BACKGROUND: CD30 is a costimulatory molecule belonging to the TNF receptor superfamily that is expressed on activated T and B cells. Several studies have demonstrated a positive correlation between expression of CD30 or increased levels of soluble CD30 and the development and severity of allergic diseases. However, thus far, the evidence for a role of CD30 in allergic diseases, such as asthma, is only indirect. OBJECTIVE: The aim of the study was to directly investigate the role of CD30 in a murine asthma model. METHODS: CD30-deficient (B6.129P2-Tnfrsf8(tm1Mak)/J) and wild-type (WT) mice were immunized to ovalbumin (OVA) to induce an asthma-like phenotype and compared in our murine asthma model. Moreover, CD30/CD30 ligand signaling was blocked in OVA-immunized WT animals by using mAbs against CD30 receptor and its ligand, CD153. RESULTS: The absence of CD30 in OVA-immunized CD30-deficient mice resulted in significantly reduced airway inflammation, serum IgE levels, and TH2 cytokine levels. The same effect was observed when CD30/CD153 signaling was blocked in OVA-immunized WT animals with mAbs against CD30 or CD30 ligand. CONCLUSION: Our results directly demonstrate that CD30/CD153 interaction plays an important role in the induction of TH2 cell-mediated allergic asthma. CLINICAL IMPLICATIONS: These findings provide evidence for a role of the costimulatory molecule CD30 in allergic asthma.
BACKGROUND:CD30 is a costimulatory molecule belonging to the TNF receptor superfamily that is expressed on activated T and B cells. Several studies have demonstrated a positive correlation between expression of CD30 or increased levels of soluble CD30 and the development and severity of allergic diseases. However, thus far, the evidence for a role of CD30 in allergic diseases, such as asthma, is only indirect. OBJECTIVE: The aim of the study was to directly investigate the role of CD30 in a murineasthma model. METHODS:CD30-deficient (B6.129P2-Tnfrsf8(tm1Mak)/J) and wild-type (WT) mice were immunized to ovalbumin (OVA) to induce an asthma-like phenotype and compared in our murineasthma model. Moreover, CD30/CD30 ligand signaling was blocked in OVA-immunized WT animals by using mAbs against CD30 receptor and its ligand, CD153. RESULTS: The absence of CD30 in OVA-immunized CD30-deficient mice resulted in significantly reduced airway inflammation, serum IgE levels, and TH2 cytokine levels. The same effect was observed when CD30/CD153 signaling was blocked in OVA-immunized WT animals with mAbs against CD30 or CD30 ligand. CONCLUSION: Our results directly demonstrate that CD30/CD153 interaction plays an important role in the induction of TH2 cell-mediated allergic asthma. CLINICAL IMPLICATIONS: These findings provide evidence for a role of the costimulatory molecule CD30 in allergic asthma.
Authors: Antonia Wallrapp; Samantha J Riesenfeld; Patrick R Burkett; Raja-Elie E Abdulnour; Jackson Nyman; Danielle Dionne; Matan Hofree; Michael S Cuoco; Christopher Rodman; Daneyal Farouq; Brian J Haas; Timothy L Tickle; John J Trombetta; Pankaj Baral; Christoph S N Klose; Tanel Mahlakõiv; David Artis; Orit Rozenblatt-Rosen; Isaac M Chiu; Bruce D Levy; Monika S Kowalczyk; Aviv Regev; Vijay K Kuchroo Journal: Nature Date: 2017-09-13 Impact factor: 49.962
Authors: Francisco Navarro; Aline Villa Nova Bacurau; Guilherme Borges Pereira; Ronaldo Carvalho Araújo; Sandro Soares Almeida; Milton Rocha Moraes; Marco Carlos Uchida; Luis Fernando Bicudo Pereira Costa Rosa; James Navalta; Jonato Prestes; Reury Frank Pereira Bacurau Journal: Eur J Appl Physiol Date: 2012-12-02 Impact factor: 3.078
Authors: Adele Hannigan; Asif M Qureshi; Colin Nixon; Penelope M Tsimbouri; Sarah Jones; Adrian W Philbey; Joanna B Wilson Journal: Mol Cancer Date: 2011-02-03 Impact factor: 27.401