Natural killer cells and B lymphocytes in L-selectin and CD18 knock out mice : marker-dependent but not lineage-dependent changes in the spleen and bone marrow

Lymphocyte homing to the lymph nodes is a well defined process, dependent on the proper function of the homing receptors LFA-1 (one of the CD18 family of integrins) and L-selectin. However, the mechanism used by lymphocytes to accumulate in the spleen is still not understood. Both B lymphocytes and Natural Killer cells are prominent in the spleen. To investigate whether CD18 integrins or L-selectin play a role in B lymphocyte and NK cell homing to the spleen, mice genetically deficient in either of these molecules were analyzed by flow cytometry. The results of this study demonstrate that neither B lymphocytes nor NK cells require the CD18 family of integrins or L-selectin for entry into the spleen. Results of this study also showed that neither cell lineage required the CD18 integrins or L-selectin for egress from their sites of birth in the bone marrow

Lymphocyte transformation in vitro in response to the carcinoembryonic antigen of the human digestive system

The carcinoembryonic antigen of the human digestive system (CEA) is a tumour-specific constituent of all human gastrointestinal tumours arising from tissues of entodermal origin and c+ the digestive organs of the fetus from two to six months of gestation. Circulating antibodies ta the CEA have been found in most patients with non-metastatic gastrointestinal cancers and in most pregnant women. In the cancer patients, antibody titres bore no relationship to the clinical course. Cell-mediated immunity to CEA was studied by measuring in vitro transformation of lymphocytes obtained from normal individuals, patients with gastrointestlnal cancers, and pregnant women. No transformation was found in any of the groups tested, suggesting that endogenous CEA does not stimulate a cell-mediated immune response. Factors affecting the reliability and sensitivity of lymphocyte transformation as a method were studied

Speaking shadows : human and divine possibility in the poetry of Paul Celan

Paul Celan (1920-1970), the Jewish poet of German descent, lived through the greatest catastrophe of European Jewry of the modern age. He survived, as his parents and innumerable others did not, and dedicated his writing, his voice, to the reality he had witnessed. It would be a mistake, however, to think of him solely as a "Jewish" poet, a term he considered anti-Semitic (see Christina Ivanovic's '''All poets are Jews:' Paul Celan's Reading of Marina Tsvetaeva"). Celan wrote of the world as such; a world that was able to reorganize itself towards the annihilation of countless human beings. In its midst, he questioned how one could live, how brotherhood could still be possible, and how a God could possibly appear in such a place. This thesis follows his questioning and pursues, along with him, the course of poetry and poetic language through the appearance of atrocity

Regulation of cell survival during B lymphopoiesis: Suppressed apoptosis of pro-B cells in P53-deficient mouse bone marrow

B cell development in mouse bone marrow (BM) is subject to quality controls that eliminate aberrant cells by apoptosis, but the intrinsic cellular mechanisms that mediate this negative B cell selection remain unclear. The p53 tumor suppressor transduces signals resulting in apoptosis and cell cycle arrest in cells that sustain DNA damage. Faulty V(D)J recombination in scid lymphocyte precursors activates a p53-dependent DNA damage checkpoint. In the present study, we have examined whether p53 is involved in apoptotic selection of normally developing B cells in BM. Double immunofluorescence labeling and flow cytometry were used to quantitate phenotypically defined B cell populations and their apoptotic rates in BM of homozygous p53-deficient mice. B220+ μ- and terminal deoxynucleotidyl transferase (TdT)+ pro-B cells were increased in both incidence and absolute number to controls. In contrast, pre-B cells were only slightly increased and the sIgM+ B lymphocyte compartment remained essentially normal. The incidence of apoptosis among p53(-/-) pro-B cells was greatly reduced, both ex vivo and in short-term culture, whereas, apoptosis of pre-B cells and B lymphocytes was not significantly different from normal. The results indicate that p53 is actively involved as an apoptosis inducer at an early quality control checkpoint in B lymphopoiesis.link_to_subscribed_fulltex

Enhanced interleukin-8 production in mononuclear cells in severe pediatric obstructive sleep apnea

Abstract Background Obstructive sleep apnea (OSA) is a risk factor for cardiovascular disease, metabolic disorders, and cognitive dysfunction. Current thinking links chronic intermittent hypoxia (CIH) with oxidative stress and systemic inflammation. However, the sequence of events leading to the morbidities associated with OSA is poorly understood in children. Monocytes are known to be altered by chronic hypoxia. Thus in this prospective study, we investigated inflammatory cytokine profiles from cultures of peripheral blood mononuclear cells (PBMC) obtained from children with severe OSA and sleep-related CIH. Methods Ten children with OSA (cases) and 5 age-matched children without OSA (controls) were recruited for study. Samples of plasma and PBMC were obtained before and after adenotonsillectomy. The levels of the inflammatory cytokines, interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12p70, and tumor necrosis factor-α (TNFα), were measured in both plasma and ex vivo culture supernatants of PBMC incubated with lipopolysaccharide (LPS) using the cytometric bead assay. Results Upon activation of PBMC by LPS, the levels of IL-8 in the culture supernatants from cases were threefold higher than in controls. The levels of the other cytokines including IL-1β, IL-6, and TNFα, in culture supernatant of PBMC from cases showed no difference from controls; nor were there significant differences in plasma cytokine levels. Conclusion We speculate that in young children with sleep-related CIH, an enhanced production capacity of IL-8 precedes the development of systemic inflammatory markers. Future work should evaluate IL-8 production capacity as a potential biomarker for OSA severity