ABSTRACT
The subacute and chronic forms are characterized by an exaggerated T-lymphocyte-mediated immune response. The precise mechanisms are unclear; however, the presence of cytokines including interferon gamma (IFN-γ), interleukin12 (IL-12), and tumor necrosis factor-α (TNF-α) in patients with HP has suggested a primarily T-helper 1 pathway. In this model, antigens presented by alveolar macrophages and dendritic cells will cause CD4+ T cells to produce IL-12 and IFN-γ, which then polarizes lymphocytes into the Th1 cell differentiation program, resulting in granulomatous inflammation. Regulatory T cells, whose role is to control the immune response, are thought to be impaired in patients with HP, resulting in uncontrolled inflammation (Figure 36.3).
