Chemokine receptor expression on T and B cells in a murine model of ovalbumin-induced allergic airway disease

Abstract In our biphasic Ovalbumin (OVA)-induced Allergic Airway Disease model, short-term exposure to OVA aerosols results in Allergic Airway Disease (AAD) whereas continued exposure leads to the resolution of disease and the development of Local Inhalational Tolerance (LIT). We have shown in adoptive transfer studies that Hilar Lymph Node (HLN) B cells of LIT mice suppress development of AAD. To understand trafficking of B cells within HLN, we assessed their expression of CXCR4 and CXCR5 chemokine receptors via flow cytometry in mice at various stages of the model: naïve, sensitized, AAD and LIT. B cell populations were divided into CD5+ and CD5- cells. Our data demonstrates that there was a significant increase in the number and percentage of total B cells expressing CXCR4 in the HLN of mice at AAD and LIT compared to naïve and sensitized mice. We also observed a significant increase in CXCR4 expression on CD5+ B cells compared to CD5- B cells. We also studied the chemokine receptor expression on T cells and observed that Foxp3+ T regulatory cells significantly increased the expression of CXCR4 at AAD and LIT. CXCR4 expression on B cells is required for germinal center development in lymphoid organs. It is unusual to find CD5+ B cells in lymph nodes. We hypothesize that these CD5+ B cells may be directly interacting with effector T cells in a regulatory manner converting them into regulatory T cells within germinal centers and hence contributing to the resolution of AAD.