The clinical importance of changes in Treg and Th17 lymphocyte subsets in splenectomized patients after spleen injury

BACKGROUND:Splenectomized patients are more prone to bacterial infections due to their immunocompromised status. Little is known about the role of T helper 17 (Th17) and T regulatory cells (Treg) in the immune system of patients after the removal of the spleen. OBJECTIVES:The aim of the present study was to analyze possible changes in CD4+ lymphocyte T subsets, especially Treg and Th17, in patients who had undergone splenectomy. MATERIAL AND METHODS:The study included a group of 67 male patients (41.74 ±16.22 years). All patients had undergone splenectomy because of spleen injury. Mean time elapsed from splenectomy to analysis was 9.1 ±4.6 years. Control samples were obtained from 20 male healthy volunteers. The percentages and absolute counts of Th17 and Treg were measured using the flow cytometry method. RESULTS:The analysis of the antibody titer against 23 serotypes of Streptococcus pneumoniae (S. pneumoniae) in the splenectomized patients revealed its elevated values compared to controls (p = 0.0016). Higher percentages and absolute counts of Treg cells were found in the splenectomized group vs controls (p < 0.000007). Lower percentages and absolute counts of the Th17 subset were found in the study group vs controls (p < 0.000002 and p < 0.00006, respectively). The Treg cell percentage was positively correlated with the antibody titer against S. pneumoniae (p < 0.02). Th17 cells were reversely correlated with the antibody titer (p < 0.004 and p < 0.001 for absolute counts and percentage values, respectively). The Th17 subset values were significantly lower in the splenectomized patients who reported a higher frequency of upper respiratory tract infections (URTI) (p < 0.0001). No correlations were found between the time elapsed since splenectomy and the Treg or Th17 cell values in the study group. CONCLUSIONS:Splenectomy results in an important deterioration of the Treg/Th17 cell balance with a predominance of immunoregulatory Tregs, which can contribute to insufficient immune response to infection.