ABO-incompatible kidney transplantation using both A2 and non-A2 living donors.

Background: Given the scarcity of cadaveric organs, efforts are intensifying to increase the availability of living donors. The current study assessed the feasibility of using ABO-incompatible living-donor kidneys to expand the donor pool.

Methods: The authors performed 18 ABO-incompatible living-donor kidney transplants between May 1999 and April 2001.

Porcine antigen presenting cells produce soluble adjuvants that stimulate B cells within and across the species.

Interactions between porcine antigen presenting cells (pAPCs) and host lymphocytes may be important in cellular and humoral rejection of porcine organ xenografts. To investigate the role of pAPCs in the activation of xenogeneic lymphocytes, porcine bone marrow cells were stimulated using porcine GM-CSF with or without porcine IL-4 to generate populations of pAPCs that had phenotypic characteristics of myeloid dendritic cells. These bone marrow-derived pAPCs were weak stimulators of xenogeneic (mouse and human) T cells in vitro but induced primary B-cell proliferation and augmented CD40-induced B-cell proliferation.

Vitamin D and its analogs as regulators of immune activation and antigen presentation.

It has been a little more than 20 years since the first appreciation that the biologically active hormonal form of the secosteroid vitamin D-classically categorized as a regulator of calcium/phosphorous metabolism and bone mineralization-can exert effects on cells of the immune system. Since then a substantial literature has accumulated to suggest that these effects are exerted on multiple immune cell types, are predominantly suppressive at pharmacologic levels, and are potent enough to have true therapeutic potential in the management or prevention of immune-mediated diseases. Less clear at present, however, are the physiological roles played by the vitamin D endocrine system in the regulation of normal and abnormal immune responses.

PKHDL1, a homolog of the autosomal recessive polycystic kidney disease gene, encodes a receptor with inducible T lymphocyte expression.

Autosomal-recessive polycystic kidney disease (ARPKD) is caused by mutation to a large gene, PKHD1, encoding a putative receptor protein, fibrocystin. We have identified, through analysis of human genomic sequence, a PKHD1 homolog, PKHDL1, in chromosome region 8q23. The PKHDL1 transcript of 13081 bp was amplified as 16 fragments and sequenced; the sequence of the murine ortholog, Pkhdl1 (chromosome region 15B3) was also determined.

Effects of 1alpha,25(OH)2D3 and its analogs on dendritic cell function.

1alpha,25-Dihydroxyvitamin D(3) (1alpha,25(OH)(2)D(3)) and non-calcemic vitamin D analogs induce a persistent state of immaturity in dendritic cells both in vitro and in vivo. These effects are transcriptional in nature, involve alterations in surface ligands as well as cytokine synthesis and release, and are dependent upon the presence of the vitamin D receptor. The vitamin D endocrine system could also play a role in altering immune function in normal physiological conditions.

Relative performance of filled and feedhorn-coupled focal-plane architectures.

Modern far-infrared and submillimeter instruments require large-format arrays. We consider the relative performance of filled-array (bare pixel) and feedhorn-coupled architectures for bolometer focal planes. Based on typical array parameters, we quantify the relative observing speeds and comment on the merits of the different architectures.

Distinctive dendritic cell modulation by vitamin D(3) and glucocorticoid pathways.

Dendritic cell (DC) maturation plays a central role in regulating immunity. We show that glucocorticoid and 1alpha,25(OH)(2)D(3) agonists modulate DCs via distinct and additive signaling pathways. Phenotypic and functional indices were examined in DCs treated with dexamethasone (DEX) and/or a 1alpha,25(OH)(2)D(3) analog (D(3) analog).

Subclinical rejection in tacrolimus-treated renal transplant recipients.

Background: Subclinical rejection, defined as histologic acute rejection in the absence of graft dysfunction, has been suggested as a cause of chronic allograft rejection. In cyclosporine-treated patients, the incidence of subclinical rejection 3 months after transplant is reported to be approximately 30%. The intent of our study was to determine the incidence of subclinical rejection in tacrolimus-treated renal allograft recipients.

Can a transplanted living donor kidney function equivalently to its native partner?

Early renal functional adaptation was examined in 81 haploidentical donor and recipient pairs, as well as long-term stability of glomerular filtration rate (GFR) in 78 recipients. GFR was determined pre- and 1 month postnephrectomy in donors and 1 month post-transplant and yearly thereafter in recipients. Compensatory increase in filtration (CIF) of transplanted and native kidneys was calculated using donor pretransplant GFR: [CIF= (GFR at 1 month/donor prenephrectomy GFR) x 100].