The Journal of Experimental Medicine
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Published online 18 December 2000.
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© The Rockefeller University Press, 0022-1007/2000/12/1763/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 12, December 18, 2000 1763-1774

Original Article

Virus-Induced Maturation and Activation of Autoreactive Memory B Cells

Amy J. Reeda, Michael P. Rileya, and Andrew J. Catona

a From The Wistar Institute, Philadelphia, Pennsylvania 19104
The Wistar Institute, Rm. 262, 3601 Spruce St., Philadelphia, PA 19104.215-898-3868215-898-3839

caton{at}wistar.upenn.edu

We have examined B cell populations that participate in distinct phases of the immune response to the influenza virus A/PR/8/34 hemagglutinin (HA) for their susceptibility to negative selection in mice that express the HA as a neo–self-antigen (HA104 mice). We demonstrated previously that specificity for the neo–self-HA causes a population of immunoglobulin G antibody-secreting cells, which dominate the primary response to virus immunization in BALB/c mice, to be negatively selected in HA104 mice. We find here that in contrast to these primary response B cells, HA-specific memory response B cells developed equivalently in HA104 and nontransgenic (BALB/c) mice. Indeed, there was no indication that HA-specific B cells were negatively selected during memory formation in influenza virus–immunized HA104 mice, even though the neo–self-HA can be recognized by memory B cells. Furthermore, HA-specific autoantibodies were induced in the absence of virus immunization by mating HA104 mice with mice transgenic for a CD4+ HA-specific T cell receptor. These findings indicate that specificity for a self-antigen does not prevent the maturation of autoreactive B cells in the germinal center pathway. Rather, the availability of CD4+ T cell help may play a crucial role in regulating autoantibody responses to the HA in HA104 mice.

Key Words: tolerance • autoantibodies • molecular mimicry • germinal center • CD4+ T cells

Abbreviations used in this paper: AP, alkaline phosphatase; ASC, antibody-secreting cell; BCR, B cell receptor; ELISPOT, enzyme-linked immunospot; HA, hemagglutinin; HAU, hemagglutinating unit(s); HI, hemagglutination inhibition; HRP, horseradish peroxidase; PNA, peanut agglutinin; PR8, influenza virus A/PR/8/34; S1, site 1; tg, transgenic.

© 2000 The Rockefeller University Press


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