Abstract
In primary Sjögren's syndrome (pSS) a complex of interconnections between epithelial barrier, innate and adaptive immunity occurs. IL-22 is a pleiotropic cytokine that in pSS may be placed at the intersection of the adaptive and innate branches of immunity. Some evidence suggests that, in pSS, IL-22 may play a prominent pro-inflammatory role driving the early phase of tissue and systemic inflammation and participating in the self-perpetuation of disease. Despite contradictory data in literature about the role of NK cells in pSS, recent data also suggest an important contribution of this subset of cells of the innate immune system in the development and perpetuation of inflammation. Here, we discuss the role of IL-22 in the pathogenesis of pSS and in epithelial barrier function.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
IL-22 and IL-22R1 overexpression in the inflamed salivary glands of primary Sjögren's syndrome (pSS) patients suggests the existence of an autocrine pro-inflammatory loop that may be responsible for the self-perpetuation of the salivary glands inflammation.
The involvement of IL-22/IL-22R1 in the pathogenesis of B- and T-cell lymphomas may suggest a role for this pathway in the development of Sjögren-associated non-Hodgkin's lymphoma.
Innate immune system through NK cells and in particular through the activating receptor NKp30 may play a key role in the early phase of inflammatory response in pSS patients.