Shortly after the discovery of T-and B-cell interactions in humoral-immune responses, interest developed in the possible occurrence of interactions between T cells during cell-mediated-immune responses. T-T interactions occur in virtually all cellmediated-immune responses including graft-versus-host (GvH) 1 reactions (1), the development of cytotoxic T cells (2, 3), mixed lymphocyte reactions (4), responses to mitogens (5), generation of helper T cells (6, 7), and the development of delayed hypersensitivity (8). More recently, they have been discovered in the activation of suppressor T cells (T~) (9-11).The purpose of this study was to investigate whether T-T cell interactions were involved in the expression of suppressor T cells in contact sensitivity system. The results indicate that suppressor T cells, which block the efferent route of contact sensitivity (Ts-eff), require the presence of another population of auxiliary T suppressor cells (Ts-aux). The Ts-aux are present in populations of immune lymph node (LN) cells but not in populations of normal LN cells. Depletion of T,-aux, either by pretreatment with cyclophosphamide (Cy), anti-0 serum + C' treatment, or by adult thymectomy, rendered the immune LN cells (TDn) nonsuppressible by Ts-eff. Materials and MethodsMice. 2-to 4-mo-old female BALB/c mice were obtained from Simonsen Laboratories, Giiroy, Calif. CBA/J male mice were obtained from The Jackson Laboratory, Bar Harbor, Maine.Antigens and Tolerogens. 2,4-dinitrobenzene-1-suifonic acid sodium salt (DNBS) was obtained from Eastman Kodak Co., Rochester, N. Y. 2,4-dinitro-1-fluorobenzene (DNFB) was obtained

Replication-defective human adenovirus (Ad) group C transducing vectors, most of which have the E1A, E1B, and E3 genes deleted, are highly inflammatory despite the fact that the parental viruses typically cause subclinical or mild infections. To investigate this paradox, the roles that the E1A, E1B, and E3 genes play in inflammation were tested by using replication-incompetent viruses carrying a deletion of the preterminal protein gene. The viruses were injected into BALB͞c mouse ears, and edema was monitored as a sensitive surrogate marker of inflammation. A virus deleted for the E1A 289R (transcription activating) protein was noninflammatory, and inhibited edema induced by empty virus particles. The E1A 243R and E1B 55-kDa (p53 binding) proteins play the most important roles in inhibition of inflammation by the noninflammatory virus. The E1B 19-kDa antiapoptotic protein inhibited edema when both the E1A 243R and E1B 55-kDa proteins were expressed but strongly induced edema when only one was expressed. E3 proteins had their greatest effect on the inhibition of edema induced by the E1A 289R protein. The results support a model in which inflammation is countered through a mechanism that involves complex genetic interactions between Ad early region proteins and offer promise for the design and construction of noninflammatory Ad gene therapy vectors that are relatively easy to grow and purify.

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