Editing Sjögren's disease (section)

=== Inflammation ===
Epithelial cells in Sjögren's disease lesions are active participants in the induction and perpetuation of the inflammatory process. Environmental and hormonal factors, in concert with an appropriate genetic background, are believed to trigger Sjögren's disease, which [[Dysregulation|dysregulates]] epithelial cells and allows aberrant [[Homing (hematopoietic)|homing]] and activation of [[dendritic cells]] (DCs), T cells, and B cells.<ref name="pmid18050195">{{cite journal | vauthors = Manoussakis MN, Boiu S, Korkolopoulou P, Kapsogeorgou EK, Kavantzas N, Ziakas P, Patsouris E, Moutsopoulos HM | title = Rates of infiltration by macrophages and dendritic cells and expression of interleukin-18 and interleukin-12 in the chronic inflammatory lesions of Sjögren's syndrome: correlation with certain features of immune hyperactivity and factors associated with high risk of lymphoma development | journal = Arthritis Rheum. | volume = 56 | issue = 12 | pages = 3977–88 | date = December 2007 | pmid = 18050195 | doi = 10.1002/art.23073 | doi-access = free }}</ref> Dendritic cells are [[antigen-presenting cells]] <!-- (APC) --> that process [[antigen]] material and present it to other T cells. Following the [[Cell migration|migration]] of lymphocytes into the glands in response to [[chemokines]] and specific [[adhesion molecule]]s, T cells interact with epithelial cells. Epithelial cells are further activated by [[proinflammatory cytokines]] (IL-1β, IFN-γ, and TNF), which are produced by adjacent T cells. The early accumulation of [[plasma cell|plasmacytoid]] dendritic cells in the target tissues, which produce high levels of type 1 IFNs, seems important, as these cells can further dysregulate the immune response through abnormal retention of lymphocytes in the tissues, and their subsequent activation. IFN-α stimulates the production of [[B-cell activating factor]] (BAFF) by epithelial cells, DCs, and T cells. BAFF stimulates aberrant B-cell maturation, leading to the emergence of self-reactive B cells, which locally produce autoantibodies, in a [[germinal centre]]-like structure (GC-like), which is also the location of [[lymphomagenesis]] (origin of [[lymphoma]]).<ref name=Voulgarelis2010/>