Journal of Experimental Medicine, Vol 161, 1357-1367, Copyright © 1985 by Rockefeller University Press
Regulation of IgG memory responses by helper and suppressor T cells activated by the type 2 antigen, polyvinylpyrrolidone
H Braley-Mullen
T cells from CAF1 mice immunized with various amounts of the type 2 antigen
polyvinylpyrrolidone (PVP) were assessed for their ability to provide help
to PVP-specific memory B cells for the production of IgG. Low doses (0.0025
micrograms) of PVP consistently activated helper T cells (Th), which were
required for the production of IgG by primed B cells. In contrast, T cells
from mice primed with higher amounts (0.25 or 25 micrograms) of PVP did not
provide significant help to the same B cells for IgG production. Moreover,
when mixed with B cells and low- dose PVP-primed Th, T cells from mice
primed with 0.25 or 25 micrograms PVP suppressed PVP-specific IgG, but not
IgM antibody responses. The suppressor cells induced by higher amounts of
PVP were eliminated either by injecting cyclophosphamide (CY) before
priming with PVP, or by treating the primed T cells with anti-Lyt-2.2 and C
before transfer. Pretreatment of suppressor T cell (Ts) donors with CY or
removal of Lyt- 2+ T cells not only eliminated Ts activity, but also
unmasked significant Th activity in the T cells from high-dose PVP-primed
mice. Thus, both low and high amounts of PVP can activate Th, although high
amounts of PVP also induce Ts, the activity of which predominates in a
normal unfractionated T cell population. The amount of PVP (0.0025
micrograms) that induces dominant help for IgG memory responses was only
marginally immunogenic for induction of primary PVP-specific IgM responses,
while 0.25 and 25 micrograms PVP, which induce dominant suppression for IgG
memory responses, are optimally immunogenic for primary IgM responses.
These results are discussed in the context of the inability of most type 2
antigens to elicit primary IgG responses or to prime memory B cells for
production of IgG, responses which are dependent on the function of
antigen-specific Th.