Yoshimoto, T., Yasuda, K., Tanaka, H., Nakahira, M., Imai, Y., Fujimori, Y. et al. Basophils contribute to T(H)2-IgE responses in vivo via IL-4 production and presentation of peptide-MHC class II complexes to CD4+ T cells. Nat. Immunol. 10, 706-712

Department of Immunology and Medical Zoology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
Nature Immunology (Impact Factor: 20). 08/2009; 10(7):706-12. DOI: 10.1038/ni.1737
Source: PubMed


Basophils express major histocompatibility complex class II, CD80 and CD86 and produce interleukin 4 (IL-4) in various conditions. Here we show that when incubated with IL-3 and antigen or complexes of antigen and immunoglobulin E (IgE), basophils internalized, processed and presented antigen as complexes of peptide and major histocompatibility complex class II and produced IL-4. Intravenous administration of ovalbumin-pulsed basophils into naive mice 'preferentially' induced the development of naive ovalbumin-specific CD4+ T cells into T helper type 2 (T(H)2) cells. Mice immunized in this way, when challenged by intravenous administration of ovalbumin, promptly produced ovalbumin-specific IgG1 and IgE. Finally, intravenous administration of IgE complexes rapidly induced T(H)2 cells only in the presence of endogenous basophils, which suggests that basophils are potent antigen-presenting cells that 'preferentially' augment T(H)2-IgE responses by capturing IgE complex.

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Available from: Yoshihiro Fujimori, Mar 11, 2014
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    • "Basophils are IgE-activated granulocytes that, unlike tissue-resident mast cells, circulate in the blood. They play a critical role in the IgE-mediated development of chronic allergic reactions and inflammation [97] [98], and they can also promote polarization towards Th2 responses by IgE-independent antigen presentation in mice [99] [100]. Basophils are recruited to a tick-feeding site and accumulate in the host skin during second and consequent (but not primary) tick infestation, where they act as important tick rejection factors [101] [102]. "
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    • "Moreover, we have shown that, in the gut mucosa of patients with inflammatory bowel disease, MCs co-localize with B cells at sites of inflammation (Merluzzi et al., 2010). Similar considerations can be made for basophils which were shown to express the lymph nodehoming marker CD62L (Yoshimoto et al., 2009). Interestingly, it has been reported that basophils of Lyn -/− mice, which develop a systemic lupus erythematosus-like disease, upregulate CD62L expression and home to the lymph nodes and spleen (Charles et al., 2010). "
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