Purpose of review Although the aetiology of sarcoidosis is not yet completely understood, immunological changes within the T-cell compartment are characteristic for an exaggerated antigen-driven immune response. In this review, we describe the most recent findings on T-cell subset responses and regulation in sarcoidosis. We discuss how future immunological research can advance the field to unravel pathobiological mechanisms of this intriguingly complex disease. Recent findings Research into the field of T-cell plasticity has recently challenged the long-held T helper type 1 (Th1) paradigm in sarcoidosis and striking parallels with autoimmune disorders and common variable immunodeficiency were recognized. For instance, it was demonstrated that Th17.1-cells rather than Th1 cells are responsible for the exaggerated IFN-gamma production in pulmonary sarcoidosis. Furthermore, impaired regulatory T-cell function and alterations within the expression of co-inhibitory receptors that control T-cell responses, such as PD-1, CTLA-4 and BTNL2, raise new questions regarding T-cell regulation in pulmonary sarcoidosis. Summary It becomes increasingly clear that Th17(.1)-cells and regulatory T-cells are key players in sarcoidosis T-cell immunology. New findings on plasticity and co-inhibitory receptor expression by these subsets help build a more comprehensive model for T-cell regulation in sarcoidosis and will finally shed light on the potential of new treatment modalities.
|Number of pages||8|
|Journal||Current Opinion in Pulmonary Medicine|
|Publication status||Published - 2016|