The regulation of interleukin 5 and interleukin 3 gene expression in human T cells

Straaten, Jeanette F.M. van; Dokter, Wha; Stulp, Ben K.; Vellenga, Edo

doi:10.1016/1043-4666(94)90017-5

Cited by 21 publications

(11 citation statements)

References 14 publications

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“…By virtue of the pattern of cytokines that they synthesize, Th2 cells are thought to control the growth and effector function of those cell types that are involved in allergic inflammatory responses [34,35,36,37,38]. As with other cytokines, regulation of interleukin-5 production is thought to result from activation of gene transcription [37]. Interleukin-5 synthesis is also regulated at the level of mRNA stability [39].…”

Section: Genomics and Biochemistry Of The Interleukin-5 Systemmentioning

confidence: 99%

“…Interleukin-5 synthesis is also regulated at the level of mRNA stability [39]. Interleukin-5 gene expression requires de novo protein synthesis, and is effectively inhibited by glucocorticoids and cyclosporine [36,37,40]. Furthermore, in vivo depletion of T cells in a mouse model of pulmonary inflammation reduces pulmonary eosinophilia, and interleukin-5 and other cytokine mRNA levels [38].…”

Section: Genomics and Biochemistry Of The Interleukin-5 Systemmentioning

confidence: 99%

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Th2 cytokines and asthma The role of interleukin-5 in allergic eosinophilic disease

Greenfeder¹,

Umland²,

Cuss³

et al. 2001

Respir Res

207

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Available online http://respiratory-research.com/content/2/2/071 IntroductionSeveral allergic diseases, such as nasal rhinitis, nasal polyps, asthma, idiopathic eosinophilic syndromes, and atopic dermatitis, have prominent inflammatory components that are characterized by pronounced eosinophilic infiltration [1]. As a result, the role of chronic pulmonary inflammation in the pathophysiology of asthma has been studied extensively in human and in animal models. In asthma, pulmonary inflammation is characterized by edema, decreased mucociliary clearance, epithelial damage, increased neuronal responsiveness, and bronchoalveolar eosinophilia [1].Eosinophils form in the bone marrow from myeloid precursors in response to cytokine activation, and are released into the circulation following an appropriate stimulus [2]. Once in the circulation they accumulate rapidly in tissue, where they synthesize and release lipid mediators that can cause edema, bronchoconstriction and chemotaxis, and secrete enzymes and proteins that can damage tissue [2].The eosinophil is therefore an ideal target for selectively inhibiting the tissue damage that accompanies allergic diseases, without inducing the immunosuppressive consequences that can arise from systemic use of pleiotropic drugs such as steroids.Interleukin-5 acts as a homodimer, and is essential for maturation of eosinophils in the bone marrow and their release into the blood [3][4][5][6]. In humans, interleukin-5 acts only on eosinophils and basophils, in which it causes maturation, growth, activation, and survival [7,8]. This specificity occurs because only those cells possess the interleukin-5 receptor. The functional high-affinity interleukin-5 receptor (250 pmol/l) is composed of two subunits: an α-subunit that is unique to interleukin-5, and a β c -subunit that is shared with interleukin-3 and granulocyte macrophage-colony stimulating factor (GM-CSF) [9,10].In animals and in humans, inhibiting interleukin-5 with monoclonal antibodies can reduce blood and bronchoReview Th2 cytokines and asthma The role of interleukin-5 in allergic eosinophilic disease AbstractInterleukin-5 is produced by a number of cell types, and is responsible for the maturation and release of eosinophils in the bone marrow. In humans, interleukin-5 is a very selective cytokine as a result of the restricted expression of the interleukin-5 receptor on eosinophils and basophils. Eosinophils are a prominent feature in the pulmonary inflammation that is associated with allergic airway diseases, suggesting that inhibition of interleukin-5 is a viable treatment. The present review addresses the data that relate interleukin-5 to pulmonary inflammation and function in animal models, and the use of neutralizing anti-interleukin-5 monoclonal antibodies for the treatment of asthma in humans. [11][12][13][14]. Therefore, exclusively inhibiting the actions of interleukin-5 can suppress at least one of the alleged causes of asthma, namely tissue damage due to eosinophil accumulation during pulmonary inflammation.Altho...

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Section: Genomics and Biochemistry Of The Interleukin-5 Systemmentioning

confidence: 99%

Section: Genomics and Biochemistry Of The Interleukin-5 Systemmentioning

confidence: 99%

Th2 cytokines and asthma The role of interleukin-5 in allergic eosinophilic disease

Greenfeder¹,

Umland²,

Cuss³

et al. 2001

Respir Res

207

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“…Although individual T cells have the capacity to produce a wide range of cytokines, distinct T cell populations and cytokine profiles exist in chronic allergic inflammatory diseases , Van Straaten et al 1994. There are a number of potential explanations for this phenomenon.…”

Section: Il-5 the Th2 Cytokine Profile And Allergic In-flammationmentioning

confidence: 99%

IL-5 and IL-5 receptor in asthma

Kotsimbos

Hamid

1997

Mem. Inst. Oswaldo Cruz

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and a soluble isoform (αIL-5Rs). Cytokines such as IL-5 produce specific and non-specific cellular responses through specific cell membrane receptor mediated activation of intracellular signal transduction pathways which, to a large part, regulate gene expression. The major intracellular signal transduction mechanism is activation of non-receptor associated tyrosine kinases including JAK and MAP kinases which can then transduce signals via a novel family of transcriptional factors named signal transducers and activators of transcription (STATS). JAK2, STAT1 and STAT 5 appear to be particularly important in IL-5 mediated eosinophil responses. Asthma is characterized by episodic airways obstruction, increased bronchial responsiveness, and airway inflammation. Several studies have shown an association between the number of activated T cells and eosinophils in the airways and abnormalities in FEV1, airway reactivity and clinical severity in asthma. It has now been well documented that IL-5 is highly expressed in the bronchial mucosa of atopic and intrinsic asthmatics and that the increased IL-5 mRNA present in airway tissues is predominantly T cell derived. Immunocytochemical staining of bronchial biopsy sections has confirmed that IL-5 mRNA transcripts are translated into protein in asthmatic subjects. Furthermore, the number of activated CD 4 + T cells and IL-5 mRNA positive cells are increased in asthmatic airways following antigen challenge and studies that have examined IL-5 expression in asthmatic subjects before and after steroids have shown significantly decreased expression following oral corticosteroid treatment in steroid-sensitive asthma but not in steroid resistant and chronic severe steroid dependent asthma. The link between T cell derived IL-5 and eosinophil activation in asthmatic airways is further strengthened by the demonstration that there is an increased number of αIL-5R mRNA positive cells in the bronchial biopsies of atopic and non-atopic asthmatic subjects and that the eosinophil is the predominant site of this increased

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“…IL-3 is produced from immunologically activated T lymphocytes (65), suggesting that IL-3 is not involved in steady-state or constitutive hematopoiesis but in inductive hematopoiesis on exposure to immunological stress (65 transcription of IL-3 is enhanced by a protein kinase C activator, phorbol myristate acetate, and calcium ionophore A23187 (75). IL-3 exerts its effects via a specific high-affinity cell surface receptor (27).…”

Section: Pharmacology Of Il-3mentioning

confidence: 99%

Neurotrophic Effect of Interleukin‐3 (IL‐3) and Its Mechanisms of Action in the Nervous System¹

1999

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The regulation of interleukin 5 and interleukin 3 gene expression in human T cells

Cited by 21 publications

References 14 publications

Th2 cytokines and asthma The role of interleukin-5 in allergic eosinophilic disease

Th2 cytokines and asthma The role of interleukin-5 in allergic eosinophilic disease

IL-5 and IL-5 receptor in asthma

Neurotrophic Effect of Interleukin‐3 (IL‐3) and Its Mechanisms of Action in the Nervous System¹

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The regulation of interleukin 5 and interleukin 3 gene expression in human T cells

Cited by 21 publications

References 14 publications

Th2 cytokines and asthma The role of interleukin-5 in allergic eosinophilic disease

Th2 cytokines and asthma The role of interleukin-5 in allergic eosinophilic disease

IL-5 and IL-5 receptor in asthma

Neurotrophic Effect of Interleukin‐3 (IL‐3) and Its Mechanisms of Action in the Nervous System1

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Neurotrophic Effect of Interleukin‐3 (IL‐3) and Its Mechanisms of Action in the Nervous System¹