Proof of Jacobi identity in generalized quantum dynamics

We prove that the Jacobi identity for the generalized Poisson bracket is satisfied in the generalization of Heisenberg picture quantum mechanics recently proposed by one of us (SLA). The identity holds for any combination of fermionic and bosonic fields, and requires no assumptions about their mutual commutativity.Comment: 9 pages, plain tex file, IASSNS-HEP-93/4

Series expansions without diagrams

We discuss the use of recursive enumeration schemes to obtain low and high temperature series expansions for discrete statistical systems. Using linear combinations of generalized helical lattices, the method is competitive with diagramatic approaches and is easily generalizable. We illustrate the approach using the Ising model and generate low temperature series in up to five dimensions and high temperature series in three dimensions. The method is general and can be applied to any discrete model. We describe how it would work for Potts models.Comment: 24 pages, IASSNS-HEP-93/1

Low Temperature Expansions for Potts Models

On simple cubic lattices, we compute low temperature series expansions for the energy, magnetization and susceptibility of the three-state Potts model in D=2 and D=3 to 45 and 39 excited bonds respectively, and the eight-state Potts model in D=2 to 25 excited bonds. We use a recursive procedure which enumerates states explicitly. We analyze the series using Dlog Pade analysis and inhomogeneous differential approximants.Comment: (17 pages + 8 figures

Long-term tolerance to skin commensals is established neonatally through a specialized dendritic cell subgroup.

Early-life establishment of tolerance to commensal bacteria at barrier surfaces carries enduring implications for immune health but remains poorly understood. Here, we showed that tolerance in skin was controlled by microbial interaction with a specialized subset of antigen-presenting cells. More particularly, CD301b+ type 2 conventional dendritic cells (DCs) in neonatal skin were specifically capable of uptake and presentation of commensal antigens for the generation of regulatory T (Treg) cells. CD301b+ DC2 were enriched for phagocytosis and maturation programs, while also expressing tolerogenic markers. In both human and murine skin, these signatures were reinforced by microbial uptake. In contrast to their adult counterparts or other early-life DC subsets, neonatal CD301b+ DC2 highly expressed the retinoic-acid-producing enzyme, RALDH2, the deletion of which limited commensal-specific Treg cell generation. Thus, synergistic interactions between bacteria and a specialized DC subset critically support early-life tolerance at the cutaneous interface

Toxin-Triggered Interleukin-1 Receptor Signaling Enables Early-Life Discrimination of Pathogenic versus Commensal Skin Bacteria

The host must develop tolerance to commensal microbes and protective responses to infectious pathogens, yet the mechanisms enabling a privileged relationship with commensals remain largely unknown. Skin colonization by commensal Staphylococcus epidermidis facilitates immune tolerance preferentially in neonates via induction of antigen-specific regulatory T cells (Tregs). Here, we demonstrate that this tolerance is not indiscriminately extended to all bacteria encountered in this early window. Rather, neonatal colonization by Staphylococcus aureus minimally enriches for antigen-specific Tregs and does not prevent skin inflammation upon later-life exposure. S. aureus α-toxin contributes to this response by stimulating myeloid cell production of IL-1β, which limits S. aureus-specific Tregs. Loss of α-toxin or the IL-1 receptor increases Treg enrichment, whereas topical application of IL-1β or α-toxin diminishes tolerogenic responses to S. epidermidis. Thus, the preferential activation of a key alarmin pathway facilitates early discrimination of microbial "foe" from "friend," thereby preventing tolerance to a common skin pathogen