Interstitial pneumonitis (IP) is the most frequent and serious pulmonary involvement in patients with dermatomyositis (DM)/polymyositis (PM) [1][2][3][4][5][6][7][8]. In one study representing the largest series of autopsy cases with DM/PM, the mean survival of patients with IP was shown to reduce to only 8 months after the onset of pulmonary symptoms [5]. We also showed that IP developed in 32% of 111 DM/PM patients and that 35% of DM/PM patients with IP died of respiratory failure in a year [8]. Moreover, it has been shown that 44-60% of IP in DM/PM, especially in DM, is resistant to high-dose corticosteroid therapy and the corticosteroid-resistant IP patients die of respiratory failure in a relatively short period [6][7][8]. Furthermore, we and others have recently shown that the corticosteroid-resistant IP is successfully treated with a T cell-specific immunosuppressant cyclosporin [8][9][10], suggesting that the activation of T cells is importantly involved in the development of corticosteroid-resistant IP in DM/PM. Therefore, in order to determine the difference in T cell activation states between corticosteroid-resistant and corticosteroidsensitive IP in DM/PM, we studied the activation markers and cytokine profiles of T cells in bronchoalveolar lavage fluids (BALF) from patients with IP in DM/PM before prednisolone therapy and then compared the activation states of T cells according to the therapeutic response of IP to prednisolone therapy. Our results indicate that activated Th1-type pulmonary T cells are importantly involved in the development of corticosteroidresistant IP in DM/PM and that the increase in CD25 + CD8 + T cells in BALF is a useful indicator for corticosteroid-resistant IP in DM/PM. 541 Activation of pulmonary T cells in corticosteroid- SUMMARYTo study the activation states and cytokine profiles of pulmonary T cells in corticosteroid-resistant and corticosteroid-sensitive interstitial pneumonitis (IP) in dermatomyositis (DM)/polymyositis (PM), we examined the activation markers and cytokine profiles of T cells in bronchoalveolar lavage fluids (BALF) from patients with IP in DM/PM before prednisolone therapy and then compared the activation states of T cells according to the therapeutic response of IP to prednisolone therapy. CD25 + CD4+ T cells in BALF were significantly increased in both corticosteroid-resistant and corticosteroidsensitive IP in DM/PM as compared with those in controls without IP. Furthermore, CD25 + CD4 + T cells in BALF were significantly more increased in corticosteroid-resistant IP than those in cortico teroidsensitive IP. Moreover, CD25+ CD8

Conclusions: Abnormal repertoires and impaired isotype expression are seen in patients with common variable immunodeficiency, these data suggested that rituximab after APBSCT can affect not only the B-cell quantities, but also the recovery of the B-cell repertoires.

Summary:We mobilized peripheral blood stem cells (PBSC) following CHOP plus rituximab (CHOP-R) therapy, and compared with the findings following CHOP therapy without rituximab. All patients were given G-CSF starting from day 11 after CHOP therapy. Patients in the CHOP-R group (n ¼ 8) were given rituximab on day 12. Target CD34 þ cells number was collected in a single leukapheresis on day 14, from all the eight patients in the CHOP-R group. PBSC mobilization kinetics, CD34þ cells yield and colony-forming ability in the graft collection, toxicity during mobilization, and engraftment after transplantation of CHOP-R group were not significantly different from those in the CHOP group (n ¼ 8). In all patients given CHOP-R therapy, CD20 þ cells and immunoglobulin heavy chain (IgH) rearrangement in the graft collection were undetectable by flow-cytometric analysis and Southern blot analysis, respectively, but with PCR analysis two of eight grafts were positive for IgH rearrangement. While further studies are needed to evaluate the efficacy of purging and the outcome of patients undergoing autologous transplantation, CHOP-R therapy can be safely and effectively used in the mobilization phase of PBSC collection, without excess clinical toxicity or deleterious effect on PBSC mobilization kinetics or engraftment time.

SummaryRecent studies have indicated that patients who received rituximab as an adjuvant to stem cell transplantation (SCT) demonstrated an increased risk of developing severe hypogammaglobulinaemia, which was found to be a result of delayed recovery of CD27 positive memory B cells and impaired isotype expression. It appears that rituximab influences both the quantity and quality of B-cell redistribution. Precisely how the B-cell repertoire regenerates after anti-CD20-mediated transient B-cell depletion in patients with nonHodgkin lymphoma (NHL) remains to be elucidated. This study performed a phenotypical analysis of B cells in 17 NHL patients who received rituximab as an adjuvant to autologous SCT. The median period after final administration of rituximab was 36 months (range, 12-43 months). Surface antigen expression of CD27, CD40 and CD80 in NHL patients was statistically significantly different from healthy controls (n ¼ 14). Moreover, B cells from NHL patients showed significantly impaired IgG and IgA production upon engagement of surface immunoglobulin receptors in the presence of interleukin (IL)-2, IL-10 and CD40 ligand in comparison with samples from healthy controls. The delayed recovery of memory B cells with an abnormal cell marker expression and function demonstrates that naive B cells may fail to differentiate into plasma cells, resulting in hypogammaglobulinaemia after autologous SCT and rituximab therapy.

We report a patient with a relapsed in bone marrow of extremities after allogeneic peripheral blood stem cell transplantation for acute lymphoblastic leukemia (ALL). The patient complained of pain in the right upper arm and left leg 15 months after transplantation. Magnetic resonance imaging (MRI) and fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) showed abnormal findings in bone marrow of upper and lower extremities. There were no findings of relapse in aspirates from the sternum and iliac bone marrow. Biopsy specimen from the iliac bone marrow showed normocellular marrow without leukemic cells. Biopsy specimen from the right humerus revealed marked leukemic cell infiltration in the bone marrow. This is apparently the first case of localized relapse of ALL in bone marrow of extremities. Physicians should be aware of unusual relapse sites of leukemia after allogeneic stem cell transplantation. MRI and FDG-PET may be of value in detecting this type of relapse. Am.