Lazy leukocyte syndrome.

A-35-year-old woman with a long-lasting history of neutropenia and recurrent infections was found to have defective neutrophil chemotaxis, random motility, and in vivo migration. Although the bone marrow granulocyte reserve was normal, the patient failed to release an appropriate amount of granulocytes after injection of etiocholanolone. These features are characteristic of the so-called "Lazy leukocyte syndrome". The clinical presentation of the five cases of this syndrome so far reported and its pathophysiological aspects are discussed.     

Genes associated with leukocyte production in mice.

We have investigated the genes influencing leukocyte production in mice by selective breeding for differences in leukocyte count and developed two major lines differing about 8-fold. In these lines we have made counter selective breeding, crossbreeding between them, and developed methods of using marker genes to search for individual genes distributed on different chromosomes. We have revealed an overall dominance of genes for low leukocyte count over those for high counts, and effects of genes at the agouti locus, certain mutant genes, and a gene or genes in the XVI linkage group. We have commented on the application and approach of quantitative genetic experimentation from both a theoretical and practical point of view and, on the basis of present results, discussed the nature of polygenes in relation to genes causing polymorphisms.     

A stochastic model of leukocyte rolling.

Selectin-mediated leukocyte rolling under flow is an important process in leukocyte recruitment during inflammation. The rolling motion of individual cells has been observed to fluctuate randomly both in vivo and in vitro. This paper presents a stochastic model of the micromechanics of cell rolling and provides an analytical method of treating experimental data. For a homogeneous cell population, the velocity distribution is obtained in an analytical form, which is in good agreement with experimentally determined velocity histograms obtained previously. For a heterogeneous cell population, the model provides a simple, analytical method of separating the contributions of temporal fluctuations and population heterogeneity to the variance of measured rolling velocities. The model also links the mean and variance of rolling velocities to the molecular events underlying the observed cellular motion, allowing characterization of the distribution and release rate of the clusters of molecular bonds that tether the cell to substratum. Applying the model to the analysis of data obtained for neutrophils rolling on an E-selectin-coated surface at a wall shear stress of 1.2 dyn/cm2 yields estimations of the average distance between bond clusters (approximately micron) and the average time duration of a bond cluster resisting the applied fluid force (approximately 0.5 s).     

Macrophages suppress CTL generation in rat mixed leukocyte cultures.

The generation of CTL in rat MLC was actively suppressed by a cell population present in spleen cell preparations from normal rats. These suppressor cells were characterized by using a variety of cell fractionation techniques. Suppressor cells were removed by passage of spleen cells through nylon wool columns or by treatment with carbonyl iron. Suppressive activity was present in the mononuclear cell fraction of spleen cells obtained by Ficoll-Hypaque density gradient centrifugation. After velocity sedimentation at unit gravity, enrichment of suppressive activity was demonstrated in the fractions containing large cells as compared to the fractions containing small cells. Populations rich in macrophages were shown to have similar suppressive activity upon CTL induction in MLC. These studies suggest that macrophages present in normal rat spleen cell preparations account for the difficulty in generating CTL in MLC prepared with rat cells.     

Measles virus-induced changes in leukocyte function antigen 1 expression and leukocyte aggregation: possible role in measles virus pathogenesis.

Measles virus (MV) infection of U937 cell or peripheral blood leukocyte cultures was shown to induce changes in the expression of leukocyte function antigen 1 (LFA-1) and cause marked aggregation of these cells. Addition of selected monoclonal antibodies specific for LFA-1 epitopes that did not neutralize MV in standard neutralization assays were found to block both virus-induced leukocyte aggregation and virus dissemination. These data suggest that MV modulation of LFA-1 expression on leukocytes may be an important step in MV pathogenesis.     

Kinetic studies of human polymorphonuclear leukocyte phosphofructokinase.

Phosphofructokinase from human polymorphonuclear leukocytes has low cooperativity and high affinity for its substrate, F-6-P. It is resistant to ATP inhibition at pH 8; however, at pH 7.1 it becomes sensitive to the effect of this compound. It is activated by F-1, 6-P2; it is not very sensitive to citrate inhibition and F-2, 6-P2 has no effect on its activity. With these kinetic characteristics we assume that perhaps the predominant L-type subunit is accompanied by an F-type component.     

Affinity of human leukocyte interferon for polyribonucleotides.

Human leukocyte interferon (HL-IF)binds to AGPOLY(A)TM, AGPOLY(U)TM and AGPOLY(I)TM. The bound interferon could be displaced from all three polyribonucleotides by including sodium chloride in the eluant. The nature of interaction of HL-IF with polyribonucleotides is electrostatic and not hydrophobic since its binding was not prevented in the presence of 50% ethylene glycol. The binding of HL-IF on AGPOLY(I)TM is stronger at lower pH since an increase in ionic strength is required to displace it.