Complement receptors regulate lipopolysaccharide-induced T-cell stimulation

Complement receptors type 1 and 2 (CR1 (CD35)/CR2 (CD21)) are known to enhance the adaptive immune response. In mice, CR1/CR2 are expressed on B cells, follicular dendritic cells, and activated granulocytes. Recently, we showed that a subset of CD44(high) and CD62L(low) T cells also expresses CR1 and CR2. We now report that CR1/CR2 are detectable on both CD4(+) and CD8(+) subsets of T cells. Lipopolysaccharide (LPS) from Gram-negative bacteria causes polyclonal activation of B cells and stimulation of macrophages and other antigen-presenting cells. We further demonstrate that LPS induced marked up-regulation of CD25 and CD69 on T cells from CR1/CR2 sufficient (Cr(+/+)), but significantly lower up-regulation on T cells from CR1/CR2 deficient (Cr(–/–)) mice. These findings point to a novel mechanism by which CR1/CR2 modulates the activation of T cells by LPS

Origin and properties of soluble CD21 (CR2) in human blood

By analysis with a panel of CD21 MoAbs it is shown that a large part of the soluble CD21 in human blood plasma is of the long isoform (CD21L), as judged by comparison with antigen produced by mouse L cells transfected with CD21L-cDNA and reactivity with the restricted CD21 MoAb R4/23. This is compatible with the hypothesis that soluble CD21 in the blood is mainly derived from follicular dendritic cells (FDC). Cells from a human keratinocyte cell line transfected with cDNA from the Burkitt lymphoma cell line Raji also produced soluble CD21L (sCD21L), whereas the short form of sCD21 (sCD21S) was the major component of sCD21 produced by the B lymphoblastoid cell line LICR-LON-HMy and the T cell line Jurkat. Confocal studies of FDC isolated from human tonsil revealed that CD21 was present in the cytoplasm. On gel filtration sCD21 from untreated serum has an apparent size considerably greater than the 130 kD found by SDS–PAGE analysis. This may be partly accounted for by the non-globular shape of the molecule, but may also indicate, as reported by others, that in its native state sCD21 is complexed with other proteins. However, no evidence of complexing with sCD23 or C3d could be found

Learning in disrupted projects: on the nature of corporate and personal learning

The majority of large, complex projects suffer disruptions. These can have unexpected and significant impacts on a project, resulting in excessive time and cost overruns. Disrupted projects therefore require careful management in order to minimize the impact of a disruption. One element of a project for which disruptions will have a particular impact is on any anticipated learning gains. Loss of learning from disruptions can often be very significant. This lost learning may be from individual workers (personal) or by the organization (corporate). An understanding of the impact of a particular disruption on learning is required to enable effective management of that disruption. This paper argues that improved management of learning in disrupted projects may come from the disaggregation of personal and corporate learning from the typically used aggregated learning curve presumptions. The literature is reviewed to explore whether a method of disaggregation can be determined from existing propositions about the behaviour of learning curves. The explorations demonstrate that the disaggregation of a learning curve is complex. The contribution of this paper derives from developing an understanding of the role of asymptotes in constructing learning curves, and the nature of the interaction between personal and corporate learning. These two aspects are argued to be crucial aspects in managing the impact of disruptions on learning. The main motivation for this work is to provide managers with an understanding of the disaggregation process, in order that they can think through the impact of a disruption on learning in their own projects