Antibodies to guinea-pig lymphokines. V. Suppression of normal lymphocyte transfer, immune lymphocyte transfer and direct reactions in the guinea-pig by anti-lymphokine globulin.

An antiserum (anti-lymphokine globulin, ALkG) directed against highly-purified products of activated lymphocytes, inhibits normal lymphocyte transfer (NLT), immune lymphocyte transfer (ILT) and direct reactions (DR) elicited by lymph node cells from strain 2 guinea-pigs in the skin of strain Bio B recipients. When injected i.d. around the site of injection of donor cells or i.v. into Bio B guinea-pigs, ALkG partially suppressed the initial inflammatory phase associated with NLT reactions and totally abolished the flare-up phase. ALkG is directed against three newly synthesized lymphocyte products (one of them being migration inhibitory factor, MIF) which are involved in the mediation of delayed hypersensitivity reactions . Since ALkG does not contain cytotoxic antibodies against guinea-pig lymphocyte cell antigens and since its inhibitory activity is not absorbed by lymphoid cells, it is probable that the inhibition of NLT reactions is not mediated by the lysis of donor or host cells but rather by the inactivation of a soluble factor elaborated as a result of the allogeneic interaction. The injection of ALkG 2 days after the initiation of the NLT reaction only produces a partial suppression of the inflammatory response associated with the flare-up phase indicating that ALkG must be present during the first 24–48 h in order effectively to inhibit the development of the NLT reaction, possibly by blocking the action of a humoral substance mediating the flare-up reaction. These findings suggest that ALkG is capable of inhibiting some product(s) of allogeneic cell interactions not only (ALkG has previously been shown to inhibit the guinea-pig mixed leucocyte reaction by reacting with a blastogenic factor produced during the MLC reaction) but also suggesting that similar lymphocyte products may be responsible for both (NLT) an (MLC) reactivity.