Serum TABM produced during anterior chamber-associated immune deviation passively transfers suppression of delayed-type hypersensitivity to primed mice

Injection of soluble protein antigen into the anterior chamber of the eyeof 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 alsoresults in a rapid rise in serum of soluble T lymphocyte-derived proteinsspecific for nominal antigen (TABM). Here, we demonstrate that serum TABMinduced in primed mice during ACAID will transfer the suppression of DTH tomice primed to the same antigen. Sera from TNP-BSA-primed mice thatreceived an anterior chamber injection of TNP-BSA, but not BSA alone,suppressed the DTH response to TNP when injected into other TNP-BSA-primedmice. Sera absorbed with Sepharose beads conjugated with either anti-TCRC(alpha), anti-TCR C(beta), anti-TABM or TNP-BSA did not containTNP-specific TABM and did not transfer suppression of DTH. These resultssuggest that the antigen-specific, TCR C(alphabeta)+ TABM that appear inserum during ACAID are able to confer on or amplify the capacity ofsensitized T cells to suppress DTH. We believe this to be the firstdemonstration of an in vivo immunologic function that is specificallyassociated with TABM produced in vivo.