CD4 T cell-independent antibody response promotes resolution of primary influenza infection and helps to prevent reinfection

Academic Article


  • 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 CB40-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 CB40-/- 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. 5827-5838 Copyright © 2005 by The American Association of Immunologists, Inc.
  • Published In

    Digital Object Identifier (doi)

    Pubmed Id

  • 2846578
  • Author List

  • Lee BO; Rangel-Moreno J; Moyron-Quiroz JE; Hartson L; Makris M; Sprague F; Lund FE; Randall TD
  • Start Page

  • 5827
  • End Page

  • 5838
  • Volume

  • 175
  • Issue

  • 9