We demonstrated in the current study that although it is dispensable for the initial immediate pulmonary inflammatory responses and HP development caused by S. rectivirgula, PKD1 in myeloid lineage cells contributes significantly to the alveolitis, proinflammatory cytokine and chemokine production, and accumulation of CXCR3+CCR6+ nonconventional Th1 cells in the lung during the development of HP caused by S. rectivirgula. Here, CXCR3 is linked to hypersensitivity pneumonitis.