No abstract

I. The levels of the brush-border enzymes sucrase (sucrose glucohydrolase, EC 3.2. I .48), isomaltase (oligo-1,6-glucosidase, EC 3. z. I . IO), maltases z and 3 (glucoamylase, EC 3. z. I . 3), lactase (8-galactosidase, EC 3.2. I . 23) and trehalase (EC 3. 2 , I. 28) and adsorbed pancreatic a-amylase (EC 3.2. I . I) have been measured at twenty-one positions along the small intestines of eighty-four pigs of different ages ranging from 3 weeks to 4 5 years. The state of dilation of the intestine at the sampling points was noted.2. The levels of sucrase and isomaltase increased with age throughout the age-range studied. Trehalase and the glucoamylases increased with age up to zoo-300 d of age. Lactase decreased with age over th? whole age range.3. For the pigs above 10 weeks of age, the distribution pattern of the brush-border enzymes along the intestine did not change with age. Each enzyme had a characteristic distribution curve, with low values at the proximal and distal ends and a peak which was proximal in the instance of lactase and trehalase and approximately mid-way along the gut with sucrase, isomaltase and the glucoamylases. 4.The pattern of distribution of the brush-border enzymes altered with age in the piglets, but approached the adult pattern by 8 weeks.5. Piglets weaned at 3 weeks had higher levels of sucrase, isomaltase and glucoamylases at 5 weeks than piglets left on the sow. At 8 weeks of age the piglets weaned at 3 weeks still had higher sucrase and isomaltase levels than those on the sow.6. There was a very close correlation between the sucrase and isomaltase levels, and between the maltase 2 and maltase 3 levels in all the samples, and a fairly close correlation between all these four enzymes.7. The level of a-amylase increased with age but showed no regular distribution pattern, its irregular fluctuations being related to the presence or absence of dilation of the intestine at the time of slaughter rather than to the position along the intestine.

Renal biopsy is rare in PSS and often reveals diverse pathological findings. Glomerulonephritis, as compared with tubulointerstitial nephritis, is associated with higher early mortality. Further studies are needed to evaluate the utility of renal biopsy and its impact on disease management.

No abstract

Sialoadhesin (Sn) is a sialic acid–binding Ig-like lectin expressed selectively on macrophage subsets. In a model of experimental autoimmune encephalomyelitis, Sn interacted with sialylated ligands expressed selectively on CD4+Foxp3+ regulatory T cells (Tregs) and inhibited their proliferation. In this study, we examined the induction of Sn ligands (SnL) on all splenic CD4+ T cells following in vitro activation. Most CD4+ Tregs strongly upregulated SnL, whereas only a small subset of ∼20% CD4+Foxp3− T cells (effector T cells [Teffs]) upregulated SnL. SnL+ Teffs displayed higher levels of activation markers CD25 and CD69, exhibited increased proliferation, and produced higher amounts of IL-2 and IFN-γ than corresponding SnL− Teffs. Coculture of activated Teffs with Sn+ macrophages or Sn+ Chinese hamster ovary cells resulted in increased cell death, suggesting a regulatory role for Sn–SnL interactions. The key importance of α2,3-sialylation in SnL expression was demonstrated by increased binding of α2,3-linkage–specific Maackia amurensis lectin, increased expression of α2,3-sialyltransferase ST3GalVI, and loss of SnL following treatment with an α2,3-linkage–specific sialidase. The induction of SnL on activated CD4+ T cells was dependent on N-glycan rather than O-glycan biosynthesis and independent of the mucin-like molecules CD43 and P-selectin glycoprotein ligand-1, previously implicated in Sn interactions. Induction of ligands on CD4+Foxp3− Teffs was also observed in vivo using the New Zealand Black × New Zealand White F1 murine model of spontaneous lupus and SnL levels on Teffs correlated strongly with the degree of proteinuria. Collectively, these data indicate that SnL is a novel marker of activated CD4+ Teffs that are implicated in the pathogenesis of autoimmune diseases.