

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42

Iwasaki, Yasuo, Shigeji Baba, and Ken Ikeda. "Interleukin 4 and Interleukin 10 in Creutzfeldt-Jakob Disease." Archives of Neurology 63, no. 6 (2006): 911. http://dx.doi.org/10.1001/archneur.63.6.911-a.

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43

Sotirović, J., A. Perić, D. Vojvodić, et al. "Serum cytokine profile of laryngeal squamous cell carcinoma patients." Journal of Laryngology & Otology 131, no. 5 (2017): 455–61. http://dx.doi.org/10.1017/s0022215117000573.

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AbstractObjectives:This study aimed to evaluate serum cytokine concentrations in healthy individuals and laryngeal squamous cell carcinoma patients.Methods:A total of 59 laryngeal squamous cell carcinoma patients and 44 healthy controls were included. Multiplex analysis of interleukins 2, 4, 5, 6, 10, 12, 13 and 17 and interferon-gamma with respect to the presence of laryngeal carcinoma, tumour–node–metastasis T stage, nodal involvement and larynx subsite was performed.Results:Statistical analysis revealed no difference in serum cytokine levels between patients and healthy controls. The serum interleukin-12 concentration was significantly higher in patients with early (T1–2) than in those with late (T3–4) stage disease and without nodal involvement (p < 0.05). Serum interleukin-10 levels were significantly higher in T3–4 stage than in T1–2 stage patients (p < 0.05). Additionally, serum interleukin 10, 12 and 13 concentrations (p < 0.05) and interleukin-6 concentration (p < 0.01) were significantly higher in patients with T1–2 stage supraglottic vs glottic tumours.Conclusion:Serum cytokines level cannot be used as laryngeal squamous cell carcinoma markers. Progression from T1–2 to T3–4 stage is followed by decreased serum interleukin-12 levels and increased interleukin-10 levels. Nodal involvement is associated with lower serum interleukin-12 levels. In patients with early stage tumours, serum interleukin 6, 10, 12 and 13 concentrations are significantly higher in those with supraglottic vs glottic tumours.

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44

Eman, Arif Rahman, Vitayani Muchtar Sri, Tabri Farida, et al. "EVALUATION OF INTERLEUKIN-12 AND INTERLEUKIN-4 LEVELS IN MULTIBACILLARY-TYPE LEPROSY PATIENT 12 MONTHS AFTER RIFAMPICIN OFLOXACIN MINOCYCLINE COMBINATION THERAPY." International Journal of Medical Reviews and Case Reports 2, no. 4 (2018): 161–65. https://doi.org/10.5455/IJMRCR.MULTIBACILLARY-TYPE-LEPROSY-INTERLEUKINS.

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Background: Leprosy is a chronic infectious disease caused by Mycobacterium leprae. In leprosy, cell-mediated immune responses are an important aspect of host resistance to mycobacterial infections and allegedly governed by anequilibrium between type 1 cytokines including Interleukin-12 (IL-12); with type 2 cytokines such as Interleukin-4 (IL-4). Currently, the World Health Organization (WHO) recommends 3 leprosy treatment regimens, one of them is Rifampicin Ofloxacin Minocycline (ROM). To date, studies on the effects of ROM on leprosy have been limited, none have specifically assessed the effects of ROM on specific immune systems, especially cytokines. Methods: The study was conducted by prospective research method. The sample of this research were all multibacillary (MB) type of leprosy patients according to WHO classification who had received ROM therapy and recorded as the patient at research location and had medical record previous of interleukin-12 and interleukin-4 levels. After 12 months of ROM therapy, blood samples were collected and calculated using the Enzyme-Linked Immunosorbent Assay (ELISA) using the Quantikine® high sensitivity (HSv) kit. Results: There was a statistically significant increase in IL-4 after 12 months of a 3-months-ROM therapy. In contrast, the levels of IL-12 after 12 months showed significant decreases. Conclusions: Increased levels of IL-4 and decreased IL-12 can be caused by many factors. Therefore, further research with a closer supervision is required.

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45

Saptarova, Liliyana M., Elvira A. Imelbaeva, Aliya V. Tukhbatova, Shamil N. Galimov, and Natalia A. Mufazalova. "The content of cytokines in the blood of patients with various stages of breast cancer." Kazan medical journal 103, no. 6 (2022): 947–54. http://dx.doi.org/10.17816/kmj70632.

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Background. Cytokine homeostasis is an important factor characterizing the general condition and adaptive capabilities of the body of patients with malignant neoplasms. However, the role of various growth factors and their significance in the development and enhancement of malignant growth in breast cancer remain poorly understood. Aim. To evaluate the levels of cytokines - tumor necrosis factor , interleukins-4, -6, -8 and -10 in the blood serum of patients with different stages of breast cancer in comparison with healthy volunteers. Material and methods. The study was conducted in 65 patients aged 25 to 67 years (mean age 44.5 [40.056.5] years). Two groups were distinguished: the first with stage 12, the second with stage 34 of breast cancer. The comparison group consisted of 15 apparently healthy women without cancer, aged 29 to 66 years (mean age 51.0 [39.061.0] years). Blood levels of tumor necrosis factor , interleukins-4, -6, -8 and -10 were studied by enzyme immunoassay. The obtained data were processed using the methods of variation statistics, the Statistica 10.0 software package. The significance of differences was assessed by calculating the median and interquartile interval, analysis of variance was performed using the KruskalWallis H-test, and Dan's Q-test was used for multiple comparisons. The critical significance level p for statistical tests was taken equal to 0.05. Results. In the group of patients with stage 12 breast cancer, an increase in the blood levels of all studied cytokines was revealed in comparison with the group of healthy women: interleukin-6 (p=0.00719), interleukin-8 (p=0.00259), tumor necrosis factor (p=0.00014), interleukin-4 (p1=0.0133), interleukin-10 (p1 0.00001). In the group of patients with stage 34 breast cancer, an increase in blood levels was characteristic of all studied cytokines: interleukin-8 (p=0.00009), tumor necrosis factor (p=0.000004), interleukin-4 (p 0.00001), interleukin-10 (p 0.00001), except for interleukin-6 (p=0.15608). The established patterns in changes in the content of cytokines in the blood of patients with breast cancer at different stages of development can serve as the basis for developing approaches to the diagnosis and treatment of the disease. Conclusion. In patients with breast cancer, the levels of tumor necrosis factor , interleukins-4, -6, -8, -10 (p 0.05) are higher than in healthy women.

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46

Puri, Raj K., and Jay P. Siegel. "Interleukin-4 and Cancer Therapy." Cancer Investigation 11, no. 4 (1993): 473–86. http://dx.doi.org/10.3109/07357909309018879.

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47

Snekvik, K. R., J. C. Beyer, G. Bertoni, et al. "Characterization of caprine interleukin-4." Veterinary Immunology and Immunopathology 78, no. 3-4 (2001): 219–29. http://dx.doi.org/10.1016/s0165-2427(01)00233-1.

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48

O'Garra, A. "The immunobiology of interleukin 4." Research in Immunology 144, no. 8 (1993): 567–68. http://dx.doi.org/10.1016/s0923-2494(05)80003-3.

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49

Baraniuk, James N. "Antisense oligodeoxynucleotides for interleukin-4." Current Allergy and Asthma Reports 4, no. 3 (2004): 186. http://dx.doi.org/10.1007/s11882-004-0024-2.

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50

Nagai, Shigenori, and Masakazu Toi. "Interleukin-4 and breast cancer." Breast Cancer 7, no. 3 (2000): 181–86. http://dx.doi.org/10.1007/bf02967457.

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