The local coupled cluster method DLPNO-CCSD(T) allows calculations on systems containing hundreds of atoms to be performed while typically reproducing canonical CCSD(T) energies with chemical accuracy. In this work, we present a scheme for decomposing the DLPNO-CCSD(T) interaction energy between two molecules into physical meaningful contributions, providing a quantification of the most important components of the chemical interaction. The method, called Local Energy Decomposition (LED), is straightforward and requires negligible additional computing time. Both the Hartree-Fock and the correlation energy are decomposed into contributions from localized or pairs of localized occupied orbitals. Assigning these localized orbitals to fragments allows one to differentiate between intra- and intermolecular contributions to the interaction energy. Accordingly, the interaction energy can be decomposed into electronic promotion, electrostatic, exchange, dynamic charge polarization, and dispersion contributions. The LED scheme is applied to a number of test cases ranging from weakly, dispersively bound complexes to systems with strong ionic interactions. The dependence of the results on the one-particle basis set and various technical aspects, such as the localization scheme, are carefully studied in order to ensure that the results do not suffer from technical artifacts. A numerical comparison between the DLPNO-CCSD(T)/LED and the popular symmetry adapted perturbation theory (DFT-SAPT) is made, and the limitations of the proposed scheme are discussed.

We definitively show that the CO stretching response to metal coordination is driven exclusively by π polarization, which quantitatively correlates with π back-donation and changes in CO bond length and frequency.

IntroductionThe induction of tolerance is central to the maintenance of immune homeostasis. Not only are dendritic cells (DCs) key elements in the development of immunity, but they also participate in the generation and maintenance of immune tolerance. Many studies have demonstrated a pivotal role for the enzyme indoleamine 2,3-dioxygenase (IDO) in immune regulation during infection, pregnancy, autoimmunity, transplantation, and neoplasia. 1,2 IDO is widely expressed in a variety of human tissues as well as in macrophages and DCs and is induced in inflammatory states via type I or type II IFN signaling. Through localized tryptophan deficiency combined with the release of proapoptotic kynurenines, DCs exert an IDO-dependent homeostatic control over the proliferation and survival of peripheral T cells and promote antigen-specific tolerance. 3,4 Murine plasmacytoid DCs (pDCs), which produce and respond to type I IFNs, have been credited with a unique ability to express functional IDO, implying an important role for these cells in the maintenance of peripheral tolerance. 5 DCs are now being exploited to improve vaccine efficacy. 6 Pathogen-pulsed DCs act, indeed, as a potent fungal vaccine in experimental hematopoietic stem cell transplantation (HSCT). 7 Protection is associated with myeloid and T-cell recovery, the activation of CD4 ϩ T-helper type 1 (Th1) lymphocytes, and the concomitant production of IL-10. This cytokine is required for the induction of regulatory T (Treg) cells, which have important functions in immune homeostasis including the onset of transplantation tolerance, inhibition of inflammation, and prevention of graft-versus-host disease (GVHD) lethality and leukemia relapse. [8][9][10] As tolerance is also one major requirement of a successful immune response to fungi, 11-13 tolerogenic DCs, including pDCs, may be pivotal in the generation of some form of dominant regulation that ultimately controls inflammation, pathogen immunity, and tolerance in transplant recipients. 14 Thymosin ␣1 (T␣1) is a naturally occurring thymic peptide 15 that promotes activation and cytokine production in human and murine mature DCs by signaling through Toll-like receptors (TLRs), including TLR9. 16 By influencing the balance of IL-12-and IL-10-producing DCs, T␣1 acts as an immune regulator capable of inducing protective immunity to Aspergillus fumigatus. 16 TLR9 stimulation can also lead to IDO activation via mechanisms including autocrine type I IFN signaling 17,18 and can promote pDC-mediated generation of CD4 ϩ CD25 ϩ cells, 19 which are an essential component of the IDO-dependent protective immunity to fungi. [11][12][13] We hypothesized that T␣1 could affect the balance of immunity and tolerance by DCs and the generation of Treg cells. We assessed here the effects of T␣1 on deriving DCs from bone marrow (murine) or peripheral blood (human) L.R. and P.P. devised the study, critically evaluated the data at regular intervals, and drafted the paper. L.R. takes responsibility for integrity of the work as a whole. K.P....