Citations

Context.— Transporting specimens can expose them to uncontrolled environmental factors. Whole blood viability is a commonly used preanalytic marker of quality for analysis of white blood cells. Objective.— To evaluate whole blood viability as a marker for transportation and specimen integrity for lymphocyte subset evaluation. Design.— More than 9000 whole blood specimens, transported during a 4-year period, and their lymphocyte subset evaluation results were analyzed retrospectively. Viability was measured by using Cellaca MX imaging cytometer, and lymphocyte and lymphocyte subset counts were determined with flow cytometry. Specimen cell viability results were stratified based on different transportation factors to discern their potential effects. Lymphocyte subset evaluation results from specimens with lower viability were compared with those from optimal viability specimens. Results.— Cell viability of transported specimens exhibited seasonal variation, decreasing during the warm summer months (median, 77.0% versus 83.4% in other seasons). The decline in viability negatively correlated with ambient temperature during transportation ( r = −0.7876). Longer transportation time (>60 hours) also caused a decrease in viability (median, 64.0%). While we observed a decrease in absolute cell counts for CD45 + lymphocytes, CD3 + T cells, CD8 + T cells, and CD19 + B cells in specimens with low viability (50%–80%), the differences were well within the assay’s total allowable error. Conclusions.— Control of preanalytic factors is critical for laboratory testing. Whole blood viability is a sensitive indicator of transport conditions and time, but it is not a specific predictor of quality for the main lymphocyte populations in cellular immunology testing.

This study demonstrates successful hematopoietic stem cell transplant of CD40L deficiency using an asymptomatic carrier mother, leading to sustained 32% CD40L expression, normal recovery of T and B cell development and diversity, and expected growth and development 7.5 years post-transplant.

Abstract We have previously shown the significant up-regulation of Il22 and increased phosphorylation of STAT3 as part of the mucosal response to C. difficile VPI 10463 infection. Others have shown that phosphorylation of STAT3 at mucosal surfaces includes IL22- and CD160-mediated components. The current study sought to determine the potential role(s) of IL22 and/or CD160 in the mucosal response to C. difficile infection. Infection of mice with C. difficile 630 led to the significant induction of STAT3 phosphorylation and a very similar set of genes in the colon as we had reported previously. C. difficile-infected mice treated with anti-IL22, anti-CD160 or both showed significantly reduced STAT3 phosphorylation in comparison to C. difficile-infected mice that had received neither antibody. In addition, C. difficile-infected mice treated with anti-IL22/CD160 induced a smaller set of genes, and at significantly lower levels than the untreated C. difficile-infected mice. These included pro-inflammatory chemokines and cytokines and anti-bacterial peptides. In addition, mice treated with anti-IL22/CD160 had a lower influx of neutrophils than the other 3 infected groups. These data demonstrate that IL22 and CD160 are together responsible for a significant fraction of the colonic STAT3 phosphorylation in C. difficile infection. They also underscore the additive effects of IL22 and CD160 in mediating both the pro-inflammatory and pro-survival aspects of the mucosal response in this infection.