International Immunology, Vol 9, 211-218, Copyright © 1997 by Oxford University Press
Y Wang, J O'Rourke and RE Cone
Injection of soluble protein antigen into the anterior chamber of the eye
of primed mice induces anterior chamber-associated immune deviation (ACAID)
which is manifested by suppression of delayed-type hypersensitivity (DTH)
to the antigen. Recently, we found that ACAID induced in primed mice also
results in a rapid rise in serum of soluble T lymphocyte-derived proteins
specific for nominal antigen (TABM). Here, we demonstrate that serum TABM
induced in primed mice during ACAID will transfer the suppression of DTH to
mice primed to the same antigen. Sera from TNP-BSA-primed mice that
received an anterior chamber injection of TNP-BSA, but not BSA alone,
suppressed the DTH response to TNP when injected into other TNP-BSA-primed
mice. Sera absorbed with Sepharose beads conjugated with either anti-TCR
C(alpha), anti-TCR C(beta), anti-TABM or TNP-BSA did not contain
TNP-specific TABM and did not transfer suppression of DTH. These results
suggest that the antigen-specific, TCR C(alphabeta)+ TABM that appear in
serum during ACAID are able to confer on or amplify the capacity of
sensitized T cells to suppress DTH. We believe this to be the first
demonstration of an in vivo immunologic function that is specifically
associated with TABM produced in vivo.
ARTICLES
Serum TABM produced during anterior chamber-associated immune deviation passively transfers suppression of delayed-type hypersensitivity to primed mice
Vision Immunology Center, Department of Pathology, University of Connecticut Health Center, Farmington 06030-3105, USA.
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