A series of arene-bridged dithorium complexes was synthesized via the reduction by potassium graphite of a Th(IV) precursor in the presence of arenes. All these compounds adopt an inverse-sandwich structure, with the arene bridging two thorium centers in a μ-η 6 ,η 6 -mode. Structural and spectroscopic data support the assignment of two Th(IV) ions and an arene tetraanion, which is an aromatic structure according to Huckel's rule. Arene exchange reactions revealed that the stability of the corresponding compounds follows the series naphthalene ≪ toluene < benzene ≈ biphenyl. Reactivity studies showed that they function as fourelectron reductants capable to reduce anthracene, cyclooctatetraene, alkynes, and azobenzene, while a mononuclear thorium anthracene complex could reduce benzene. Density functional theory calculations unveiled that the bonding interactions consist of δ bonds between thorium 6d and 5f orbitals and arene π* orbitals, showing a significant covalent character, able to stabilize highly reduced arene ligands.

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Allergic asthma is a common airway inflammatory disease in which B cells play important roles through IgE production and antigen presentation. SNP (single nucleotide polymorphism) analysis showed that Atg (autophagy-related) allele mutations are involved in asthma. It has been demonstrated that macroautophagy/autophagy is essential for B cell survival, plasma cell differentiation and immunological memory maintenance. However, whether B cell autophagy participates in asthma pathogenesis remains to be investigated. In this report, we found that autophagy was enhanced in pulmonary B cells from asthma-prone mice. Autophagy deficiency in B cells led to attenuated immunopathological symptoms in asthma-prone mice. Further investigation showed that IL4 (interleukin 4), a key effector Th2 cytokine in allergic asthma, was critical for autophagy induction in B cells both in vivo and in vitro, which further sustained B cell survival and enhanced antigen presentation by B cells. Moreover, IL4-induced autophagy depended on JAK signaling via an MTOR-independent, PtdIns3K-dependent pathway. Together, our data indicate that B cell autophagy aggravates experimental asthma through multiple mechanisms.