• Oral presentation
• Open Access

• Received: 11 January 2005
• Published: 17 February 2005

One of the most important but as yet unanswered questions in inflammation research is not why chronic inflammation occurs but why it does not resolve. Current models of inflammation stress the role of antigen-specific lymphocyte responses and attempt to address the causative agent. However, recent studies have begun to challenge the primacy of the lymphocyte and have begun to focus on an extended immune system in which stromal cells, such as macrophages and fibroblasts, play a role in the persistence of the inflammatory lesion.

In this lecture I will illustrate how fibroblasts play an important role in regulating the switch from acute resolving to chronic persistent inflammation associated with the pathology of diseases such as rheumatoid arthritis [1]. In chronic inflammation the normal physiological process of the death and emigration of unwanted inflammatory effector cells becomes disordered leading to accumulation of leucocytes [2–4] within lymphoid aggregates that resemble those seen in lymphoid tissue [5]. I will describe how fibroblasts from the rheumatoid joint provide survival and retention signals for leucocytes leading to their inappropriate and persistent accumulation within inflamed tissue [6]. Our work suggests that targeting the stromal microenvironment is likely to be an important strategy for future anti-inflammatory therapies.