antibody response and impaired class switch recombination. Analysis of memory B-cell and switched memory B-cells revealed normal values. As LEKTI is prominently expressed in the thymus, we hypothesize that SPINK5 is required for maturation of antigen-specific T-cells in the thymus and that its defect may cause abnormal class switch recombination. Based on the resulting antibody deficiency, treatment with IVIG may be beneficial. doi:10.1016/j.clim.2006.04.547 Su.121. UV-Induced Immunosuppression and Cutaneous Apoptosis Requires the Proapoptotic Protein Bid. Sanjay Pradhan, Christopher Thrash, Sudheer Mantena, Santosh Katiyar, Craig Elmets, Laura Timares. Dermatology, University of Alabama at Birmingham, Birmingham, AL. Apoptosis plays an important role in eliminating UV- mutagenized cells but its role in immunosuppression is not clear. We have shown that Langerhans cells (LCs) normally undergo apoptosis after successful antigen presentation by recruiting proapoptotic Bid (BH3 interacting death domain) protein, and that Bid null ( / ) LCs resist apoptosis and mediate exaggerated immune responses. However, the role Bid plays in response to UV-induced damage in LCs and keratinocytes is not known. Therefore, we first compared UVB-induced sunburn responses and the forma- tion of sunburn cells after UVB exposure in C57Bl/6 wild type (WT) and Bid / mice. Then, to determine if apoptosis-resistant Bid / LCs respond differently from WT LCs to UVB exposure, we examined the levels of LCs remaining in epidermis and UV-induced immunosuppression to hapten sensitization. Sunburn responses were measured 24 hours after graded doses of UVB exposure on shaved backs and ears of mice. The minimal dose of UVB required to produce a sunburn response was less than 50 mJ/cm2 for WT mice, and greater than 100 mJ/cm2 for Bid / mice (p b 0.003). This correlated with a marked reduction in apoptotic cells (TUNEL+) and retention of LC (I-A+) density in the epidermis. UV-induced immunosuppression is thought to correlate with the level of DNA damage in LCs, suggesting a role for LC apoptosis in mediating suppres- sion. We tested immunosuppression of hapten sensitization and contact hypersensitivity in Bid / mice and found they were resistant, inhibited by only 29% as compared to 98% in WT mice (p b 0.03). Thus, Bid / epidermal cells undergo reduced apoptosis and provide an enhanced immu- nogenic environment for maintaining LC function after UVB exposure. doi:10.1016/j.clim.2006.04.548 Su.122. CD8+ IL-17 Producing T-cells Are Important in Effector Functions for the Elicitation of Contact Hypersensitivity. Donggou He, Lizhi Wu, Hee Kyung Kim, Hui Li, Craig Elmets, Hui Xu. Dermatology, University of Alabama, Birmingham, AL. Allergen induced contact hypersensitivity (CHS) has been considered to be primarily mediated by CD8+ CTL and/or Tc1 cells. IFN-g, the prototype Tc1 (Th1) cytokine, has been implicated as the primary inflammatory cytokine for CHS. However, accumulating evidence indicates that IFN-g may not play a major role in the elicitation of CHS. Therefore, effector mechanisms for CHS remain to be fully defined. The current studies specifically examine the role of IL-17, a pro- inflammatory cytokine, in the elicitation of CHS and characterize hapten primed T-cells that produce IFN-g and IL-17. Results indicated that neutralization of IL-17 prior to hapten challenge suppressed CHS, which was independent of CD4+ T-cells. However, neutralization of IL-17 did not have significant effects on the proliferation of primed T-cells and the CHS following re-challenge of the treated animals after three weeks rest. In contrast, anti-IFN-g antibody had little effect on CHS. While both CD4+ and CD8+ primed T-cells produced IL-17, the level in CD8+ was higher than in CD4+ T- cells. Further analysis demonstrated that distinct subpopu- lations of CD4+ and CD8+ T-cells produced IL-17 or IFN-g. While the activity of CD4+ and CD8+ IL-17 producing cells was stimulated by IL-23, it was inhibited by IL-12, a strong stimulator for IFN-g producing Th1 or Tc1 cells. These data, for the first time, demonstrate that IL-17 has important functions at the elicitation phase of CHS and hapten primed T-cells produce IL-17. Moreover, hapten primed CD8+ IL-17 producing cells are distinct from IFN-g producing Tc1 cells and are designated as T-IL-17 by us. To our knowledge, identification of CD8+ T-IL-17 and its functions in immune responses were not previously reported. The studies provide insights into a novel mechanism for CHS and may lead to new strategies for treatment of allergic contact dermatitis. doi:10.1016/j.clim.2006.04.549 Su.123. Hom S 4, An Ige-Reactive Autoantigen Belonging to a Novel Subfamily of Calcium-Binding Proteins Can Induce Th1-Mediated Autoreactivity. Karl Aichberger, 1 Irene Mittermann, 5 Renate Reininger, 2 Susanne Seiberler, 5 Ines Swoboda, 5 Susanne Spitzauer, 2 Tamara Kopp, 3 Georg Stingl, 3 Wolfgang Sperr, 1 Peter Valent, 1 Andreas Repa, 4 Barbara Bohle, 5 Dietrich Kraft, 5 Rudolf Valenta. 5 1 Department of Internal Medicine I, Division of Hematology, Medical University of Vienna, Vienna, Austria; 2 Clinical Institute for Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, Austria; 3 Department of Dermatology, Division of Immunology, Allergy and Infectious Diseases, Medical University of Vienna, Vienna, Austria; 4 Department of Pediatrics, Division of Neonatology and Intensive Care, Medical University of Vienna, Vienna, Austria; 5 Department of Pathophysiology, Division of Immunopathology, Medical University of Vienna, Vienna, Austria. Skin inflammation in atopic dermatitis (AD) usually starts with Th2 and IgE-mediated responses against exogenous allergens and, for unknown reasons, often resembles features of a Th1-driven reaction in the chronic stages. We here report the characterization of a human protein, Hom s 4, recognized by IgE autoantibodies from AD patients. The Abstracts S201