| First Author | Kashiwakura JC | Year | 2012 |
| Journal | J Clin Invest | Volume | 122 |
| Issue | 1 | Pages | 218-28 |
| PubMed ID | 22133880 | Mgi Jnum | J:184412 |
| Mgi Id | MGI:5320857 | Doi | 10.1172/JCI59072 |
| Citation | Kashiwakura JC, et al. (2012) Histamine-releasing factor has a proinflammatory role in mouse models of asthma and allergy. J Clin Invest 122(1):218-28 |
| abstractText | IgE-mediated activation of mast cells and basophils underlies allergic diseases such as asthma. Histamine-releasing factor (HRF; also known as translationally controlled tumor protein [TCTP] and fortilin) has been implicated in late-phase allergic reactions (LPRs) and chronic allergic inflammation, but its functions during asthma are not well understood. Here, we identified a subset of IgE and IgG antibodies as HRF-interacting molecules in vitro. HRF was able to dimerize and bind to Igs via interactions of its N-terminal and internal regions with the Fab region of Igs. Therefore, HRF together with HRF-reactive IgE was able to activate mast cells in vitro. In mouse models of asthma and allergy, Ig-interacting HRF peptides that were shown to block HRF/Ig interactions in vitro inhibited IgE/HRF-induced mast cell activation and in vivo cutaneous anaphylaxis and airway inflammation. Intranasally administered HRF recruited inflammatory immune cells to the lung in naive mice in a mast cell- and Fc receptor-dependent manner. These results indicate that HRF has a proinflammatory role in asthma and skin immediate hypersensitivity, leading us to suggest HRF as a potential therapeutic target. |
