Adaptive Immunity in Interstitial Lung Diseases and Pulmonary Hypertension

The lungs are constantly exposed to inhaled agents that may induce an inflammatory response. The inflammatory response encompasses several stages, starting with the influx of activated inflammatory cells, and ending with tissue repair and restoration of tissue function. When the delicate balance between inflammation and resolution becomes dysregulated, ongoing inflammation can lead to tissue remodeling or fibrosis. In interstitial lung diseases and pulmonary hypertension, the big question is whether the observed changes in adaptive immunity are a critical trigger for disease onset and progression in susceptible patients or a consequence of established disease. The findings described in this thesis contribute to our knowledge on the immune-related pathogenesis of interstitial lung diseases and pulmonary hypertension. Combining the immunological mechanisms with disease behavior, response to therapy and patients’ perspectives will help to advance patient-tailored care.

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