Abstract
Despite over a century of research, the causative agent(s) in sarcoidosis, a heterogeneous granulomatous disorder mainly affecting the lungs, remain elusive. Following identification of genetic factors underlying different clinical phenotypes, increased understanding of CD4+ T-cell immunology, which is believed to be central to sarcoid pathogenesis, as well as the role of B-cells and other cells bridging innate and adaptive immunity, is now contributing to novel insights into the mechanistic pathways influencing disease resolution or chronicity. Hopefully, new perspectives and state-of-the-art technology may help to shed light on the still-elusive enigma of sarcoid aetiology. This perspective article highlights a number of recent advances in the search for antigenic targets in sarcoidosis, as well as the main arguments for sarcoidosis as a spectrum of autoimmune conditions, either as a result of an external (microbial) trigger and/or due to defective control mechanisms regulating the balance between T-cell activation and inhibition.
Footnotes
This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.
Conflict of interest: Dr. Kaiser has nothing to disclose.
Conflict of interest: Dr. Eklund has nothing to disclose.
Conflict of interest: Dr. Grunewald has nothing to disclose.
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