Combined Oral and Intravenous Immunization Stimulates Strong IgA Responses in Both Systemic and Mucosal Compartments.

To investigate the influence of immunization routes onIgG, IgA and IgM production in systemic and mucosal compartments, we immunized mice with keyhole limpet hemocyanin (KLH) via oral, intranasal (i.n.) or subcutaneous (s.c.) routes alone or combined with the intravenous (i.v.) route. We found that administering antigen intravenously could affect antibody production and formation of antibody secreting cells (ASCs) depending on the immunization route previously used. Combined oral/i.v. immunization but not s.c./i.v. immunization caused a great increase of IgA ASCs in the spleen and enhanced IgA production in the small intestine and serum. Combined i.n./i.v. immunization could also increase IgA ASCs in the spleen and enhance IgA production in serum but had no effect on IgA production in the small intestine. Oral/i.v. immunization caused increase of IgG ASCs in both the spleen and bone marrow. In comparison, combined i.n./i.v. and s.c./i.v. immunization could increase IgG ASCs in the spleen but not in bone marrow. Intravenous administration of KLH in mice that had been immunized via oral, i.n. or s.c. routes caused some increase of IgM ASCs in the spleen but not in bone marrow. In conclusion, combined oral and i.v. administration of an antigen can induce fast and strong immune responses, especially for IgA, in both systemic and mucosal compartments.

Potential regulatory role of in vitro-expanded Vδ1 T cells from human peripheral blood.

γδ T cells represent a relevant proportion of T lymphocytes that express T cell receptors (TCRs) encoded by the γ and δ T cell receptor genes. Whereas the most circulating γδ T cell type, Vδ2 T cells, has been described and studied intensively, the potential role of Vδ1 T cells remains largely unclear. Here, we identified that expanded peripheral blood Vδ1 T cells stimulated with anti-human TCR Vδ1 monoclonal antibody (mAb) in vitro predominantly expressed forkhead box p3 (Foxp3). In addition, these cells also expressed other regulatory T cell-related molecules, such as CD25, glucocorticoid-induced TNFR family-related protein and cytotoxic T lymphocyte-associated protein-4 (CTLA-4), and held the potent capacity for the production of transforming growth factor beta 1 (TGF-ß1). These autocrine and/or paracrine TGF-ß1 could bind TGF-ß1 receptors on Vδ1 T cells and induce sustained Foxp3 expression. Moreover, Foxp3 expression coincided with high CD25 expression. CD25(high) Vδ1 T cells exhibited stronger suppression on CD4(+) T cell proliferation compared with TGF-ß1-induced CD25(high) CD4(+) regulatory T cells. Therefore, our phenotypic and functional analyses first demonstrate the potential regulatory property of anti-human TCR Vδ1 mAb-activated Vδ1 T cells. These results will broaden our understanding about the role of peripheral blood Vδ1 T cells under physical and pathological conditions.