when you are wrong you need not fall on

your sword or sadly reflect that when you listen to people or companies that they are often wrong.

Shoot BCG and then fire....

Diabetologia. 2013 Nov 5. [Epub ahead of print]

Why were we wrong for so long? The pancreas of type 1 diabetic patients commonly functions for decades.

Faustman DL.

Source

Immunobiology Laboratory, Massachusetts General Hospital, Harvard Medical School, Building 149, 13th Street, Room 3602, Boston, MA, 02129, USA, Faustman@helix.mgh.harvard.edu.

Abstract

The type 1 diabetes field has held firm to the dogma that the pancreas is no longer viable, and thus incapable of producing insulin, within 1 to 2 years of diagnosis for the majority of patients. A new study in this issue of Diabetologia (DOI: 10.1007/s00125-013-3067-x ), based on a hypersensitive assay, has found detectable C-peptide, a marker of insulin production, in individuals with long-standing type 1 diabetes. This new study confirms and expands a decades-long track record of research finding intact pancreatic islet cells in advanced disease. Because the evidence, stemming back to 1902, was largely histological in nature, it was dismissed as lacking functional corroboration. This new study in patients with long-term diabetes shows appropriate functioning of pancreatic islet cells after exposure to a mixed-meal stimulus. The weight of evidence now makes it clear that a large fraction of patients with long-standing diabetes have low level, but persistent functioning of pancreatic islet cells enduring more than a decade after disease onset.

Sci Rep. 2013 Nov 6;3:3153. doi: 10.1038/srep03153.

Homogeneous expansion of human T-regulatory cells via tumor necrosis factor receptor 2.

Okubo Y, Mera T, Wang L, Faustman DL.

Source

Immunobiology Laboratory, Massachusetts General Hospital and Harvard Medical School, Rm 3602, MGH-East, Bldg 149, 13th Street, Boston, MA 02129.

Abstract

T-regulatory cells (Tregs) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity, and asthma. Clinical applications of Tregs have not been fully realized because standard methods of expansion ex vivo produce heterogeneous progeny consisting of mixed populations of CD4 + T cells. Heterogeneous progeny are risky for human clinical trials and face significant regulatory hurdles. With the goal of producing homogeneous Tregs, we developed a novel expansion protocol targeting tumor necrosis factor receptors (TNFR) on Tregs. In in vitro studies, a TNFR2 agonist was found superior to standard methods in proliferating human Tregs into a phenotypically homogeneous population consisting of 14 cell surface markers. The TNFR2 agonist-expanded Tregs also were functionally superior in suppressing a key Treg target cell, cytotoxic T-lymphocytes. Targeting the TNFR2 receptor during ex vivo expansion is a new means for producing homogeneous and potent human Tregs for clinical opportunities.