Tissue fibroblasts are not passive players in the initiation and resolution of inflammation: They act as innate immune sentinels, and engage in critical soluble and contact mediated interactions with both tissue resident and recruited inflammatory leukocyte subpopulations. They are now known to have active roles in determining the switches governing progression from acute to chronic inflammation, and also those governing resolution or the progression to chronic, persistent inflammation. The “switch to resolution” is an important signal that permits tissue repair to take place and enables immune cells to return to draining lymphoid nodes in order for immunological memory to become established. However in RA, certain fibroblast subpopulations become persistently activated and contribute to the inappropriate recruitment and retention of leukocytes in a site or organ-dependent manner, leading to tissue and site specific initiation and subsequent relapse of chronic persistent inflammatory disease; effectively a “switch to persistence”. This talk will review the field of stromal cell: leukocyte interactions, examining recent data from work with early arthritis fibroblasts and potential for therapeutic targeting.
Disclosure of Interest None Declared
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