Rationale: There is growing evidence that residents cells, such as fibroblasts and epithelial cells, can drive the persistent accumulation of dendritic cells (DC) in chronically inflamed tissue, leading to the organization and the maintenance of ectopic lymphoid aggregates. This phenomenon occuring through a chemokine mediated retention mechanism has been documented in various disorders, but not in fibrotic interstitial lung disorders in which the presence of organized lymphoid follicles has been documented. Objectives: To characterize the distribution of DC in fibrotic lung, and to analyze the expression of the main chemokines known to regulate DC recruitment. Methods: Lung resection tissue (idiopathic pulmonary fibrosis (IPF), n = 12; non-specific interstitial pneumonia (NSIP), n = 5; control lungs, n = 5) was snap frozen for subsequent immunohistochemical techniques on serial sections and RT-PCR analysis. Main Results: Results were similar in IPF and NSIP lungs which were heavily infiltrated by immature DC in established fibrosis and in areas of epithelial hyperplasia. Altered epithelial cells and fibroblasts, particularly in fibroblastic foci, frankly expressed all chemokines (CCL19, CCL20, CCL22 and CXCL12) susceptible to favor the recruitment of immune cells. Lymphoid follicles were infiltrated by maturing DC which could originate from the pool of DC accumulating in their vicinity. Conclusions: These findings suggest that resident cells in pulmonary fibrosis can sustain chronic inflammation by driving the accumulation of DC with the potential to mature locally within ectopic lymphoid follicles. Future strategies should consider DC or chemokines as therapeutic targets in the treatment of pulmonary fibrosis.