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Letteratura scientifica selezionata sul tema "IL-4"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 11 marzo 2023

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Articoli di riviste sul tema "IL-4"

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, n. 04 (18 aprile 2017): 20446–50. http://dx.doi.org/10.18535/jmscr/v5i4.115.

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2

Kelly-Welch, A., E. M. Hanson e A. D. Keegan. "Interleukin-4 (IL-4) Pathway". Science Signaling 2005, n. 293 (12 luglio 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, n. 8 (15 aprile 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 e P. Rothman. "STF-IL-4: a novel IL-4-induced signal transducing factor." EMBO Journal 13, n. 6 (marzo 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 e A. D. Steinberg. "Activation of CD 4-, CD 8- thymocytes with IL 4 vs IL 1 + IL 2." Journal of Immunology 141, n. 7 (1 ottobre 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, n. 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 e 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, n. 2 (15 gennaio 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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Noben-Trauth, N., L. D. Shultz, F. Brombacher, J. F. Urban, H. Gu e 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, n. 20 (30 settembre 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 e 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, n. 5 (1 settembre 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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Reich, Adam, Justyna Szczęch e Dominik Samotij. "Biologics for Itch: IL-4/IL-13, IL-31, IL-17, and IL-23 Antagonists". Current Dermatology Reports 6, n. 4 (17 ottobre 2017): 263–72. http://dx.doi.org/10.1007/s13671-017-0204-7.

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Più fonti

Tesi sul tema "IL-4"

1

Dawson, Charlotte Helen. "STAT 6 and IL-4 signalling". Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245716.

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2

Nieuwenhuizen, Natalie. "Immune and allergic responses to Anisakis pegreffii, with focus on the roles of IL-4, IL-13 and the IL-4 receptor alpha". Doctoral thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/3115.

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Includes bibliographical references (p. 117-127).
The fish-parasitizing nematode Anisakis pegreffii induces gastrointestinal disease and allergy when ingested by humans, and can cause occupational allergy in seafood processing workers. The present study examines immune and allergic responses to A. pegreffii in wildtype and gene deficient mice, with special focus on interleukin(IL)-4, IL-13, and the IL-4 receptor alpha (IL-4Rα). Experimental murine models of Anisakis infection, Anisakis-induced anaphylaxis and Anisakis-induced dermatitis were established in order to gain insight into the immune responses generated against Anisakis and unravel mechanisms of allergic disease.

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3

Oksuz, Samet. "Targeting IL-4 locus for epigenetic reprogramming". University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1423581203.

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4

Govender, Melissa. "Investigating the role of IL-4/IL-13 signalling through the IL-4 receptor alpha (IL-4Rα) on keratinocytes in murine models of Leishmania major and Schistosoma mansoni". Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/24890.

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Keratinocytes represent the major cell type in the skin. During cutaneous leishmaniasis (CL) and schistosomiasis, the skin is important during the parasite life cycle. While Th1 immunity is required to control CL, protection during schistosomiasis requires Th2 immunity. Paradoxically, Th2 characteristic IL-4 secreted early during L. major infection in mice, can drive a Th1 response by instructing dendritic cells to produce IL-12. Additionally, keratinocytes at the site of L. major infection in C57BL/6 mice, were postulated to be the source of the IL-4. We investigated if IL-4/IL-13 signalling via the IL-4Rα on keratinocytes contributed to early immunity during CL and schistosomiasis. Keratinocyte-specific IL-4Rα deficient (KRT14creIL-4Rα-/lox) BALB/c and C57BL/6 mice were generated by gene targeting and site-specific recombination (cre/loxP) under control of the KRT14 locus. In the L. major footpad model, KRT14creIL-4Rα-/lox BALB/c mice developed increased swelling, high parasite burdens, and cytokine and antibody secretion similar to littermate controls. L. major-infected KRT14creIL-4Rα-/lox C57BL/6 mice had decreased footpad swelling, low parasite burdens, a dominant Th1 cytokine response, and low type 1 and 2 antibody titres, similar to littermate control and resistant C57BL/6. In the L major ear model, KRT14creIL-4Rα-/lox BALB/c mice developed increased swelling, high parasite burdens, Th1 and Th2 cytokines, and high antibody titres, similar to littermate controls. L. major LV39-infected KRT14creIL-4Rα-/lox BALB/c mice showed significantly decreased parasite burdens in the ear, compared to littermate controls. L. major-infected KRT14creIL-4Rα-/lox C57BL/6 mice in the ear model, had decreased swelling, low parasite burdens, a dominant Th1 immune response, and low type 1 and 2 antibody titres, similar to littermate control and C57BL/6 mice. In the Schistosoma model, survival of S. mansoni-infected KRT14creIL-4Rα-/lox BALB/c mice was similar to littermate controls during mortality studies. During acute infection, S. mansoni-infected KRT14creIL-4Rα-/lox BALB/c mice showed gut pathology, hepatosplenomegaly, cytokine production, low type 1 and high type 2 antibodies, similar to littermate controls. In comparison to littermate controls, S. mansoni-infected KRT14creIL-4Rα-/lox BALB/c mice had smaller granulomas. Collectively, our results indicate that IL-4/IL-13 signalling through the IL-4Rα on keratinocytes is not required for control during CL or acute schistosomiasis, but does contribute to efficient granuloma formation during acute schistosomiasis.

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5

Мозгова, Юлія Анатоліївна, Юлия Анатольевна Мозговая e Yuliia Anatoliivna Mozghova. "Динаміка вмісту IL-4 та IL-6 при хронічному тонзиліті в дітей". Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32359.

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Хронічне запалення піднебінних мигдаликів є розповсюдженим захворюванням дитячого віку, що несприятливо впливає на зростаючий організм. На хронічний тонзиліт страждає більше 2-3% дітей раннього віку, 6-7% - дошкільного та 8-9% школярів. При цитуванні документа, використовуйте посилання http://essuir.sumdu.edu.ua/handle/123456789/32359

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6

Pizzuti, Lucas. "Síntese de 4-(fur-2-il)- e 4-(tien-2-il)-pirimidinas a partir de β-Alcoxivinil trifluormetil cetonas". Universidade Federal de Santa Maria, 2005. http://repositorio.ufsm.br/handle/1/10401.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
The cyclocondensation of the 1,1,1-trifluoro-4-methoxy-4-(2-heteroaryl)-3-buten-2-ones (heteroaryl = furyl and thienyl) with urea and amidines (acetamidine, benzamidine, guanidine, 1H-pyrazole-1-carboxamidine and 2-methyl-2-thiopseudourea) for synthesis of two 4-(2-heteroaryl)-6-trifluoromethylpyrimidinones and a series of ten 4-(2-heteroaryl)-6-trifluoromethylpyrimidines is reported. The reaction of the 1,1,1-trifluoro-4-methoxy-4-(2-heteroaryl)-3-buten-2-ones with urea was carried out in the presence of boron trifluoride etherate as a catalyst, at 50°C for 20 hours. The reactions of the same substracts with amidines were carried out in the presence of a 1 M solution of sodium hydroxide at r.t.-50°C for 1 hour. Under this conditions, only aromatic pyrimidines were obtained in 48-67%.
Este trabalho relata a síntese e isolamento de duas 4-(2-heteroaril)-6-trifluormetilpirimidinonas e uma série de dez 4-(2-heteroaril)-6-trifluormetilpirimidinas (heteroaril = furil e tienil), a partir da ciclocondensação de 1,1,1-trifluor-4-metoxi-4-(2-heteroaril)-3-buten-2-onas com uréia e amidinas (acetamidina, benzamidina, guanidina, 1Hpirazolil-1-carboxamidina e 2-metil-2-tiopseudouréia). A reação de 1,1,1-trifluor-4-metoxi-4-(2-heteroaril)-3-buten-2-onas com uréia ocorreu na presença de BF3.Et2O como catalisador, à 50°C por 20 horas. As reações dos mesmos substratos com amidinas ocorreu na presença de uma solução 1 M de NaOH à t.a.-50°C por 1 hora. Nestas condições, foram obtidas somente pirimidinas aromáticas com rendimentos entre 48-67%.

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7

Cirocco, Robert E. "Cytokine analisys in atlantic bottlenose dolphins: molecular characterization of IL-4, IL-6, and IL-10". FIU Digital Commons, 2001. http://digitalcommons.fiu.edu/etd/2370.

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The health status of wild and captive Atlantic Bottlenose dolphins (Tersiops truncatis) is difficult to ascertain. Mass strandings of these animals have been attributed to pollutants, as well as bacterial infections. Using human Enzyme Linked Immuno-Assays (ELISA) for immunological cytokines, I measured soluble cytokine levels with respect to their health status. In a retrospective analysis of dolphin sera, there was a trend of higher cytokine levels in “sick” animals. I cultured dolphin lymphocytes in the presence of a mitogen (PHA), a super antigen (Staph-A), Lipopolysaccharide (LPS), and a calcium flux inducer (PMA). Levels of messenger RNA, from these cultured cells, were assayed with Polymerase Chain Reaction (PCR) using primers for the human cytokines IL-2, EL-4, IL- 6, IL-10, Tumor Necrosis Factor, and Interferon gamma. Only IL-4, IL-6, and IL-10 messages were obtained, inferring similar nucleotide homology to the human primer sequences. The PCR products were sequenced. Sixteen IL-4 sequences, twelve IL-6 sequences and seven IL-10 sequences were obtained and analyzed. Each cytokine exhibited the same nucleotide sequence in all dolphins examined. There was no difference in the cytokine profile in response to the various stimuli. The derived amino acid composition for each of the dolphin cytokines was used for molecular modeling, which showed that dolphin IL-4, IL-6, and IL-10 were structurally similar to the corresponding proteins of Perissodactyla.

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8

Vale, Mariana Lima. "Atividade analgesica das interleucinas 4, 10 e 13 (IL-4, IL-10 e il-13) na dor inflamatoria experimental : papel de celulas residentes e citocinas". reponame:Repositório Institucional da UFC, 2000. http://www.repositorio.ufc.br/handle/riufc/2569.

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VALE, Mariana Lima. Atividade analgesica das interleucinas 4, 10 e 13 (IL-4, IL-10 e il-13) na dor inflamatoria experimental : papel de celulas residentes e citocinas. 2000. 140 f. Dissertação (Mestrado em Farmacologia) - Universidade Federal do Ceará. Faculdade de Medicina, 2000.
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The release of cyclo-oxigenase products and sympathomimetics amines, the final mediators of inflammatory pain, is preceded by the generation of cytokines by resident cells. In recent years a number of cytokines such as IL-4, IL-10, IL-13, IL-6, TGF-β e IFN-α have been described to inhibit the production of TNF-α, IL-1β, IL-6 and IL-8 (cytokines regarded as pró-inflammatory) and possibly to exert their modulatory effect on macrophages and mast cells. Since it is known the capacity of those cytokines to inhibit the production of pro-inflammatory cytokines and the pivotal role of resident cells in the development of inflammatory pain we have decided to test the possibility of IL-4, IL-13 and IL-10 to modulate inflammatory pain. In short, IL-4 (1 – 5ng/animal), IL-13 (0.4 - 2.5ng/animal) or IL-10 (0.4 - 10ng/animal) was given 30 min before acetic acid (AAc) or zymosan (Zym) administration in the writhing model. IL-4 (2.5 e 5 ng/animal), IL-13 (1 e 2.5 ng/animal) or IL-10 (2 e 10 ng/animal) were injected, ip, 30 min before Zym (1 mg/animal; intra-articular) in the rat knee joint incapacitation test up to the 4th hour (the number of leukocytes was determined in the articular exsudate 6 hours later). Doses of those cytokines that exerted maximum effect in the writhing test were also injected 30 min before the hot plate test. These same doses were injected ip before naloxone administration in the AAc-induced writhing model in mice. TNF-α and IL-1β were determined in the supernatant of a macrophage culture which were collected from peritoneal fluid of mice treated with Zym and pre-treated with the cytokines under test. Our results show that interleukins 4, 13 and 10 inhibit writhing response in mice induced by AAc or Zym up to 58.7, 89.2 and 52%, and up to 62.6, 61.7 and 74.4%, respectively (p<0.05). Similar results were observed in the rat knee joint incapacitation test induced by Zym: 49.2, 56.6, 69,9% of inhibition (p<0.05). The same interleukins were able to inhibit Zym-induced leukocyte influx into articular cavity (53.8, 92.1 e 62% of inhibition, respectively - p<0,05). The analgesic activity of IL-4, IL-13 and IL-10 seems to be peripheral, since these cytokines presented no effect in the reaction time of the animals on hot plate test. This antinociceptive effect seems to have no relation with endogen opioid release since naloxone (opioid receptor antagonist) had no effect in reverting the antinociceptive effect of cytokines in the AAc-induced writhing in mice. However, IL-4 and IL-10 inhibit the release of TNF-α (42 e 41.2%, respectively - p<0.05) and of IL-1β (61.9 e 80.9%, respectively - p<0,05) by macrophages stimulated in vivo by Zym, indicating that their antinociceptive activities may be due to the inhibition of those cytokines release by resident cells.
Já está estabelecido que a liberação de produtos da cicloxigenase e aminas simpatomiméticas, mediadores finais da dor inflamatória é precedido pela geração, por células residentes, de uma cascata de citocinas. Recentemente dados do nosso laboratório demonstraram que no modelo de contorções abdominais (CA) a ativação dessa cascata é dependente também da presença de células residentes como macrófagos e mastócitos. Dados da literatura apontam algumas citocinas capazes de modular negativamente a função dessas células: IL-4,. IL-10, IL-13, IL-6, TGF-β e IFN-α . Com base nesses dados, o objetivo do presente trabalho foi estudar uma possível atividade analgésica de três citocinas: IL-4, IL-13 e IL-10. Para tanto injetou-se, via ip, IL-4 (1–5ng/animal), IL-13 (0.4-2.5ng/animal) ou IL-10 (0.4-10ng/animal) 30 min antes da administração de zymosan (Zym) ou ácido acético (AAc) para o teste de CA. IL-4 (2.5 e 5ng/animal), IL-13 (1 e 2.5ng/animal) ou IL-10 (2 e 10ng/animal) foi injetada, ip, 30 min antes do Zym (1 mg/animal; intra-articular) e logo após foi medida a incapacitação articular (IA) até a 4ª hora e na 6ª hora foi feita a contagem de leucócitos no fluido articular. As interleucinas estudadas também foram administradas (30 min antes) na dose que melhor inibiu as CA no teste da placa quente (PQ) e em camundongos que haviam recebido ou não a naloxona previamente ao estímulo (AAc) no teste de CA. IL-4 (5 ng/animal) ou IL-10 (10 ng/animal) foi injetada ip 30 min antes do Zym (ip) e após 15 min os animais foram sacrificados e o exsudato peritoneal foi colhido e posto em cultura para a dosagem de IL-1β e TNF-α no sobrenadante. No presente trabalho ficou demonstrado que as interleucinas-4, 13 e 10 são analgésicas tanto no modelo de CA induzidas por AAc (58.7, 89.2, 52% de inibição, efeito máximo, respectivamente, p<0.05) ou Zym (62.6, 61.7, 74.4% de inibição, efeito máximo, respectivamente, p<0.05) como também no modelo de IA induzido por Zym (49.2, 56.6, 69,9% de inibição, efeito máximo, respectivamente, p<0.05). As citocinas estudadas foram capazes de inibir o influxo de leucócitos para a cavidade articular (53.8, 92.1 e 62%, respectivamente - p<0,05). Foi demonstrado que o efeito analgésico parece ser de domínio periférico visto que nenhuma das citocinas modificou o tempo de reação na PQ, teste algesimétrico sensível apenas para drogas que exercem efeito central. Também foi demonstrado que a atividade analgésica das interleucinas testadas não depende da liberação de opióides endógenos, visto que o pré-tratamento com naloxona não foi capaz de reverter a atividade analgésica de nenhuma das interleucinas no modelo de CA. Contudo essa atividade analgésica parece depender da inibição da liberação de citocinas por células residentes visto que IL-4 e IL-10 foram capazes de diminuir a liberação de TNF-α (42 e 41.2% de inibição respectivamente - p<0.05) e IL-1β (61.9 e 80.9% de inibição respectivamente - p<0,05) por macrófagos peritoneais residentes.

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Toor, Iqbal Singh. "Investigating the role of eosinophils in cardiac remodelling following myocardial infarction". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31187.

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Myocardial infarction (MI) occurs following acute thrombotic occlusion of a coronary artery, and triggers a robust inflammatory response. Within hours, neutrophils are recruited to the infarcted myocardium followed by the infiltration of pro-inflammatory Ly6Chi monocytes. Transition from the pro-inflammatory macrophage phenotype (M1) to an anti-inflammatory, pro-resolution phenotype (M2-like) is critical to successful infarct healing. Interventions that polarize macrophages towards an anti-inflammatory 'M2-like' phenotype improve infarct healing in the experimental MI mouse model and reduce subsequent adverse remodelling of the myocardium, but the endogenous mechanisms that regulate repair are not well understood. Furthermore, differences in the resolution of inflammation in C57BL/6 and BALB/c mice, which are two of the commonly used wild-type mouse strains in experimental MI have not been characterised. We previously found that low peripheral blood eosinophil count is associated with increased short-term risk of mortality in low-intermediate risk patients with ischaemic heart disease. This suggests that eosinophils may have a role in the successful remodelling and repair of the heart following myocardial infarction. Eosinophils express a number of immuno-modulating cytokines and lipid mediators implicated in the resolution of inflammation. Increasingly prominent is interleukin-4 (IL-4), a cytokine that has been found to maintain the anti-inflammatory M2-like phenotype in macrophages. We therefore hypothesised that IL-4Rα signalling and recruitment of eosinophils to the myocardium following infarction are key in regulating the subsequent inflammatory response and scar tissue formation during infarct repair and cardiac remodelling. Experimental MI was induced by permanent left anterior descending artery ligation in isofluorane anaesthetized 12-15 week-old male wild-type (WT) BALB/c, WT C57BL/6, IL4Rα-/-, IL-4Rαflox/-, IL-4Rαflox/-LysMCre mice and eosinophil-deficient ΔdblGATA mice. Cardiac function was characterised by high-resolution ultrasound and immune cell infiltration by flow cytometry of single cell infarct and remote zone tissue digests. Blood eosinophil count and 6-month all-cause mortality were assessed in 732 consecutive patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction (STEMI). The rate of mortality due to cardiac rupture was significantly higher in C57BL/6 mice in comparison with BALB/c mice at Day 7 post-MI. This was associated with a higher proportion of pro-inflammatory Ly-6Chi macrophages infiltrating the infarct zone tissue of C57BL/6 mice following MI. An accompanying reduction in the number of splenic Ly-6Chi monocytes post-MI, suggestive of splenic monocyte mobilisation, was seen in C57BL/6 mice but not found in BALB/c mice. Furthermore, C57BL/6 mice had a delayed transition in macrophage polarisation towards an anti-inflammatory phenotype. Disruption of IL4Rα signalling, in mice null for the IL4Rα gene, resulted in increased F4/80+ macrophage and pro-inflammatory Ly6Chi macrophage infiltration of the infarct zone and reduced expression of the anti-inflammatory macrophage marker CD206, compared to wild-type controls. Furthermore, expression of GATA3 and ST2, both associated with the immunosuppressive function of (CD4+ Foxp3+) regulatory T cells, was reduced in infarct zone regulatory T cells from IL4Rα-/- mice. These findings were associated with defective wound healing with impaired angiogenesis, increased scar size, disarrayed infarct zone collagen deposition, accompanied by modified expression of plod2 that encodes the collagen cross-linking enzyme lysyl hydroxylase 2. Resulting in greater left ventricular dilatation and loss of cardiac function, as well as a higher 7- day mortality due to cardiac rupture in IL4Rα-/- mice. This indicates that successful infarct repair requires the engagement of IL-4Rα signalling to facilitate the accumulation of anti-inflammatory macrophages and highly immunosuppressive ST2+ regulatory T cells in the heart following MI. Resident cardiac macrophages from naïve hearts of IL-4Rαflox/-LysMCre mice failed to undergo LysMCre-mediated deletion of the IL-4Rα gene, potentially because low or absent expression of Lyz2 (encoding lysozyme M). In both ST-elevation MI (STEMI) patients and mice after acute MI, there was a decline in peripheral blood eosinophil count, with activated eosinophils being recruited to the infarct zone and paracardial adipose tissue of mice. The transcription factors GATA-1 plays a role in the differentiation of eosinophils from eosinophil progenitor cells. Deletion of GATA-1 results in loss of the eosinophil lineage and has been exploited to develop the eosinophil-deficient ΔdblGATA mouse. ΔdblGATA mice were used to address the role of eosinophils in cardiac remodelling following MI. ΔdblGATA mice had increased left ventricular dilatation and reduced ejection fraction after induction of MI, relative to wild-type mice. ΔdblGATA mice had increased scar size with disarrayed infarct zone collagen deposition, accompanied by modified expression of the genes plod2 and lox, which are associated with collagen cross-linking. The proportion of CD206+ anti-inflammatory macrophages was less in the infarct zone of ΔdblGATA mice, but was restored by adoptive transfer of eosinophils from WT mice. Furthermore, adverse cardiac remodelling in eosinophil-deficient ΔdblGATA mice was rescued by provision of IL-4 complex following MI. In conclusion, an enhanced inflammatory response following MI underlies the increased risk of cardiac rupture seen with WT C57BL/6 mice in comparison to WT BALB/c mice. WT BALB/c mice are protected from cardiac rupture, which was associated with an absence of splenic monocyte mobilisation following ischaemic injury. The resolution of inflammation was found to be dependent on IL4Rα signalling which is crucial for cardiac repair and remodelling, through modulating inflammatory cell recruitment and phenotype, as well as scar formation. Eosinophils are recruited to the heart post-MI and are essential for regulating cardiac repair and remodelling, likely through provision of IL-4. Therefore, we were able to show that IL-4Rα signalling and recruitment of eosinophils to the myocardium following infarction are both key in regulating the subsequent inflammatory response and scar tissue formation during infarct healing and cardiac remodelling.

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Dheda, Keertan Unkha Jairam. "The expression and role of IL-4 and IL-4(delta)2 in tuberculosis with and without HIV co-infection". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445411/.

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Background: Tuberculosis progresses despite potent Thl responses. A putative explanation is the presence of a subversive Th2 response. However interpretation is confounded by a novel cytokine, IL-452, a splice variant and inhibitor of IL-4. Methods: The expression of Thl cytokines (IFN-y), IL-452, Th2 cytokines (IL-4) and sCD30 was investigated in whole blood, lung lavage and mononuclear cell cultures from donors with TB, TB-HIV co-infection, and matched controls. Results: After validation of a fluorogenic real-time RT-PCR assay, the half-life of IL- 4 mRNA, but not IL-452, was found to be prolonged in TB vs controls (P<0.002). mRNAs for IL-4 and IL-452 were elevated in unstimulated cells from blood and lung lavage of patients vs controls (p<0.005). Patients with TB expressed significantly greater mRNA levels of both cytokines in T-cells (p<0.05 compared to controls where expression was predominantly in non-T cells). Radiological disease correlated with the IL-4/IFN-y ratio and sCD30 (p<0.005). Tuberculosis antigen upregulated expression of IL-4 relative to IL-462 in mononuclear cell cultures from tuberculosis patients (P<0.05). By contrast, though HIV-TB co-infected donors had increased IL-4 in blood and lung lavage, in lung the predominant form was IL-452. After chemotherapy, in tuberculosis and in HIV-TB co-infection, IL-4 mRNA levels remained unchanged whilst IL-462 increased (p<0.05). Conclusions: A Th2-like response, prominent in T cells, and driven by TB antigen, is present in TB and is modulated by treatment suggesting a role for IL-4 and its antagonist, IL-452 in the pathogenesis of TB and their ratio as a possible marker of disease activity. Furthermore, enhancement of IL-4 mRNA stability, a hitherto undescribed regulatory mechanism in human TB, may facilitate the immunopathological effect of IL-4. The specific antigens inducing the IL-4 response require identification to facilitate future vaccine development strategies. Further studies are required to determine whether IL-4 facilitates systemic HIV progression in co-infected patients.

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Libri sul tema "IL-4"

1

Samolot bombowy DB-3/Ił-4. Warszawa: Dom Wydawniczy Bellona, 2006.

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2

Mutin, U. G. Lichnai︠a︡ voĭna mekhanika Il-4. Staryĭ Oskol: Rosa, 2012.

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3

1948-, Spits Hergen, a cura di. IL-4: Structure and function. Boca Raton, FL: CRC Press, 1992.

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4

Kotelnikov, Vladimir. Il-4: "vozdushnye kreĭsera" Stalina. Moskva: I︠A︡uza, 2009.

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5

Lazara, Silvia Ferri de, Giulia D'Amaro Valle e Enoch Battagin. Cos'è il contemporaneo? 4: What is the contemporary? 4. Padova: CLEUP, 2012.

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6

Trevisi, Giuseppe. Il delitto Fanin: 4 novembre 1948. Bologna: Il Mulino, 1998.

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7

Il gastigamatti: Commedia in 4 atti. Firenze: FirenzeLibri, 2010.

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8

Giuseppe, Verdi. Il trovatore: Dramma in 4 parti. Roma: Gremese Editore, 1988.

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Giuseppe, Verdi. Il Trovatore: Dramma in 4 parti. Roma: Gremese Editore, 1988.

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10

Natacha, Godeau, a cura di. Shrek 4: Il était une fin. [Paris]: Hachette jeunesse, 2010.

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Capitoli di libri sul tema "IL-4"

1

Ranasinghe, Charani, Sreeja Roy, Zheyi Li, Mayank Khanna e Ronald J. Jackson. "IL-4 and IL-13 Receptors". In Encyclopedia of Signaling Molecules, 2549–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101978.

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2

Ranasinghe, Charani, Sreeja Roy, Zheyi Li, Mayank Khanna e Ronald J. Jackson. "IL-4 and IL-13 Receptors". In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101978-1.

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3

Pelaia, Girolamo, Alessandro Vatrella e Rosario Maselli. "Anti-IL-4/IL-13 Biologics". In Asthma: Targeted Biological Therapies, 67–81. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46007-9_6.

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4

Borish, Larry, John W. Steinke, Marion Kasaian e Samuel J. Goldman. "IL-4- and IL-13-directed approaches". In New Drugs and Targets for Asthma and COPD, 115–21. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320808.

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5

Schroeder, John T. "Diagnostic Components: T Helper Cell Cytokines (IL-4, IL-5, IL-9, IL-10, IL-13, IL-17)". In Encyclopedia of Medical Immunology, 221–26. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9194-1_298.

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6

Keegan, Achsah, Keats Nelms e William E. Paul. "The IL-4 Receptor — Signaling Mechanisms". In Advances in Experimental Medicine and Biology, 211–15. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-0987-9_21.

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7

Clair, R. P. "Saturday, September 4, 2010—Chicago, IL". In Zombie Seed and the Butterfly Blues, 323–25. Rotterdam: SensePublishers, 2013. http://dx.doi.org/10.1007/978-94-6209-308-9_60.

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8

Clair, R. P. "Saturday, September 4, 2010—Chicago, IL". In Zombie Seed and the Butterfly Blues, 327. Rotterdam: SensePublishers, 2013. http://dx.doi.org/10.1007/978-94-6209-308-9_61.

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9

Shirokaze, J., K. Yanagida, K. Shudo, K. Konomoto, K. Kamiya e K. Sagara. "IL-4 Production Using Macroporous Microcarrier". In Animal Cell Technology: Developments Towards the 21st Century, 877–81. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0437-1_141.

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10

Khan, Manzoor M. "Regulation of IL-4 and IL-5 Secretion by Histamine and PGE2". In Advances in Experimental Medicine and Biology, 35–42. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1891-4_5.

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Atti di convegni sul tema "IL-4"

1

Kalinauskaitė-Žukauskė, Virginija, Andrius Januškevičius, Ieva Janulaitytė e Kęstutis Malakauskas. "IL-4, IL-8, IL-13, IL-17, IL-33 serum levels changes in acute allergic asthma model". In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp237.

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2

Muchtar, R. Masri. "294 Polymorphism promotor gene of il-4 and il-4 level at graves disease patients". In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.294.

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3

Haque, S. Jaharul, Rikhia Chakraborty, Pankaj Sharma, Suzy Comhair, Sudakshina Ghosh, Weiling Xu, Manoj M. Veleeparambil et al. "Antioxidant-Mediated Negative Regulation Of IL-4/IL-13 Signaling". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2794.

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4

Kalinauskaitė-Žukauskė, Virginija, Andrius Januškevičius, Ieva Janulaitytė e Kęstutis Malakauskas. "LSC - 2019 - IL-4, IL-8, IL-13, IL-17, IL-33 serum levels changes in acute allergic asthma model". In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4083.

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5

Butova, Tatiana, Mykhailo Kuzhko, Dmytro Butov e Nataliya Piriatinskaa. "Association between IL-2,IL-4 gene polymorphisms and pulmonary MDRTB". In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3035.

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6

Yadav, Aravind, Rakesh Naidu e Gopala Krishnan Govindasamy. "IL-4, IL-13 And IL-4RA Gene Polymorphisms And The Risk For Developing Idiopathic Nonallergic Rhinitis". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4191.

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7

Punia, Navneet, Jennifer Thomson, Irene Babirad e Roma Sehmi. "IL-4 And IL-13 Prime The Transmigrational Responses Of Hemopoietic Progenitor Cells". In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4034.

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8

Wirth, F., A. Lubosch, C. Zöller, K. Huck e I. Nakchbandi. "Osteoblasten stimulieren die Hämatopoese durch IL-4 Produktion". In Jahreskongress DVO OSTEOLOGIE 2021. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1722115.

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9

Le Floc’H, Audrey, Jeanne Allinne, Kirsten Nagashima, George Scott, Dylan Birchard, Seblewongel Asrat, Matthew Sleeman, Andrew Murphy e Jamie Orengo. "Il-4 and IL-13 act independently and synergistically to drive type 2 inflammation". In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5206.

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10

Blauvelt, Andrew, e Susanne Kammerer. "Novel IL-4/IL-13 blocker shows high efficacy with only modest conjunctivitis signal". In 2022 American Academy of Dermatology Annual Meeting, a cura di Peter van de Kerkhof. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/8aee17f2.

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Rapporti di organizzazioni sul tema "IL-4"

1

Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang e Chenming Xu. Association of IL-4 and IL-10 Polymorphisms with Preterm Birth Susceptibility: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2022. http://dx.doi.org/10.37766/inplasy2022.4.0044.

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Review question / Objective: The aim of our systematic review and meta-analysis was to summarize the effects of IL-4 and IL-10 gene polymorphism and clarify their possible association with PTB. Condition being studied: World Health Organization (WHO) defines preterm birth (PTB) as babies born alive before 37 weeks of pregnancy are completed. The new estimates show that the prevalence of PTB during 2014 ranged from 8.7% to13.4% of all live births, about 15 million preterm babies born each year. Besides, PTB is the leading cause of death worldwide for children below 5 years of age. Babies born preterm are at an increased risk of short-term and long-term complications attributed to immaturity of multiple organ systems, such as cerebral palsy, intellectual disabilities, vision and hearing impairments, and impaired cognitive development. PTB has become a worldwide public health problem, but its etiology remains unclear. Accumulating evidence shows that PTB is a syndrome that can be attributed to a variety of pathological processes(5). Inflammatory diseases and genetic background are known risk factors for PTB, many studies had shown that genetic variations in proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 α (IL-1 α) are associated with increased risk of PTB, but the relationship between genetic polymorphism in anti-inflammatory cytokines and risk of PTB remains controversial.

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2

Gilroy, Jill M. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, ottobre 2001. http://dx.doi.org/10.21236/ada403390.

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3

Gooch, Jennifer L. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, luglio 1999. http://dx.doi.org/10.21236/ada390684.

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4

Gooch, Jennifer. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, luglio 2000. http://dx.doi.org/10.21236/ada384372.

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5

Sachdev, Deepali. Role of IRS-1 Phosphorylation in IGF-1 and IL-4 Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, giugno 2001. http://dx.doi.org/10.21236/ada396609.

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6

Sachdev, Deepali. Role of IRS-1 Phosphorylation in IGF-1 and IL-4 Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, giugno 2002. http://dx.doi.org/10.21236/ada407504.

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7

Sachdev, Deepali. Role of IRS-1 Phosphorylation in IGF-1 and IL-4 Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, giugno 2003. http://dx.doi.org/10.21236/ada418308.

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8

Liu, Miao, Hongan Wang, Jing Lu, Zhiyue Zhu, Chaoqun Song, Ye Tian, Xinzhi Chen et al. Vitamin D supplementation in the treatment of Myasthenia Gravis A protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, settembre 2022. http://dx.doi.org/10.37766/inplasy2022.9.0129.

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Review question / Objective: The patients should meet the internationally recognized diagnostic criteria for myasthenia gravis and be definitely diagnosed as myasthenia gravis, excluding MG patients caused by congenital, drug and other factors, as well as patients with serious primary diseases, autoimmune diseases or mental diseases. Patients are not restricted by race, region, gender, age, background, course of disease and other factors. We will focus on trials using vitamin D as an intervention at any dose and in any regimen (eg daily/weekly/monthly intake). The control group was routinely given western medicine, including cholinesterase inhibitors, glucocorticoids, immunosuppressants, alone or in combination, or placebo. The intervention group was treated with vitamin D on the basis of western medicine treatment in the control group. The specific dosage form and dose were not limited, and the shortest course of treatment should be 4 weeks. Main outcome measures: (1) Quantitative score of myasthenia gravis (QMG); (2) Recurrence rate; (3) Effective. Secondary outcome measures: (1) The level of serum acetylcholine receptor antibody (AchRab); (2) The levels of inflammatory factors such as IL-6 and IL-10; (3) Clinical absolute score; (4) TCM syndrome score scale; (5) Quality of life score (QOL); (6) Incidence rate of adverse events. All randomized controlled trials (RCT) literatures from the establishment to September 2022 were retrieved and classified.

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Shomer, Ilan, Louise Wicker, Uzi Merin e William L. Kerr. Interactions of Cloud Proteins, Pectins and Pectinesterases in Flocculation of Citrus Cloud. United States Department of Agriculture, febbraio 2002. http://dx.doi.org/10.32747/2002.7580669.bard.

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The overall objective was to understand the cloud flocculation of citrus juice by characterization of the interactions between proteins and pectins, and to determine the role of PE isozymes in catalyzing this phenomenon. Specific objectives were to: 1. identify/characterize cloud-proteins in relation to their coagulable properties and affinity to pectins; 2. to determine structural changes of PME and other proteins induced by cation/pectin interactions; 3. localize cloud proteins, PME and bound protein/pectates in unheated and pasteurized juices; 4. to create "sensitized" pectins and determine their effect on clarification. The original objectives were not changed but the methods and approach were modified due to specific research requirements. Two i postulates were: 1. there is a specific interaction of cloud proteins with de-esterified regions of ! pectin and this contributes to cloud loss; 2. isozymes of pectin-methyl-esterase (PME) vary in efficiency to create sensitized pectins. The appearance of citrus fruit juice is an important quality factor and is determined by the color and turbidity that .are conferred by the suspended particles, i.e., by the cloud and its homogeneity. Under some circumstances the cloud tend to flocculate and the juice clarifies. The accepted approach to explain the clarification is based on pectin demethoxylation by PME that promotes formation of Ca-pectate. Therefore, the juice includes immediate heat-inactivation upon ~ squeezing. Protein coagulation also promotes cloud instability of citrus fruit extracts. However, the clarification mechanism is not fully understood. Information accumulated from several laboratories indicates that clarification is a more complex process than can be explained by a single mechanism. The increasing trend to consume natural-fresh juice emphasizing the importance of the knowledge to assure homogeneity of fresh juice. The research included complementary directions: Conditions that induce cloud-instability of natural- juice [IL]. Evaluate purification schemes of protein [USA]. Identifications of proteins, pectin and neutral sugars ([IL]; Structure of the cloud components using light and electron microscopy and immuno-labeling of PME, high-methoxyl-pectin (HMP) and low-methoxyl-pectin (LMP); Molecular weight of calcium sensitized pectins [US]; Evaluation of the products of PME activity [US]. Fractions and size distribution and cloud components [IL-US]. The optimal pH activity of PME is 7 and the flocculation pH of the cloud is 3-4. Thus, the c roles of PME, proteins and pectins in the cloud instability, were studied in pH ranges of 2- 7. The experiments led to establish firstly repeatable simulate conditions for cloud instability [IL]. Thermostable PME (TS-PE) known to induce cloud instability, but also thermolabile forms of PME (TL-PE) caused clarification, most likely due to the formation and dissolution of inactive :. PE-pectin complexes and displacement of a protective colloid from the cloud surface [US]. Furthermore, elimination of non-PME protein increases TS-PE activity, indicating that non-PME proteins moderate PME activity [US]. Other experiments Concomitantly with the study of the PME activity but promotes the association of cloud-proteins to pectin. Adjusting of the juice pH to f 7 retains the cloud stability and re-adjusting of the pH to 40% DE reacts to immuno-labeling in the cloud fragments, whereas

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Elmann, Anat, Orly Lazarov, Joel Kashman e Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, marzo 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.

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