Sweet syndrome after kidney transplantation.

The association between Sweet syndrome (acute febrile neutrophilic dermatosis) and malignancies, infection, and drugs has been well established, but the disorder has never been reported in a solid organ transplant recipient. We have presented the first reported case of Sweet syndrome connected with solid organ transplant. Our patient is a 38-year-old man who underwent deceased donor kidney transplant for focal and segmental glomerulosclerosis and after resuming dialysis 6 weeks posttransplant, was readmitted 2 months later with high fevers and multiple head, neck, chest, and back lesions. Cultures were negative, and skin biopsy was consistent with Sweet syndrome. The lesions responded to higher doses of prednisone. Sweet syndrome has been linked to multiple drugs and malignancies, but has also been linked with states of altered immunity. Posttransplant immunosuppression may be related to this occurrence.

Migratory activity and functional changes of green fluorescent effector cells before and during experimental autoimmune encephalomyelitis.

Homing behavior and function of autoimmune CD4+ T cells in vivo was analyzed before and during EAE, using MBP-specific T cells retrovirally engineered to express the gene of green fluorescent protein. The cells migrate from parathymic lymph nodes to blood and to the spleen. Preceding disease onset, large numbers of effector cells invade the CNS, with only negligible numbers left in the periphery. In early EAE, most (>90%) infiltrating CD4+ cells were effector cells. Migratory effector cells downregulate activation markers (CD25, OX-40) but upregulate several chemokine receptors and adsorb MHC class II on their membranes. Within the CNS, the effector cells are reactivated, with upregulated proinflammatory cytokines and downmodulated T cell receptor-associated structures, presumably reflecting autoantigen recognition in situ.

Suppression of experimental autoimmune encephalomyelitis with a TNF binding protein (TNFbp) correlates with down-regulation of VCAM-1/VLA-4.

The effect of a novel TNF binding protein (TNFbp), a polyethylene glycol-linked form of the type I soluble receptor of TNF, on the expression of adhesion molecules has been investigated with a passive transfer model of experimental autoimmune encephalomyelitis (EAE) in SJL/J mice. The expression of L-selectin, VLA-4 and LFA-1 on spleen cells of EAE animals treated with TNFbp or saline was examined by FACS analysis. The expression of VCAM-1 and ICAM-1 was investigated by immunochemistry in spinal cord tissue of SJL/J mice with EAE. In animals sensitized for EAE and treated with TNFbp, the expression of VCAM-1 in the central nervous system as well as VLA-4 on spleen cells was clearly diminished. Reduction in VCAM-1 staining and VLA-4 expression corresponded to inhibition of inflammation in the spinal cord and to prevention of clinical signs of EAE. The results have also shown that myelin basic protein responses as well as non-antigen-specific responses were not diminished in animals treated with TNFbp. The findings suggest that TNFbp might prevent EAE development by modulating the expression of VCAM-1 and VLA-4.