NBR1 is a new PB1 signalling adapter in Th2 differentiation and allergic airway inflammation in vivo.

نویسندگان

  • Jun-Qi Yang
  • Hongzhu Liu
  • Maria T Diaz-Meco
  • Jorge Moscat
چکیده

Allergic airway inflammation is a disease in which T helper 2 (Th2) cells have a critical function. The molecular mechanisms controlling Th2 differentiation and function are of paramount importance in biology and immunology. Recently, a network of PB1-containing adapters and kinases has been shown to be essential in this process owing to its function in regulating cell polarity and the activation of critical transcription factors. Here, we show in vivo data showing that T-cell-specific NBR1-deficient mice show impaired lung inflammation and have defective Th2 differentiation ex vivo with alterations in T-cell polarity and the selective inhibition of Gata3 and nuclear factor of activated T c1 activation. These results establish NBR1 as a novel PB1 adapter in Th2 differentiation and asthma.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

NBR1 is a new PB1 signaling adapter in Th2 differentiation and allergic airway inflammation in vivo

Table SI. Splenic immune cell populations unchanged in conditional NBR1-deficient mice CD4 CD8 B220 NK1.1 CD11b + F4/80 CD11c F4/80 NBR1fl/fl 17.6 ± 1.0 13.9 ± 0.7 59.7 ± 2.1 3.7 ± 0.7 5.9 ± 0.5 4.1 ± 0.3 NBR1fl/fl CreOX40 17.9 ± 0.8 14.6 ± 0.4 60.0 ± 0.9 4.3 ± 0.5 5.9 ± 0.6 4.8 ± 0.6 Single-cell suspension from spleen were stained by FACS. Percentages (Means ± SE) of positive cells gated on ly...

متن کامل

Allergic airway inflammation induces a pro-secretory epithelial ion transport phenotype in mice.

The airway epithelium is a central effector tissue in allergic inflammation and T-helper cell (Th) type 2-driven epithelial responses, such as mucus hypersecretion contribute to airflow obstruction in allergic airway disease. Previous in vitro studies demonstrated that Th2 cytokines also act as potent modulators of epithelial ion transport and fluid secretion, but the in vivo effect of allergic...

متن کامل

Notch Ligand DLL4 Alleviates Allergic Airway Inflammation via Induction of a Homeostatic Regulatory Pathway

Notch is a pleiotropic signaling family that has been implicated in pathogenesis of allergic airway diseases; however, the distinct function of individual Notch ligands remains elusive. We investigated whether Notch ligands, Jagged1 and DLL4, exert differential effects in OVA-induced allergic asthma. We found that whilst Jagged1 inhibition mitigated Th2-dominated airway inflammation, blockage o...

متن کامل

Inactivated Mycobacterium phlei inhalation ameliorates allergic asthma through modulating the balance of CD4+CD25+ regulatory T and Th17 cells in mice

Objective(s): Th2 response is related to the aetiology of asthma, but the underlying mechanism is unclear. To address this point, the effect of nebulized inhalation of inactivated Mycobacterium phlei on modulation of asthmatic  airway  inflammation was investigated. Materials and Methods: 24 male BALB/c mice were randomly divided into three groups: control group (Group A), asthma model group (G...

متن کامل

Enhanced Th2 cell differentiation and allergen-induced airway inflammation in Zfp35-deficient mice.

Studies of human asthma and of animal models of allergic airway inflammation revealed a crucial role for Th2 cells in the pathogenesis of allergic asthma. Kruppel-type zinc finger proteins are the largest family of a regulatory transcription factor for cellular development and function. Zinc finger protein (Zfp) 35 is an 18-zinc finger motif-containing Kruppel-type zinc finger protein, while it...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • The EMBO journal

دوره 29 19  شماره 

صفحات  -

تاریخ انتشار 2010