Fig. 1

Pathogenesis of HTLV-1 associated pulmonary disease. The production of IFN-γ by HTLV-1 infected cells that have infiltrated into the lung induces CXCL10 production by diverse cell types including monocytes and neutrophils, recruiting more CXCR3 expressing, activated T cells and macrophages to the lungs, amplifying the inflammatory process in a positive feedback loop. HTLV-1 infected cells also produce CCL3, which further enhances lymphocyte migration to the area of inflammation, and this is facilitated by increased expression of cell adhesion molecules in response to IL-1α from HTLV-1 infected cells. The production of pro-inflammatory cytokines and chemokines is further augmented by the clonal proliferation of HTLV-1 infected cells in response to IL-2 acting in an autocrine and paracrine manner. Lung epithelial cells may also contribute to this process by producing pro-inflammatory cytokines (dotted line). This inflammatory process involves the interstitium, airways and alveoli, resulting in a lymphocytosis that is detectable in bronchoalveolar lavage fluid, and peribronchiolar lymphocyte infiltration which is apparent histologically