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CD4 T Cell-Independent Antibody Response Promotes Resolution of Primary Influenza Infection and Helps to Prevent Reinfection¹

Byung O. Lee, Javier Rangel-Moreno^*, Juan E. Moyron-Quiroz^*, Louise Hartson^*, Melissa Makris^*, Frank Sprague^*, Frances E. Lund^* and Troy D. Randall^2,*

^* Trudeau Institute, Saranac Lake, NY 12983; and Vaccine Research Institute of San Diego, San Diego, CA 92109

It is generally believed that the production of influenza-specific IgG in response to viral infection is dependent on CD4 T cells. However, we previously observed that CD40-deficient mice generate influenza-specific IgG during a primary infection, suggesting that influenza infection may elicit IgG responses independently of CD4 T cell help. In the present study, we tested this hypothesis and show that mice lacking CD40 or CD4 T cells produce detectable titers of influenza-specific IgG and recover from influenza infection in a manner similar to that of normal mice. In contrast, mice completely lacking B cells succumb to influenza infection, despite the presence of large numbers of functional influenza-specific CD8 effector cells in the lungs. Consistent with the characteristics of a T-independent Ab response, long-lived influenza-specific plasma cells are not found in the bone marrow of CD40^–/– and class II^–/– mice, and influenza-specific IgG titers wane within 60 days postinfection. However, despite the short-lived IgG response, CD40^–/– and class II^–/– mice are completely protected from challenge infection with the same virus administered within 30 days. This protection is mediated primarily by B cells and Ab, as influenza-immune CD40^–/– and class II^–/– mice were still resistant to challenge infection when T cells were depleted. These data demonstrate that T cell-independent influenza-specific Ab promotes the resolution of primary influenza infection and helps to prevent reinfection.

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