Primary Sjögren’s syndrome (pSS) is an autoimmune disease characterized by lymphocytic infiltration leading to destruction of acinar and ductal cells and loss of glandular parenchyma. Although sicca symptoms are pivotal manifestations of pSS, extraglandular involvement also occurs. Pulmonary involvement in pSS consists of interstitial lung disease, obstructive small airway disease, pulmonary arterial hypertension (PAH), bullous disease, and lymphoma1. Recent evidence suggests that cytokine-mediated mechanisms are critical in pSS, but the precise cytokine pattern driving lung injury remains unclear2–4. Because of current availability of therapies that modulate selected cytokines, in-depth knowledge of the cytokine profile associated to specific tissue damage is necessary. We analyzed circulating concentrations of several prototypical TH1 [interferon-γ (IFN-γ)], TH2 [interleukin 4 (IL-4), IL-6, IL-10], and TH17 (IL-17) cytokines in patients with pSS according to the presence or absence of pulmonary involvement. From an outpatient cohort with pSS according to the preliminary classification criteria5 we selected patients who had pulmonary involvement demonstrated by high-resolution computed tomography scans of the lungs, and at least one of the following: pulmonary function test, spirometry, or lung biopsy. For comparisons, we selected age and gender-matched pSS patients without pulmonary manifestations and normal chest radiograph. We excluded … Address correspondence to Dr. L.M. Amezcua-Guerra; E-mail: lmamezcuag{at}gmail.com