Removal Of Dead Cells Research Articles

Possible immunoregulatory role for CD5+B cells

CD5 + B cells represent a subpopulation of B cells which have the characteristic of employing unmutated immunoglobulin variable region genes. These cells are found to be increased early in ontogeny. The percentage of CD5 + B cells is highest in the fetus and decreases after birth. The antibodies produced by CD5 + B cells are polyreactive and are the natural autoantibodies. These autoantibodies may not be pathogenic. CD5 + B cells are elevated in certain autoimmune disease states and are the malignant cell type in B-CLL, with a strong genetic component involved in determining elevated CD5 + B cell states. Elevated CD5 + B cells are found in immunodeficient states (young, aged, and autoimmune). CD5 + B cells may normally act as a first-line defense against invading foreign pathogens but are not involved in the specific immune response. There is some evidence, at least in newborns, that CD5 + B cells may affect the emerging B cell repertoire of conventional B cells via idiotype cascade. However, the action of CD5 + B cells in the newborn may be quite different than their activity in the adult. Nonimmunoglobulin-producing CD5 + B cells may be immunosuppressors. In this report, a unique subpopulation of CD5 + B cells was investigated. These cells were found only in the spleens of aged NZB mice. The CD5 + B cells were clonal and possessed extra chromosomes and did not appear to be producing antibodies. These cells were capable of rapid proliferation in unirradiated recipients. By taking advantage of this proliferative capability, the effect of exogenous clonal CD5 + B cells on recipient immune system was evaluated. Clonal CD5 + B cells from NZB mice were immunosuppressive and decreased the numbers of conventional B cells as well as the level of "natural antibodies." In summary, CD5 + B cells may play different roles in the immune system depending upon environment, age, and their differentiation state (i.e., proliferation versus antibody secretion). The natural antibody produced by CD5 + B cells may be involved in maintenance functions such as removal of dead cells and first-line defense mechanisms. In addition, CD5 + B cells may themselves regulate the immune system and produce a factor which is immunosuppressive. An understanding of the various functions of CD5 + B cells may elucidate fundamental immunoregulatory circuits.

Naturally occurring cell death in the cerebral cortex of the rat and removal of dead cells by transitory phagocytes

Regressive phenomena are common during the development of the nervous tissue. Among them, naturally occurring cell death has been observed in several regions of the nervous system. Cell death in the somatosensory cortex and medial cortical regions (hind limb, frontal cortex 1, frontal cortex 2, retrosplenial agranular, retrosplenial granular [Zilles K. et al. (1980) Anat. Embryol. 159, 335–360]) as well as in the cortical subplate (future subcortical white matter) in the rat mainly occurs during the first 10 days of postnatal life with peak values of 3.1 dead cells per 1000 live neurons at the end of the first week. Cell death progresses from birth to day 7 with a predominance of dead cells in the subplate and in layers II–III. Later, dead cells are more dispersed in the cerebral cortex, but a significant amount is still present in the subcortical white matter. This pattern correlates with the arrival and settlement of cortical afferents at the different cortical levels, as described in other studies, and points to the likelihood that transitory cellular populations are important clues in the modelling of the cerebral cortex during normal development. Transitory populations of macrophages (amoeboid or nascent microglial cells) that appear in great numbers during the same period and in the same regions are involved in the removal of dead cells.

Hemocytes of Leiobunum limbatum and two other species of harvestmen (Arachnida, Opiliones): Morphological classification and functional aspects.

The hemocytes of Leiobunum limbatum, Mitopus morio, and Opilio ravennae number from about 8,000 (juveniles) to 41,000 (pregnant females) per microliter of hemolymph. Five different types of hemocytes occur in all three species and both sexes. According to their ultrastructural appearance and their similarities to other arthropod hemocytes these five types are designated as prohemocyte, plasmatocyte, granulocyte, coagulocyte, and spherulocyte. From the ultrastructural point of view the prohemocytes are interpreted as stem cells for plasmatocytes which on their part differentiate into granulocytes. Transitional stages which would indicate the origin of coagulocytes and spherulocytes could not be found. Granulocytes and spherulocytes are interpreted as being storage cells; coagulocytes burst when hemolymph is transferred to a microscopic slide. Plasmatocytes are involved in the removal of dead cells or cell fragments. Plasmatocytes are demonstrated as being able to phagocytize and digest bacteria.

Establishment of Lymphoblastoid Cell Lines from Marek's Disease Primary Tumors

Seven lymphoblastoid cell lines were developed from 15 Marek's disease primary lymphomas treated to remove adherent cells (46.7% success rate) and 1 cell line was developed from 15 untreated lymphomas (6.7% success rate). These cell lines are designated as MDCC-RP22 through MDCC-RP29. Tumor materials were from 1515 × 71 chickens infected with either JM-111S clone or the GA-22 clone of Marek's disease virus. Factors contributing to the establishment of cell lines include, in addition to the removal of adherent cells at the initial stage of culture, the periodic adjustment and the concentration of viable cells, including the removal of dead cells. The cell lines bear T-cell surface markers and Marek's disease tumor associated surface antigen (MATSA). MDCC-RP22 and MDCC-RP23 are high virus producers.

Effect of added cold shocked cells upon the viability of pony stallion spermatozoa

Cold shocked pony stallion spermatozoa, which had been warmed to room temperature, were found to have a detrimental effect upon the survival and motility of spermatozoa stored at 21°C. Within the first twenty minutes of storage, aliquots with added dead cells declined from their initial mean percent alive by 50.5 percent. Controls, however, only exhibited a decline of 8 percent from the original value. Motility, in aliquots with added dead spermatozoa, virtually ceased by the end of 60 minutes storage, whereas controls showed substantial motility after 80 minutes storage. These results indicate that removal of dead cells from semen or inactivation of their toxic products could help extend spermatozoan viability.

Acid hydrolases and nitrogen mustard cytotoxicity

Acid Hydrolases and Nitrogen Mustard Cytotoxicity. Cohen, A. M. (1978). Toxicol. Appl. Pharmacol. 43 , 85–97. The role of acid hydrolases in the cytocidal action of nitrogen mustard (HN 2 ) in rat intestine crypt epithelial cells was studied. An eight-fold increase in crypt cel β-glucuronidase activity was observed at 24 hr after HN 2 injection (2 mg/kg, ip). The activity of acid phosphatase and cathepsin D was not significantly altered by HN 2 administration. Inhibition of DNA synthesis and widespread pycnosis and karyorrhexis of crypt cells preceded significant increases in β-glucuronidase activity. However, loss of intestinal DNA prelabeled with tritiated 5-iodo-2′-deoxyuridine occurred subsequent to significant increases in β-glucuronidase activity. A single injection of cycloheximide (1 mg/kg, ip) given at either 30 min before or 30 min after HN 2 delayed the development of crypt cell histopathology. A second injection of cycloheximde at 8 hr after HN 2 prevented further development of crypt histopathology and completely blocked the increase in β-glucuronidase activity and the loss of prelabeled DNA observed at 24–30 hr after HN 2 alone. These studies suggest that acid hydrolases do not play a major role in the initiation of the processes responsible for the death of proliferating crypt cells exposed to HN 2 . However, the results are consistent with a possible role for certain of these enzymes in the degradation and removal of dead cells from the crypt epithelium.

Brain-tumor therapy. Quantitative analysis using a model system.

A recently developed colony-formation assay has been used to evaluate in vivo 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) therapy of a transplantable rat brain-tumor model. A comparison of the in vitro colony-forming capacity of treated and untreated tumor cells permits calculation of the fraction of clonogenic tumor cells surviving in vivo therapy; The plateau that we previously observed o the BCNU dose-response curve is not the result of repair of potentially lethal damage, since no change in the 0.1% of surviving clonogenic tumor cells occurs during the first 2 to 4 days after treatment. Although reanalysis of the dose-response curve indicates that sublethal damage exists, its repair is probably minimal. The most likely explanation for the observed limitation of the BCNU effect is the drug's failure to reach all clonogenic cells. A dose of BCNU that kills more than 99.9% of clonogenic tumor cells within 30 minutes of treatment results in only a 60% decrease in tumor weight by Day 14. This disparity is explained by retarded removal of dead cells, and, along with a previously determined 90% cell-kill threshold necessary to appreciate increased animal survival, demonstrates the inherent limitations of measurements of tumor size (including brain scans and clinical patient evaluations) in evaluating the efficacy of brain-tumor therapy. Following at LD10 dose of BCNU the surviving clonogenic tumor cells increase in number after latency period of 2 to 4 days; during regrowth the cell doubling time is 40 hours. Marked variability in tumor response and regrowth was noted. The determination of information regarding disturbed tumor cell kinetics and tumor heterogeneityis essential for the proper planning of combination chemotherapy and multimodality regimens.

The myocardial conduction system in sudden death in infancy.

THE ultimate mechanism responsible for sudden unexpected death in infancy remains unknown. Current hypotheses tend toward the concept of an instantaneous interruption in some basic physiologic function such as the control of respiration or cardiac action.1 In 1968 James2 proposed the hypothesis that these deaths are due to lethal disturbances in the conduction system triggered by focal histopathologic changes in the atrioventricular bundle and the atrioventricular node. The histologic features that he described are focal resorptive degeneration of conduction tissue cells, cell death, removal of dead cells by macrophages and replacement with collagen produced by young fibroblasts. These abnormalities were . . .