CD8α(+) dendritic cells are an obligate cellular entry point for productive infection by Listeria monocytogenes.

CD8α(+) dendritic cells (DCs) prime cytotoxic T lymphocytes during viral infections and produce interleukin-12 in response to pathogens. Although the loss of CD8α(+) DCs in Batf3(-/-) mice increases their susceptibility to several pathogens, we observed that Batf3(-/-) mice exhibited enhanced resistance to the intracellular bacterium Listeria monocytogenes. In wild-type mice, Listeria organisms, initially located in the splenic marginal zone, migrated to the periarteriolar lymphoid sheath (PALS) where they grew exponentially and induced widespread lymphocyte apoptosis.

Preparation, characterization and in vitro efficacy of an acid-modified beta-TCP material for dental hard-tissue remineralization.

A blended material composed of beta-tricalcium phosphate (beta-TCP) and fumaric acid (FA) was prepared using a mechanochemical process. The structure and properties of the TCP-FA material was probed using particle size analysis, infrared, (31)P and (13)C solid-state nuclear magnetic resonance (NMR) spectroscopy, powder X-ray diffraction and calcium bioavailability. NMR studies showed that orthophosphate environments within beta-TCP remain largely unaffected in the presence of FA during mechanochemical processing; alternately, (13)C data indicated the carboxylic groups of FA are strongly affected during processing with beta-TCP.

Immunological reversal of autoimmune diabetes without hematopoietic replacement of beta cells.

Type 1 diabetes mellitus results from the autoimmune destruction of the beta cells of the pancreatic islets of Langerhans and is recapitulated in the nonobese diabetic strain of mice. In an attempt to rescue islet loss, diabetic mice were made normoglycemic by islet transplantation and immunization with Freund's complete adjuvant along with multiple injections of allogeneic male splenocytes. This treatment allowed for survival of transplanted islets and recovery of endogenous beta cell function in a proportion of mice, but with no evidence for allogeneic splenocyte-derived differentiation of new islet beta cells.

Absence of lymph nodes in NOD mice treated with lymphotoxin-beta receptor immunoglobulin protects from diabetes.

Pregnant nonobese diabetic (NOD) mice were treated with lymphotoxin-beta receptor immunoglobulin fusion protein (LTbetaR-Ig) or control human immunoglobulin on days embryonic day 11 (E11) and E14, and offspring were followed for the development of anti-beta-cell antibodies, islet pathology, and hyperglycemia. The development of anti-beta-cell surface antibodies was abrogated in treated mice compared with controls. Autopsy examination of the mice at 30 weeks of age revealed normal development of secondary lymphoid structures in the control animals; however, mice treated with LTbetaR-Ig had no axillary, inguinal, popliteal, or peripancreatic lymph nodes.