NGF increased p-Akt expression in CD3+T lymphocytes. Here we have observed two novel growth functions of NGF on T cell biology. NGF is mitogenic to T lymphocytes and promotes survival of T lymphocytes by inhibiting TNF-α induced apoptosis. doi:10.1016/j.clim.2009.03.456 S.83. Th17, Th1 and Treg Subsets are Increased in Systemic Sclerosis (SSc) Patients Janette Furuzawa-Carballeda, Luis Llorente, Javier Cabiedes, Luis Fajardo-Hermosillo, María Inés Vargas-Rojas, Tatiana Rodriguez-Reyna. Instituto Nacional de Ciencias Médicas y Nutrición, Mexico, Mexico SSc is an autoimmune disease characterized by fibrosis and vasculopathy. A key feature of the inflammatory lesions is the presence of T cells. High levels of IL-17 have been reported. This study suggested that the T-cell activity in SSc takes place outside the conventional Th1/Th2 subsets. Aim. To quantify T cell subsets in peripheral blood from SSc patients. Methods. Blood samples from 153 consecutive SSc patients were obtained. Clinical evaluation and organ involvement were determined using the Medsger severity scale. Controls were collected from age-and sex-matched healthy volunteers (n = 12; mean age = 30.3 ± 8.5yrs); active SLE patients(n = 13; mean age = 36.7 ± 12.2yrs)and active RA patients(n = 12; mean age = 46.8 ± 15.3yrs). Mononuclear cells were analyzed by flow cytometry to determine the absolute number (cel/ml) of Th1 (CD4+/CD14-/IFN-γ+), Th2 (CD4+/ CD14-/IL-4+), Th17 (CD4+/CD14-/CD4/IL-17+), Treg (CD4+/ CD14-/FoxP3+) and T CD4+/IFN-γ+/IL17+subsets. Patients were classified according to skin involvement in diffuse (n = 63; age = 44.4 ± 13.2yrs; disease evolution = 8.2 ± 5.9yrs) and limited (n = 90; age = 46.8 ± 13.5; disease evolution = 11.1 ± 10.1). Results. Th17, Th1 and Treg subsets were increased in SSc and active RA groups vs. healthy control and SLE groups (Th17: limited = 135.4 ± 20.0; diffuse = 222.8 ± 108.4; vs. healthy control = 26.93 ± 4.0; SLE = 9.3 ± 2.2; p b 0.001. Th1: limited = 97.5 ± 22.0; diffuse = 113.7 ± 55.0; vs. healthy con- trol = 7.9 ± 3.9; SLE = 3.3 ± 1.6; p b 0.006. Treg: limited = 165.4 ± 24.2; diffuse = 157.6 ± 33.3; vs. healthy control = 81.0 ± 9.3; SLE = 45.0 ± 9.6; p b 0.04). There were no differences between active RA and SSc patients. There were no statistical differences in T CD4+/IFN- γ+/IL17+subset, by age, time of disease evolution and treatment between SSc groups. Conclusion. Th17, Th1 and Treg subsets are increased in patients with SSc. doi:10.1016/j.clim.2009.03.457 S.84. Role of C-Chemokine Receptor 2 (Ccr2) in Murine Model of Kawasaki's Disease Hernan Martinez 1 , Marlon Quinones 1 , Fabio Jimenez 1 , Carlos Estrada 1 , Kassandra Clark 1 , Kazuo Suzuki 3 , Noriko N. Miura 2 , Naohito Ohno 2 , Seema Ahuja 1 . 1 UTHSCSA, San Antonio, TX; 2 Chiba University Graduate School of Medicine, Tokio, Japan; 3 Tokyo University Pharmaceutical and Life Sciences, Tokyo, Japan Mounting evidence suggests that immune responses trig- gered by unidentified infectious agent(s) may underlie the pathogenesis of Kawasaki Disease (KD); an illness character- ized by coronary vessel inflammation (CVI) mostly affecting young children and associated with high circulating levels of the CC chemokine ligand 2 (CCL2). We used a murine KD model based on exposure to Candida Albicans Water Soluble extract (CAWS) antigens as a trigger for development of CVI to elucidate the role of the CCL2′s receptor CCR2 in KD. Ccr2 null mice (Ccr2-/-), Rag1-/-(T and B cell deficiency) and matched controls (WT) received two 5-day cycles of daily intraperitoneal CAWS injections and were euthanized after 8 weeks. The incidence and severity of CVI after CAWS exposure was significantly attenuated in Ccr2-/-mice. This resistant phenotype was associated with reduced macro- phage infiltration and lower circulating levels of known KD- pathogenic factors such as anti-MPO antibodies and MMP9. Two lines of evidence suggested that resistance to CVI in Ccr2-/-mice might be linked to effects on T and B cells inter- actions. First, Rag1-/-mice became susceptible to CVI only after being reconstituted with T+B cells from WT but not Ccr2-/-mice. Second, genetic inactivation of CCR2 blunted the depletion of circulating regulatory T cells (CD4+, CD25+, and Foxp3+Tregs) observed in WT mice following exposure to CAWS. Collectively, our data suggest that CCR2 plays a critical role in the pathogenesis of CAWS induced CVI, possibly orchestrating immune regulation through its effects on T cell responses. doi:10.1016/j.clim.2009.03.458 S.85. Chronic GVHD Appears to Cause Genomic Instability in Oral Mucosal Cells After Allogeneic Hematopoeitic Cell Transplantation (HCT) Faisal Khan, Sarah Sy, Polly Louie, Douglas Stewart, James Russell, Jan Storek. University of Calgary, Calgary, AB, Canada Genomic Instability (GI) is typically a precancerous/can- cerous state but is also reported in non-neoplastic chroni- cally inflamed tissues. Chronic Graft-versus-host-disease (GvHD) after allogeneic HCT may produce chronically inflamed tissues. Since chronic GvHD and second malignancy are frequent in oral and rare in nasal mucosa, we determined whether GI occurs in oral and nasal mucosal cells and, if yes, whether it is related to chronic GVHD. We examined epithelial cells from oral and nasal mucosa of 85 subjects that include long-term (4-22 yrs, n = 25) and short-term (1- 3 months, n=27) survivors of allo-HCT. Controls included survivors of auto-HCT (n = 18), patients treated with inten- sive chemotherapy without HCT (n = 5) and healthy volun- teers (n = 10). DNA extracted from blood leukocytes and cells of nasal and oral mucosa was PCR amplified for 15 microsatellite markers. Fragment size analysis was done to identify novel allele peaks (GI). GI was detected in 68% of oral specimens and 4% of nasal specimens in long-term allo- HCT survivors (p b 0.001). Number of microsatellites showing GI in oral mucosa was higher in patients with than without history of clinical oral GVHD (p = 0.02). GI was found in oral mucosa of only 3.7% short-term allo-HCT survivors and was S155 Abstracts