Anti-IL9 monoclonal antibody, clone E0403D23 Functional Grade

IL9 is a cytokine produced by activated T cells and particularly from the Th2 subset. This protein shows pleiotropic activities on various cell types such as T and B lymphocytes, mast cells, erythroid and myeloid precursors and neuronal cell lines. The IL9 receptor is a member of the hematopoietin receptor superfamily and associates with the gamma chain of the IL2 receptor to transduce the signal inside the cells. IL9 transgenic mice, constitutively expr essing large amounts of this cytokine, are highly susceptible to the development of thymic lymphomas after irradiation or injection of a chemical mutagen. In the human, constitutive IL9 expression has been found in cell lines and lymph nodes from patients with Hodgkin disease or large cell anaplastic lymphomas and an IL9-mediated autocrine loop has been demonstrated for one Hodgkin cell line in vitro.

Th9 cells preferentially produce IL-9 and participate in allergic responses and asthma. Differentiation of Th9 cells is induced by IL-4 and TGF-beta, and then the cells are amplified by OX40 signals. The transcription factors PU.1, IRF4, and BATF are required for Th9 differentiation. BATF3 is an AP-1 family transcription factor that is highly homologous to BATF; however, its role in Th9 cells is poorly defined. Here, we show that OX40 signaling induced the expression of Batf3 and that its overexpression in the presence or absence of OX40 signaling increased the expression of IL-9 in Th9 cells. BATF3 physically interacted with IRF4 and was bound to the Il9 locus. A transient reporter assay revealed that the BATF3-IRF4 complex induced Il9 promoter activity. BATF3 rescued Il9 expression and restored the capacity to induce the airway inflammation in Batf KO Th9 cells. Thus, BATF3 itself is sufficient for the induction of Th9 cell differentiation and can substitute for BATF during Th9 cell differentiation.