In vitro activation of immune lymph node cell proliferation by photohapten-modified cells in murine contact photosensitivity.

Painting of 3,3',4',5-tetrachlorosalicylanilide (TCSA) plus ultraviolet A (UVA) irradiation to the same site induces contact photosensitivity (CPS), but at the same time results in death of the photohapten-modified cells. Using an in vitro immune lymph node cell (LNC) proliferation system, we investigated the mechanism of induction and elicitation of CPS by TCSA painting plus UVA irradiation. The proliferation of LNC from TCSA-photosensitized mice was not augmented by the addition of TCSA-photocoupled syngeneic spleen cells (SC) or epidermal cells (EC), whereas the picryl chloride immune LNC proliferation was activated by trinitrophenyl-coupled (TNP-coupled) SC or EC. While the viability of SC and EC was unchanged even after TNP haptenization, cells showed very low levels of viability after TCSA photohaptenization. This suggests that the inability of photoTCSA-modified cells to activate LNC proliferation is because of their low viability. Nylon wool column purified lymph node T cells from TCSA-photosensitized mice were activated by photohapten-conjugated SC or photohaptenized EC fragments only in the presence of peritoneal macrophages (M phi). The function of live M phi was not replaced by interleukin-1 (IL-1), suggesting that M phi were required for processing and/or presentation of photohapten rather than simply providing IL-1. Our in vitro study implies that photoTCSA-modified cells generated in vivo require intact antigen-presenting cells to effectively induce and elicit the CPS reaction.