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Quantitative studies of the growth of mouse embryo cells in culture and their development into established lines

by George J. Todaro, Howard Green - J. Cell , 1963
"... Disaggrcgatcd mouse embryo cells, grown in monolaycrs, undcrwcnt a progrcssivc dcclinc in growth ratc upon succcssivc transfer, the rapidity of the decline dcpcnding, among othcr things, on the inoculation density. Ncvcrthclcss, ncarly all culturcs dcvclopcd into cstablishcd lincs within 3 months of ..."
Abstract - Cited by 256 (3 self) - Add to MetaCart
Disaggrcgatcd mouse embryo cells, grown in monolaycrs, undcrwcnt a progrcssivc dcclinc in growth ratc upon succcssivc transfer, the rapidity of the decline dcpcnding, among othcr things, on the inoculation density. Ncvcrthclcss, ncarly all culturcs dcvclopcd into cstablishcd lincs within 3 months of culture. Thc first sign of thc emcrgcncc of an established line was the ability of thc cells to maintain a constant or rising potential growth ratc. This occurred while thc cultures wcrc morphologically unchangcd. Thc growth rate continued to incrcasc until it cqualcd or cxcccdcd that of the original culturc. The carly cstablishcd cclls showed an increasing mctabolic autonomy, as indicated by dccrcasing dependence on ccll-to-ccll fccding. It is suggcstcd that the process of cstablishmcnt involvcs an altcration in ccll pcrmcability propcrtics. Chromosome studics indicatcd that thc cells rcsponsiblc for thc upturn in growth rate wcrc diploid, but latcr the population shifted to the tctraploid range, often very rapidly. Still later, marker chromosomes appcarcd. Different lines acquired diffcrcnt propcrtics, dcpcnding on thc culture conditions cmploycd; one line dcvclopcd which is cxtrcmcly scnsitivc to contact inhibition.
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Human immunity to the meningococcus. I. The role of humoral antibodies

by Irving Goldschneider, Emil C. Gotschlich, Malcolm S. Artenstein - Journal of Experimental Medicine , 1969
"... Meningococcemia and meningococcal meningitis in man appear to be infrequent complications of the host-parasite relationship. Ordinarily, exposure to a strain of Neisseria mertingitidis results in carriage of the organism in the nasopharynx for weeks or months (1--4), producing either a mild pharyngi ..."
Abstract - Cited by 97 (5 self) - Add to MetaCart
Meningococcemia and meningococcal meningitis in man appear to be infrequent complications of the host-parasite relationship. Ordinarily, exposure to a strain of Neisseria mertingitidis results in carriage of the organism in the nasopharynx for weeks or months (1--4), producing either a mild pharyngitis or no symptoms at all (5, 6). Even during an epidemic, the great majority of individuals exposed to the epidemic strain of meningococcus become asymptomatic carriers rather than clinical cases with systemic disease (7). Viewed in this light, the occurrence of meningococcal disease is related more to the unique susceptibility of the individual host than to the innate virulence of the infecting organism. Several epidemiol0gical findings suggest that individuals who are susceptible to systemic meningococcal disease lack humoral antibodies to meningococci. First, except for outbreaks among military recruits (8, 9) and other dosed populations (10), meningococcal meningitis is a disease of infancy and early childhood (11, 12). This is true both in epidemic and interepidemic periods. Susceptibility to many so-called "diseases of childhood, " bacterial and viral, has been shown
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Receptors for C3b and C3bi promote phagocytosis but not release of toxic oxygen from human phagocytes

by D. Wright, Samuel, C. Silversten - 158:2016. MACROPHAGES IN MURINE MALARIA , 1983
"... Monocytes, macrophages, and polymorphonuclear ieukocytes (PMN) 1 bear receptors for C3 and for the Fc domain of IgG that allow these phagocytes to bind particles coated with the corresponding ligands (1). The consequences of ligand-receptor interaction, however, are different for IgG and C3. While F ..."
Abstract - Cited by 80 (2 self) - Add to MetaCart
Monocytes, macrophages, and polymorphonuclear ieukocytes (PMN) 1 bear receptors for C3 and for the Fc domain of IgG that allow these phagocytes to bind particles coated with the corresponding ligands (1). The consequences of ligand-receptor interaction, however, are different for IgG and C3. While Fc receptors constitutively promote phagocytosis of IgG-coated particles, the ability of C3 receptors to promote phagocytosis is regulated. Murine peritoneal macrophages do not ingest C3-coated erythrocytes, but macrophages ~activated " by a T-cell derived lymphokine readily ingest them (2). Similarly, human PMN, monocytes, and cultured monocytes (which resemble macrophages) do not phagocytose particles coated with C3b or C3bi, but cultured monocytes adherent to immobilized fibronectin (FN) or serum amyioid P component do phagocytose both C3b and C3bi-coated particles (3). Complement receptors thus appear to exist in one of two states: Receptors in the "inactive " state bind ligands but fail to promote ingestion, while receptors in the "active " state bind iigands and promote ingestion. Ligation of Fc receptors signals not only phagocytosis but also the synthesis and release of 02- and H20~, powerful oxidants that either alone or in concert with leukocyte enzymes efficiently kill many potential pathogens (4). We have examined the ability of C3 receptors to promote the release of toxic oxygen from human phagocytes. Here we report that neither the C3b nor the C3bi receptor causes the release of H20 ~ from monocytes, cultured monocytes, or PMN. Further, the complement receptors of cultured monocytes cannot be rendered capable of triggering H202 release even under conditions in which they readily promote phagocytosis.

Human immunity to the meningococcus. II. Development of natural immunity

by Irving Goldschneider, Emil C. Gotschlich, Malcolm S. Artenstein , 1969
"... Serum from most young adults contains antibodies to pathogenic strains of meningococci (1). The strongest evidence that these antibodies are protective derives from the fact that resistance to meningococcal disease and the presence of aatimeningococcal antibodies, as determined by the serum bacteric ..."
Abstract - Cited by 54 (2 self) - Add to MetaCart
Serum from most young adults contains antibodies to pathogenic strains of meningococci (1). The strongest evidence that these antibodies are protective derives from the fact that resistance to meningococcal disease and the presence of aatimeningococcal antibodies, as determined by the serum bactericidal reaction, are closely correlated at all ages (1). Of particular importance is the observation (2, 3) that infants in the neonatal period are highly resistant to meningococcal disease, but that they are extremely susceptible by 6 months of age. The curves of increasing susceptibility to systemic meningococcal infection during the first 6 months of life and of the development of physiological hypogammaglobulinemia (4) are reciprocally rdated. Results of the preceding study (1) indicate that natural immunization against meningococcal disease occurs during childhood. Thus, between ages 2 and 12 yr there is a progressive increase of approximately 5 % per year in the number of children having serum bactericidal activity to strains of pathogenic meningococci. In the present study, it will be shown that immune sensitization occurs, in large part, as a result of the asymptomatic carriage of meningococci in the nasopharynx. Group specific, cross-reactive, and type-specific meningococcal antigens are seen to participate in the immunizing process. It will be further shown that immunity in the newborn infant is associated with the transplacental passage of gamma G antimeningococcal antibodies. Metkods Baa~iologi¢al Tedmiques.--Bacteriological techniques, serum bactericidal reaction, and indirect immunofluorescence were performed as described previously (1). Absorption of Serum and Gamma CdobuUn.--Human sera were obtained from the same sources as described previously (1).
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Delayed hypersensitivity-type granuloma formation and dermal reaction induced and elicited by a soluble factor isolated from Schistosoma mansoni eggs

by Dov L. Boros, Kenneth, S. Warren , 1970
"... Granulomatous inflammation plays a major role in the pathogenesis of a wide variety of diseases caused by infectious agents, including mycobacteria (tuberculosis, leprosy); fungi (coccidioidomycosis, histoplasmosis); worms (schistosomiasis, fllariasis); and possibly viruses and protozoa (1, 2). Alth ..."
Abstract - Cited by 43 (6 self) - Add to MetaCart
Granulomatous inflammation plays a major role in the pathogenesis of a wide variety of diseases caused by infectious agents, including mycobacteria (tuberculosis, leprosy); fungi (coccidioidomycosis, histoplasmosis); worms (schistosomiasis, fllariasis); and possibly viruses and protozoa (1, 2). Although it has long been suspected that the granuloma may be a manifestation of delayed hypersensitivity, significant data supporting this concept have been gathered only in the past 15 yr (2). As recently as 1967 a review of granulomatous hypersensitivity concluded that the evidence was still insufficient to include the granuloma in the spectrum of delayed responses (2). Since then, the Schistosoma mansoni egg granuloma, a quantifiable model of granulomatous inflammation (3), has been established as a form of delayed hypersensitivity. Mice previously exposed to schistosome eggs develop larger granulomas more rapidly than control unsensitized animals (4). The anamnestic reaction is specific in relation to other worm genera (4), to the two other schistosome species infective to man (5), and even to the different life cycle stages of S. mansoni itself (6). Sensitization is transferrable from infected to uninfected inbred mice by lymph node and spleen cells, but not by serum (4). Finally, the granulomatous response is strongly inhibited by a series of immunosuppressive
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A receptor for antibody on B lymphocytes. I. Method of detection and functional significance

by A. Basten, J. F. A. P. Miller, J. Sprent, J. Pye , 1972
"... Antibody-antigen complexes bind to the surface of some mouse lymphocytes (1-2). Recent evidence has suggested that this property may be characteristic of some nonthymus-derived "B " lymphocytes: (3), not of thymus-derived "T " lymphocytes (4). A similar conclusion has been reache ..."
Abstract - Cited by 31 (2 self) - Add to MetaCart
Antibody-antigen complexes bind to the surface of some mouse lymphocytes (1-2). Recent evidence has suggested that this property may be characteristic of some nonthymus-derived "B " lymphocytes: (3), not of thymus-derived "T " lymphocytes (4). A similar conclusion has been reached independently in our laboratory from studies originally designed to examine the relationship between antigen-binding cells and "memory " cells in primed mice. In these experiments, use was made of the sensitive technique of radioautography to establish the presence of a receptor for antibody on lyrnphocytes. Thoracic duct lymphocytes (TDL) were selected as the main source of lymphoid cells because of their high viability and low contamination with other cell types. The identity of lymphocytes binding antibody was established by examination of cell populations either enriched for T cells or B cells or containing the two cell types in known numbers. The T cell content was assessed by means of independent genetic markers such as 0 C3H antigen or H-2 antigen in the case of chimeric mice. When this figure was compared with the proportion of antibody-binding lymphocytes, an inverse relationship was observed. An exact correlation was therefore demonstrable between the number of lymphocytes binding antibody and the number of B cells in the population. In other words, the receptor is carried by all B cells, not by just a subclass of B cells. The identification of a marker of this kind on all B cells has permitted the develop-
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The Fc receptor on thymusderived lymphocytes. III. Mixed lymphocyte reactivity and cell-mediated lympholytic activity of Fc- and Fc + T lymphocytes

by D. Stout, Donal B. Murphy, Hugh O. Mcdevitt, Leonard A. Herzenberg , 1976
"... As our knowledge of the cellular basis for immunity has increased, it has become apparent that the generation of effector lymphocytes does not simply involve reaction of precursors with antigen and subsequent differentiation to effector stage. Thus far, in most models of cellular and humoral immunit ..."
Abstract - Cited by 25 (2 self) - Add to MetaCart
As our knowledge of the cellular basis for immunity has increased, it has become apparent that the generation of effector lymphocytes does not simply involve reaction of precursors with antigen and subsequent differentiation to effector stage. Thus far, in most models of cellular and humoral immunity studied, the generation of optimal immune responses requires an active collaboration between precursor cells and ~accessory " T cells, whose function is to enhance or initiate some stage(s) in the subsequent differentiation of the precursor (1-3). The T cell which collaborates with B cells in the generation of IgG antibody responses is termed a "helper " T cell (1). The T cell which collaborates with progenitors of cytotoxic lymphocytes in the generation of cell-mediated cytolytic responses is termed an "amplifer " T cell (2). These amplifier and helper T cells have their negative counterparts in a population of T cells termed "suppressor " T cells. It is the function of suppressor T cells to actively prevent the generation of effector cells (4-6). It thus appears that the immune system exerts self-control through a network of positive and negative regulator T cells.

Cell-to-cell interaction in the immune response. VI. Contribution of thymus-derived cells and antibody-forming cell precursors to immunological memory

by J. Sprent , 1971
"... Interaction between thymus-derived (T) 1 and nonthymus-derived (B) cells occurs in the primary humoral antibody response of mice to heterologous erythrocytes (1-3) and serum proteins (4, 5). Unequivocal evidence has shown that the B cells are the antibody-forming cell precursors (AFCP) (6-8) and tha ..."
Abstract - Cited by 21 (6 self) - Add to MetaCart
Interaction between thymus-derived (T) 1 and nonthymus-derived (B) cells occurs in the primary humoral antibody response of mice to heterologous erythrocytes (1-3) and serum proteins (4, 5). Unequivocal evidence has shown that the B cells are the antibody-forming cell precursors (AFCP) (6-8) and that immunological specificity characterizes both T and B cells before intentional antigenic stimulation (9). Although it is known that the faculty of immunological memory is carried by small lymphocytes (10), the relationship between memory and T and B cells is not clear. Answers to the following questions must be sought: Is collaboration between T and B cells obligatory for the generation of memory cells (in thymus-dependent humoral antibody responses)? Do both T and B cells carry memory and, if so, is the memory directed towards the same or different antigenic determinants? Is collaboration between T and B cells essential to activate memory cells in secondary antibody responses or does priming entail a qualitative change in B cells which permits them to interact directly with antigen without the need for the participation of T cells? Cell transfer experiments to date have led to different conclusions; in one case it appeared that T cells
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2-Deoxyglucose selectively inhibits Fc and complement receptor-mediated phagocytosis in mouse peritoneal macrophages

by B Josef Michl, Diane J. Ohlbaum, Samuel C - II. Dissociation of the irthibitory effects of 2-Deoxyglucose on phagocytosis and ATP , 1976
"... Before the identification of specific receptors for the Fc portion of immunoglobulin G (1) and the third component of complement (2) on the surface of phagocytic leukocytes, Fenn (3) and others (4) suggested that the phagocytosispromoting properties of serum opsonins could be accounted for by the ca ..."
Abstract - Cited by 21 (5 self) - Add to MetaCart
Before the identification of specific receptors for the Fc portion of immunoglobulin G (1) and the third component of complement (2) on the surface of phagocytic leukocytes, Fenn (3) and others (4) suggested that the phagocytosispromoting properties of serum opsonins could be accounted for by the capacity of these proteins to alter the physicochemical characteristics of the surfaces of pathogenic microorganisms. Although immunoglobulins and complement probably do alter the charge and topegraphic distribution of components on the surface of a particle, it is now evident that it is the specific and coordinated interaction between particle-bound ligands (immunoglobulin G and/or complement) and their corresponding receptors (the Fc and C3 receptors) on the plasma membranes of phagocytic leukocytes which is responsible for the ingestion of opsonized particles by these cells (5). In contrast, a variety of nonpathogenic (rough) strains of bacteria as well as carbon particles, latex, and boiled yeast cell walls (zymosan) are readily ingested by phagocytic leukocytes in the absence of serum opsonins. The phagocytosis of these particles is mediated by unidentified plasma membrane components
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Taxoi Binds to Cellular Microtubules

by James J. Manfredi, Jerome Parness, Susan Band Horwitz
"... ABSlRACT Taxol is a low molecular weight plant derivative which enhances microtubule assembly in vitro and has the unique ability to promote the formation of discrete microtubule bundles in cells. Tritium-labeled taxol binds directly to microtubules in vitro with a stoichiometry approaching one (Par ..."
Abstract - Cited by 17 (0 self) - Add to MetaCart
ABSlRACT Taxol is a low molecular weight plant derivative which enhances microtubule assembly in vitro and has the unique ability to promote the formation of discrete microtubule bundles in cells. Tritium-labeled taxol binds directly to microtubules in vitro with a stoichiometry approaching one (Parness, J., and S. 8. Horwitz, 1981, J. Cell Biol. 91:479-487). We now report studies in cells on the binding of [aH]taxol and the formation of microtubule bundles. [aH]Taxol binds to the macrophagelike cell line, J774.2, in a specific and saturable manner. Scatchard analysis of the specific binding data demonstrates a single set of high affinity binding sites. Maximal binding occurs at drug concentrations which produce maximal growth inhibition. Conditions which depolymerize microtubles in intact and extracted cells as determined by tubulin immunofluorescence inhibit the binding of [aH]taxol. This strongly suggests that taxol binds specifically to cellular microtubules. Extraction with 0.1 % Nonidet P-40 or depletion of cellular ATP by treatment with 10 mM NaNa prevents the characteristic taxol-induced bundle formation. The binding of [aH]taxol, however, is retained under these conditions. Thus, there must be specific cellular mechanisms which are required for bundle formation, in addition to the direct binding of taxol to cytoplasmic microtubules.
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