A survey of 150 cases with sporotrichosis seen at the Dermatological Clinic of Kurume University Hospital from February 1962 to October 1986 was reported. The proportion of cases with sporotrichosis to the total number of outpatients was 0.17%. Greater percentage of cases fell into the less than 10 years old or more than 40 years old groups. The male to female ratio was 1:1.46, and 38 cases occurred in farmers. Geographic distribution was remarkable, especially around the Chikugo and Yabe river. Sixty-four cases showed the cutaneous lymphangitic type and 85 cases the localized cutaneous type and one case atypical type. The face and upper extremities were the most affected. The sporotrichin test was positive in 117 of 131 cases. The causative organism was demonstrated in tissue sections in 69% of the cases.

IntroductionTransplantation of hematopoietic organs (eg, bone marrow) into immunocompetent hosts induces the activation of alloreactive T cells of both recipient and donor origins, thus causing the host 3 graft reactions expressed clinically as graft rejection and the graft 3 host reactions manifested as graft-versus-host disease (GVHD), respectively. It has become evident that dendritic cells (DCs) play crucial roles in the initiation of both types of alloresponses. 1,2 Host 3 graft reactions are mediated primarily by host T cells that recognize either intact donor major histocompatibility complex (MHC) molecules expressed on donor DCs (direct presentation) or donor-derived peptide antigens being presented by host DCs (indirect presentation). Likewise, donor T cells that recognize intact host MHC molecules on host DCs or host-derived peptide antigens presented by donor DCs function as main effector leukocytes for GVHD. 3,4 Both CD4 ϩ and CD8 ϩ T cells are involved in the above bidirectional allogeneic immune responses, thus providing an additional level of complicity. 5,6 Many therapies have been developed to prevent the onset of allogeneic immune responses after organ transplantation. For example, GVHD, a major complication after allogeneic bone marrow transplantation, has been prevented and treated clinically by conventional immunosuppressive agents and, in selected cases, by ex vivo removal of T cells from the donor inoculum before in vivo infusion. 7,8 GVHD in experimental animals has been successfully treated by more innovative immunomodulatory strategies that are designed to: (1) trigger clonal anergy of effector T cells by blocking costimulatory molecules 9-13 ; (2) control the expansion and differentiation of effector T cells by administration of recombinant cytokines or cytokine inhibitors 7,14-17 ; or (3) interfere with effector T-cell trafficking by blocking adhesion molecules. [18][19][20] Our ultimate goal is to develop a new strategy that is designed to selectively kill alloreactive T cells.Recently, we have created "killer" DCs by introducing the CD95L cDNA into a fully mature DC line (XS106) derived from A/J mice. 21 The resulting CD95L-transduced killer DC clone, when pulsed with ovalbumin (OVA), induced rapid apoptosis of OVA-reactive T cells and prevented the induction of delayedtype hypersensitivity (DTH) responses to OVA in syngeneic A/J mice. Likewise, contact hypersensitivity responses to dinitrofluorobenzene (DNFB) were suppressed almost completely by administration of DNFB-pulsed killer DCs. On the other hand, when administered into allogeneic BALB/c hosts, killer DCs inhibited only partially the host immune responses to A/Jassociated MHC molecules. We have interpreted these results to suggest that killer DCs may deliver apoptotic signals only to the host T cells that recognize allo-MHC molecules via direct presentation. Thus, we have hypothesized that complex alloimmune responses may be suppressed more efficiently if one can Figure 1A). Materials and methods Animals and cell linesAll ...