Intraperitoneal application of ZPS, such as PS A1 from B. fragilis or Sp1 from S. pneumoniae, with adjuvant, promotes CD4+ T cell-dependent intra-abdominal abscess pathology [5],[13], whereas subcutaneous ZPS application without adjuvant induces regulatory IL-10-secreting CD4+ T cells that protect from abscess formation [14]. The gene discussed is CD4; the disease is abdominal abscess.