Peptide immunization indicates that CD8(+) T cells are the dominant effector cells in trinitrophenyl-specific contact hypersensitivity

The identity of the effector T cell population involved in contact hypersen sitivity is still questionable with evidence promoting both CD4(+) or CD8() T cells. Previous experimental studies have relied on the in vivo depleti on of T cell subsets using antibody, or the use of knock-out mice with defi ciencies in either CD4(+) or CD8(+) T cell-mediated immunity. To address th e role of the class I- and class II-mediated pathways of T cell activation in contact hypersensitivity responses in mice with an intact immune system, we utilized various trinitrophenyl-derivatized peptides, which bind specif ically with H-2K(b) (major histocompatibility complex class I) or H-2I-A(b) (major histocompatibility complex class II). The subcutaneous injection of major histocompatibility complex class II-specific, but not of class I-bin ding, hapten-derivatized peptides in incomplete Freund's adjuvant induced s pecific, albeit low, contact hypersensitivity responsiveness to trinitrochl orobenzene. When bone-marrow-derived dendritic cells, however, were pulsed with the same peptides and administered intradermally, the opposite result was observed, namely that the class I binding peptides induced contact hype rsensitivity responses similar to that observed after epicutaneous trinitro chlorobenzene application. In contrast, dendritic cells pulsed with major h istocompatibility complex class II binding peptides did not reproducibly se nsitize for contact hypersensitivity responses. Surprisingly, both immuniza tion protocols efficiently induced CD8(+) effector T cells. These results s upport the notion that CD8(+) T cells are the dominant effector population mediating contact hypersensitivity responsiveness and that the CD4(+) T cel l subset only contributes little if at all.