Information on environmental factors important for the development, perpetuation, or course of RA is surprisingly scarce. Smoking is the only conventional environmental factor that has been linked reproducibly to an increased risk of developing RA. Other exposures, such as silica dust and mineral oils, have been reported in a few studies. It has not yet been possible to verify frequently hypothesized stimuli such as microbial infections with the methods used to date. Smoking was initially considered as an unspecific risk factor, of interest mainly from a public health perspective. However, newer studies indicate that smoking is a specific trigger of RA, as discussed in more detail below.


Studies on specific immune reactions in RA have been confined almost entirely to those involving autoantibodies. As described above, they were initially restricted to the measure of rheumatoid factors, but more recently, antibodies specific for citrullinated proteins have been shown to be of great importance. This is discussed in detail below, since their presence covariates with genetic and environmental factors, providing an important tool in subgrouping patients into different entities of RA. In the process of joint inflammation and cartilage and bone destruction, many different cells and molecules of the immune system participate. Some of them are illustrated in Figure 2. However, even if some of these inflammatory processes are revealed in detail, a specific trigger has still not been identified.

In recent years, advances within the field of cytokine regulation and cytokine-directed therapy have largely dominated the research field of RA, illustrating how therapeutic progress is possible even though the role of adaptive immunity in the disease is not fully understood. Cytokines are soluble molecules that mediate the communication between cells of the immune system but also with other cells of the body, such as the endothelium. Interestingly, the first cytokine that was targeted, tumor necrosis factor (TNF), belongs to the innate immune system. Blocking IL-1, another cytokine belonging to the innate immune system, has not proven to be as effective as TNF blockade for the majority of the RA patients. Recent clinical trails blocking a third cytokine in this family, IL-6, show promising results. This cytokine exerts effects within both the innate and the adaptive immune systems.

Temporarily eliminating B-cells, which are the producers of antibodies, has also proven a successful therapy. A third alternative, blocking the interaction between cells presenting antigens and T- cells, has resulted in an approved therapy. Together, these treatment- based data also demonstrate the significant role of the various parts of the innate as well as adaptive immune system for disease progression.

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