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Updated: Jul 27, 2026

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
Published on: June 16, 2011
Thyrocytes isolated from autoimmune-diseased thyroids secrete soluble tumor necrosis factor-R1 that is related to
M LaBue1, K K Colburn, L M Green
1J.L. Pettis Memorial Veterans Medical Center, Research Service-151, Loma Linda, California, USA.
Abstract:
Soluble tumor necrosis factor (TNF)-alpha receptors have the potential to modulate TNF-alpha activity during autoimmune thyroiditis. In this study we examined cell-surface TNF-alpha receptors and soluble TNF-alpha receptor production by thyrocytes from normal and MRL-lpr(-/-) (diseased) mice, which spontaneously develop autoimmune thyroiditis. We found that murine thyrocytes possess the 55-kd receptor (TNF-R1). Examination of soluble TNF-R1 production revealed that diseased thyrocytes produced sevenfold more soluble TNF-R1 than normal thyrocytes. Furthermore, basal protein kinase C (pKC) activity in diseased thyrocytes was 67% higher than that found in normal murine thyrocytes. The elevated basal pKC activity in diseased thyrocytes was related to their enhanced production of soluble TNF-R1 because inhibition of pKC activity with calphostin C caused soluble TNF-R1 production to decrease significantly. Additionally, soluble TNF-R1 production by murine thyrocytes was not a result of cell-surface receptor shedding but through secretion of a truncated version of TNF-R1. This was evident when cell-surface TNF-R1 levels were unchanged after treatment of diseased thyrocytes with calphostin C. Also, the 28-kd form of TNF-R1, which corresponds to the soluble receptor, was present in the intracellular membranes of the diseased thyrocytes.
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