Disease relevance of IL25

• Transgenic overexpression of human IL-17E results in eosinophilia, B-lymphocyte hyperplasia, and altered antibody production [1].
• We have generated IL-25-deficient (il25(-/-)) mice and found that they are highly susceptible to experimental autoimmune encephalomyelitis (EAE) [2].
• Mechanism of interleukin-25 (IL-17E)-induced pulmonary inflammation and airways hyper-reactivity [3].

High impact information on IL25

• Infusion of mice with IL-25 induced IL-4, IL-5, and IL-13 gene expression [4].
• We now show that IL-25 also regulates the development of autoimmune inflammation mediated by IL-17-producing T cells [2].
• Thus, IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity [2].
• Taken together, these data indicate that IL-17E regulates hematopoietic and immune functions, stimulating the development of eosinophils and B lymphocytes [1].
• IL-17E, a novel proinflammatory ligand for the IL-17 receptor homolog IL-17Rh1 [5].

Biological context of IL25

• IL-17E also potentiated the upregulation of CXCL-8 transcripts observed with TGF-beta1 [6].
• IL-25-induced AHR is dependent on the production of Th type-2 cytokines, and removal of IL-13 and its signal transduction pathway prevents IL-25-induced airways inflammation and AHR [3].

Anatomical context of IL25

• Expression of IL-17E and of eosinophil major basic protein was evaluated by immunohistochemistry in bronchial biopsies from subjects with asthma [6].
• IL-17E upregulates the expression of proinflammatory cytokines in lung fibroblasts [6].
• Our results suggest a potential proremodeling effect of IL-17E on airway smooth muscle cells through the induction of ECM and that its receptor is upregulated by proinflammatory conditions [7].
• Recently, it has been demonstrated that a novel IL-17 family cytokine IL-25 (IL-17E) is a product of activated Th2 cells and mast cells [8].
• The receptor for interleukin-17E is induced by Th2 cytokines in antigen-presenting cells [9].

Analytical, diagnostic and therapeutic context of IL25

• In situ hybridization of transgenic tissues revealed that IL-17Rh1 (IL-17BR/Evi27), a receptor that binds IL-17E, is up-regulated [1].
• METHODS: Expression of IL-17B receptor (IL-17BR), a receptor for IL-17E, was evaluated by immunofluorescent staining, Western blot, and real-time PCR in human primary lung fibroblasts [6].
• Mediator production was analyzed by using real-time PCR and ELISA after stimulation of fibroblasts with IL-17E alone or in combination with TNF-alpha and TGF-beta1 [6].

References