Immunoglobulin D enhances immune surveillance by activating antimicrobial, proinflammatory and B cell–stimulating programs in basophils

Kang Chen et al. Nat Immunol. 10 (8):889-898. (2009)

Speaker: Miao-his Hsieh (謝妙禧)                                Time: 14:00~15:00, Nov. 25, 2009

Commentator: Dr. Trai-Ming Yeh (葉才明老師)  Place: Room 601

Abstract:

　　IgD has been discovered more than 40 years. It was reported that IgD-deficient mice have normal immune response to pathogen infection. In addition, while B cell losing IgM function, IgD can largely substitute and compensate.[1] But up to date, the functions of IgD are still enigmatic.[2] Authors observed IgD⁺IgM^- B cells in the upper respiratory mucosa, especially tonsil and nasal mucosa. In tonsil, IgD⁺IgM^- B cells located in the gemrminal center and extrafollicular area. IgD⁺IgM⁺ B cells could activate by T cell-dependent and T cell-independent pathway and underwent class-switch to IgD⁺IgM^- B cells. Previous studies found that IgD could recognized bacteria.[3] Here, authors confirmed the possibility of binding Gram-negative bacteria and its products by IgD. Since IgD recognized respiratory bacteria, they want to know which leukocyte can bind IgD and help toeliminate microbial infection. In vivo and in vitro data show that IgD bind  basophil and through a protease-sensitive, IL-3- or IL-4-inducible receptors. IgD-activated basophils trigger innate and adaptive immune response after sensing pathogen at the upper respiratory mucose by releasing immunostimulating, proinflammatory factors, antimicrobial factor and B cell-activating factors. In clinial research, the patients with periodic fever syndroms and autoinflammatory syndromes can find that IgD class-switched B cell and ‘IgD-armed’ basophil out of control. In conclusion, this study proved that IgD could bind basophils achieve immune surveillance by immunity and inflammation. It may be providing another treatment methods for periodic fever syndroms and autoinflammatory syndromes.

Reference:

1. Nitschke, L. et al. Immunoglobulin D-deficient mice can mount normal immune responses to thymus-independent and -dependent antigens. Proc. J. Exp. Mcd. 1993. 90(3) 1887-1891

2. Claudia Lutz et al. IgD can largely substitute for loss of IgM function in B cells. Nature 1998. 393(6) 797-801

3. Forsgren, A. et al. Many bacterial species bind human IgD. J. Immunol. 122(4), 1468–1472