Sjögrens syndrome—the non-apoptotic model of glandular hypofunction

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Abstract
The ‘classical’ model to explain glandular hypofunction in Sjögrens syndrome (SS) is tissue loss secondary to immune attack mediated by a combination of apoptosis and cytotoxic cell death (reviewed recently by Ramos-Casals and Font [1]). In this model, the process of glandular destruction is made self-sustaining by the continued production of novel ‘self’ antigens, secondary to apoptotic bleb formation or cell-death [2]. Failure of the organ is thought to follow directly from tissue loss. For over six decades, research into SS has been directed towards understanding the mechanisms of destruction of salivary and lacrimal acinar tissue. Over this time, the only role envisaged for salivary glands themselves in the pathological process, has been that of a ‘reactor’ for infiltrating lymphocytes.

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