Pancreatic Lymph Nodes Are Required for Priming of β Cell Reactive T Cells in NOD Mice

Nonobese diabetic (NOD) mice develop spontaneous autoimmune diabetes that results from the destruction of insulin secreting β cells by diabetogenic T cells. The time and location of the encounter of autoantigen(s) by naive autoreactive T cells in normal NOD mice are still elusive. To address these issues, we analyzed diabetes development in mice whose spleen or pancreatic lymph nodes (panLNs) had been removed. Excision of panLNs (panLNx) at 3 wk protected mice against insulin autoantibodies (IAAs), insulitis, and diabetes development almost completely, but had no effect when performed at 10 wk. The protection afforded by panLNx at weaning was not due to modifications of the immune system, the absence of autoreactive T cells, or the increase in the potency of regulatory T cells. That panLNs are dispensable during adult life was confirmed by the capacity of 10-wk-old panLNx irradiated recipients to develop diabetes upon transfer of diabetogenic T cells. In contrast, splenectomy had no effect at any age. Partial excision of mesenteric LN at 3 wk did not prevent accelerated diabetes by cyclophosphamide as panLNx did. Thus, in normal NOD mice, autoreactive T cell initial priming occurs in LNs draining the target organ of the disease from 3 wk of age

Poly[di-μ2-chlorido-μ2-(1,4-dioxane-κ2 O:O′)-cadmium(II)]

In the title complex, [CdCl2(C4H8O2)]n, two different CdII ions are present, one in a general position and one with site symmetry 2. The CdII ions are coordinated by two O atoms from two 1,4-dioxane ligands and four chloride anions in a slightly distorted octa­hedral geometry and is connected to neighboring CdII ions by two bridging chloride anions, generating infinite linear chains along the a axis. These chains are further inter­connected by bridging 1,4-dioxane ligands, affording a three-dimensional network