bluuebunny/crossref_metadata_2025_split huggingface dataset:
STUDIES ON THE SENSITIZATION OF ANIMALS WITH SIMPLE CHEMICAL COMPOUNDS
Authors: Maguire Henry C. , Chase Merrill W. 
Published: June 2004

A method of establishing regular and intense sensitivity to picric acid is described, based upon an initial sensitization by a "split-adjuvant" technique in which the intradermal injection of mycobacteria in paraffin oil precedes or follows the administration of allergen to the same sites. When subsequent contact applications of picric acid are later made, the degree of sensitivity rises in steps such that reactivity occurs in tests made with low concentrations of picric acid, in the range of 0.06–0.006% but varying somewhat from one experiment to another. This heightening of picric acid reactivity represents an anamnestic response in the area of delayed hypersensitivity.
The characteristics of contact reactions to the weak allergen, picric acid, differ from those encountered with covalently binding haptens, PCI and DNCB. A slow evolution from an initial micropapular reaction to full reaction requires about 3 days, leading often to a micaceous scale, with histological evidence of vesiculation even while the reaction is still feeble, and to an infiltrate containing a significant number of polymorphonuclear leukocytes.
Substitution of an emulsion of picric acid in complete Freund's adjuvant as a priming experience proved to be much less efficient.
The split-adjuvant technique offers a general plan for sensitizing with weak allergens. Indeed, technically, sensitization can be acquired even when, for priming, the allergen is applied topically over intradermal depots of mycobacteria in paraffin oil. Compatibility between sensitizer and adjuvant is not required.
THE SELECTIVE INHIBITION OF MACROPHAGE PHAGOCYTIC RECEPTORS BY ANTI-MEMBRANE ANTIBODIES
Authors: Holland Phillip , Holland Nancy H , Cohn Zanvil A. 
Published: June 2004

Rabbit antibodies were prepared against purified mouse macrophages, erythrocytes, and liver lysosomes. In the presence of complement each of these reagents was capable of lysing mouse erythrocytes and macrophages. In the absence of complement, all antisera agglutinated mouse erythrocytes and at high concentration produced a cytotoxic effect on macrophages. At IgG concentrations of 100 µg/ml, no morphological evidence of cytotoxicity was evident. These data suggest the presence of common antigens on the erythrocyte and macrophage plasma membrane.
Anti-macrophage, anti-erythrocyte, and anti-lysosomal γ-globulins and IgG, employed at subtoxic concentrations, all inhibited the attachment and ingestion of opsonized erythrocytes and mycoplasma. This occurred without significant reduction in the phagocytosis of polystyrene particles, formalinized erythrocytes, and yeast cell walls. Each of the anti-membrane IgG antibodies was capable of blocking the Fc receptor on the macrophage plasma membrane. Attachment to the macrophage membrane occurred by means of the Fab region. However, a role for the Fc portion of the molecule was suggested since pepsin-digested IgG was unable to block the receptor.
Each of the IgG antibodies produced a partial blockade of the complement receptor and reduced the ingestion of EAC1,4,2,3 by approximately 50%.
THE IMMUNOLOGICALLY SPECIFIC RETENTION OF RECIRCULATING LONG-LIVED LYMPHOCYTES IN LYMPH NODES STIMULATED BY XENOGENEIC ERYTHROCYTES
Authors: Thursh Donald R. , Emeson Eugene E. 
Published: June 2004

The lymph nodes of mice actively or adoptively immunized to sheep RBC and/or chicken RBC selectively retain long-lived lymphocytes after challenge with the appropriate antigen. This retention is demonstrable within 8 hr of the time of stimulation, though it probably begins even before this, and it is essentially complete within the first 24 hr. A similar selective retention is seen in nodes regional to the injection of some nonimmunogenic substances such as turpentine, but not others such as colloidal carbon or syngeneic RBC.
In animals adoptively immunized to sheep and chicken RBC simultaneously, there is a preferential accumulation of the labeled long-lived lymphocytes of donors immunized to sheep RBC in lymph nodes challenged with sheep RBC, and a preferential accumulation of lymphocytes (labeled with a different radioisotope) from donors immunized to chicken RBC in lymph nodes challenged with this antigen. This immunologically specific component is demonstrable whether the antigen is given before or after adoptive immunization, suggesting that the only labeled cells capable of specific localization in this system are those cells that normally remain in the recirculating pool. In the present experiments, 31 out of 31 sets of antigenically stimulated lymph nodes have shown radiochemical evidence of immunological specificity in the distribution of donor lymphocytes between them, while corresponding sets of nonstimulated lymph nodes have shown only small random variations in the distribution of donor cells. Two different mechanisms are postulated whereby antigenic stimulation can alter the traffic of recirculating long-lived lymphocytes through stimulated lymph nodes. One affects recirculating cells of a particular immunological specificity, while the other affects recirculating cells without regard to their immunological specificity.
SYNERGY AMONG LYMPHOID CELLS MEDIATING THE GRAFT-VERSUS-HOST RESPONSE
Authors: Cantor Harvey , Asofsky Richard 
Published: June 2004

Two types of thymus-derived (T) lymphocytes have been shown to cooperate in the induction of graft-versus-host responses. One cell type is found in highest concentrations in the peripheral blood and lymph node, is extremely sensitive to anti-thymocyte serum (ATS) in vivo, and is probably part of the recirculating lymphoid cell pool (3). The second cell type, found in highest concentrations in the thymus and spleen, is relatively resistant to small doses of ATS in vivo. Both cell types are substantially depleted after neonatal thymectomy.
Moreover, since synergism was also obtained using appropriate mixtures of cells from either parental strain in F1 hosts, it was possible to show that the nonrecirculating cells determined the specificity of the response and were probably the precursors of effector cells in this response. The recirculating T cell appeared to amplify this response. The implications of these data are discussed.
MATERNALLY INDUCED TRANSPLANTATION IMMUNITY, TOLERANCE, AND RUNT DISEASE IN RATS
Authors: Beer Alan E. , Billingham R. E. , Yang S. L. 
Published: June 2004

A previous report that the offspring of outbred Sprague-Dawley rats, born of mothers presensitized or tolerant with respect to tissue antigens of the Lewis strain, and reinoculated with Lewis cells during their pregnancy, reject test grafts of Lewis skin in an accelerated manner has been confirmed. This "maternally induced" alteration in reactivity of the progeny has been found to be long lasting, immunologically specific, and probably not due to transfer of humoral antibody. It has been established that the reexposure of the mothers to donor cellular antigen during pregnancy augmented the influence of the prior states of tolerance or sensitivity.
To obviate the complications inherent in working with the outbred Sprague-Dawley rats, the key experiments summarized above were repeated with isogenic Fischer rats as parents and Lewis rats as the tissue donors as before. With this combination it was found that a state of prior sensitization or tolerance in the mothers resulted in the apparent induction of tolerance in some of their progeny. Reinoculation of either the tolerant or sensitized mothers during pregnancy slightly increased the incidence and degree of impairment of their offsprings' capacity to reject Lewis skin grafts. A single intraperitoneal injection of 100 x 106 million Lewis lymphoid cells into normal Fischer rats in the 14th–16th day of pregnancy also weakened the reactivity of their progeny to Lewis test grafts.
Further to test the premise that this weakened reactivity might be due to maternal induction of tolerance, by antenatal transmission of alien cells, the lymphohematopoietic tissue system of adult Fischer females was replaced by that from Lewis donors with the aid of cyclophosphamide. It was anticipated that when these animals were mated with Fischer males, sufficient Lewis leukocytes might cross the placentas to induce high degrees of tolerance. Although normal sized healthy litters were born, about 50% of the infants succumbed to graft-versus-host (GVH) or runt disease within 40 days, many of them giving evidence of being tolerant of Lewis grafts. The mothers, too, developed chronic GVH disease. The offspring of Fischer females made chimeric with cells from (Fischer x Lewis)F1 hybrid donors, as well as their mothers, remained healthy.
Intraperitoneal injection of normal Fischer females, in the 15th–17th day of pregnancy, with 100 million lymphoid cells from specifically sensitized Lewis rats, also caused fatal runt disease to develop in about 50% of their offspring, but left the mothers unscathed.
Taken together, these various findings indicate that in some genetic contexts at least the extent of the natural surreptitious transplacental cellular traffic can be considerably augmented experimentally, though how this comes about and why lymphocytic cells that are foreign to the mother can apparently gain access to fetuses more readily than her own cells remain to be determined.
DEVELOPMENT OF CHICKEN LYMPHOID SYSTEM
Authors: Choi Yong Sung , Good Robert A. 
Published: June 2004

Development of Ig-synthesizing cells in the bursa of chick embryo was studied by immunohistochemical staining method as well as by in vitro incorporation of leucine-3H into Ig. Ig-synthesizing cells are first detected in the bursa of a 14 day old chick embryo and increase with the maturation of the embryo. Acrylamide gel analysis of leucine-3H-labeled Ig shows that synthesis of nonsecretory IgM-H0 precedes that of secretory IgM-H, reflecting an ontogenetic sequence of development of lymphoid cells synthesizing IgM.
Since IgM-H0 is not secreted, we further studied biochemical differences between two heavy chains. The difference is attributable to lack of galactose attachment to H0 chains. It is proposed that during differentiation of lymphoid cells synthesizing and secreting Ig, attachment of galactose may play an obligatory role in the development of cellular capacity for Ig secretion.
IMMUNE AND NATURAL ANTIBODIES TO SYNGENEIC MURINE PLASMA CELL TUMORS
Authors: Herberman Ronald B. , Aoki Tadao 
Published: June 2004

Cytotoxic antibody to a plasma cell tumor antigen was produced in syngeneic BALB mice by immunization with viable or inactivated plasma cell tumors. Antibody with the same specificity was found in the sera of normal BALB and other strains of mice. This natural antibody reacted with an antigen with characteristics indistinguishable from the previously described alloantigen, PC.1, and with viral envelope antigen, χVEA. The incidence of cytotoxic reactivity and the antibody titers reached a peak in normal BALB mice at 3–4 months of age, and were lower in 9–12-month old mice. The sera of germfree mice had lower reactivity; but when the mice were transferred to conventional conditions, their sera soon became as active as those of conventional mice.
A virus common to all plasma cell tumors, which is present in latent form in some normal tissues of BALB and other PC.1 positive strains, is suggested as the cause for the PC.1 antigen and for the appearance of natural antibody to it. The considerable evidence for the close association of a virus with plasma cell tumors is presented.
THE EFFECTS OF MERCAPTOETHANOL AND OF PERITONEAL MACROPHAGES ON THE ANTIBODY-FORMING CAPACITY OF NONADHERENT MOUSE SPLEEN CELLS IN VITRO
Authors: Chen Chang , Hirsch James G. 
Published: June 2004

Nonadherent mouse spleen cells exhibited poor viability and little or no capacity to form antibodies to sheep red cells in the Mishell-Dutton culture system. Viability and antibody-forming capacity could be restored by addition to these cultures of low concentrations of mercaptoethanol (10–4–10–5 M), or by addition of appropriate numbers of mouse peritoneal macrophages. Macrophage concentrations lower than optimal resulted in lower lymphoid cell viability and correspondingly fewer plaque-forming cells, whereas excess macrophages resulted in marked inhibition of antibody formation despite good viability of the lymphocytes. Restoration of the nonadherent cells with mercaptoethanol was thus much simpler and more reproducible than it was with macrophages; furthermore, the number of plaque-forming cells developed in cultures restored with mercaptoethanol was approximately fourfold higher than it was in cultures restored with optimal numbers of macrophages.
In the presence of mercaptoethanol, the plaque-forming capacity of the nonadherent spleen cells was not increased when small numbers of macrophages were added to the system, nor was it decreased when the few macrophages present in the nonadherent cells were further reduced or eliminated. Excess macrophages inhibited antibody formation in the cultures containing mercaptoethanol as they did in control cultures.
Optimal restoration of plaque-forming capacity to the nonadherent spleen cells with mercaptoethanol required the reducing agent to be present throughout the 4 or 5 day culture period. Addition of mercaptoethanol 1 or more days after initiation of culture, or transfer of the cells to a medium free of mercaptoethanol before completion of the culture resulted in a reduction in the numbers of plaque-forming cells.
The results suggest that mouse lymphoid cells do not require macrophages in order to form antibodies to sheep red cells in vitro, provided mercaptoethanol is present in the culture medium. The mechanism of action of mercaptoethanol under these conditions is not completely clear, but one of its effects is to promote the viability of lymphoid cells in the cultures.
A CLASSIFICATION OF THE MURINE LEUKEMIA VIRUSES
Authors: Eckner Robert J. , Steeves Richard A. 
Published: June 2004

Coinfection of neonatal BALB/c mice with helper-dependent Friend spleen focus-forming virus (SFFV), as contained in the Friend virus (FV) complex, and antigenically distinct Moloney leukemia virus (MolLV) resulted in the recovery of a MolLV pseudotype of SFFV, abbreviated SFFV(MolLV). The antigenic alteration of SFFV was observed by following its neutralization kinetics in vitro by specific Friend or Moloney typing antiserum.
Effective pseudotype production was accomplished only when N-tropic LLV-F (the natural helper virus in the FV complex) was inhibited in B-type mice coinfected with an NB-tropic MolLV or other murine leukemia virus (MuLV) preparation. SFFV pseudotypes could not be prepared by using murine viruses other than leukemia viruses. SFFV prepared after two serial passages in the presence of MolLV was effectively neutralized by Moloney antiserum, but not by Friend typing antiserum; therefore, the envelope of the pseudotype virus, SFFV(MolLV), is homogeneous. Pseudotype virus was antigenically stable in the absence of continued mixed infection of BALB/c mice with SFFV(MolLV) and MolLV. However, SFFV(MolLV) was easily converted back to the LLV-F type after only one passage in BALB/c mice coinfected with NB-tropic LLV-F. The antigenic interconversion between LLV-F and MolLV types demonstrated that SFFV is defective with respect to the expression of neutralizable envelope antigens.
Analysis of the neutralizable envelope antigens of nine SFFV(MuLV) pseudotypes by a panel of seven typing antisera made possible a "type-specific" SFFV(MuLV) envelope classification. Two major categories have been identified which correspond to the Gross (G) and Friend-Moloney-Rauscher (FMR) subgroups. Further, the FMR subgroup was divided into four types on the basis of distinct neutralization patterns. These results indicated that the specificity observed by cytotoxic G vs. FMR antisera is different from that observed by neutralization kinetics. We therefore suggest that the specific antigens revealed by virus neutralization tests be referred to as type specific.
LYSOSOMES OF THE ARTERIAL WALL
Authors: Peters T. J. , Müller M. , de Duve Amo C. 
Published: June 2004

Smooth muscle cells were dissociated from normal rabbit aorta by incubating the tissue in Hanks' solution containing elastase, collagenase, and hyaluronidase. The isolated cells contained significant amounts of the following acid hydrolases: N-acetyl-ß-glucosaminidase, N-acetyl-ß-galactosaminidase, ß-galactosidase, ß-glucuronidase, α-mannosidase, ß-glucosidase, acid phosphatase, and cathepsins C and D. The cells were disrupted and fractionated by isopycnic centrifugation on sucrose density gradients in the Beaufay automatic zonal rotor.
Lysosomes with a modal density of 1.16 were identified by the distribution of these acid hydrolases and by the latency of N-acetyl-ß-glucosaminidase and ß-galactosidase. Other particulate enzymes studied in these sucrose gradients included cytochrome oxidase and monoamine oxidase (mitochondria), 5'-nucleotidase and leucyl-ß-naphthylamidase (plasma membrane), and catalase (? peroxisome).
This microanalytical subcellular fractionation technique is applicable to the study of milligram quantities of many other tissues, both normal and pathological.
THE INTERACTION BETWEEN TOXOPLASMA GONDII AND MAMMALIAN CELLS
Authors: Jones Thomas C. , Yeh Shirley , Hirsch James G. 
Published: June 2004

Macrophage, fibroblast, and HeLa cell cultures have been infected with Toxoplasma gondii, and observations have been made on parasite entry and fate.
A special procedure was devised for studying the entry of toxoplasmas by electron microscopy. Toxoplasmas were centrifuged onto the cells in the cold; fixation 1–3 min after warming yielded specimens showing numerous examples of parasites in the process of entering cells. The mechanism of entry into macrophages, fibroblasts, and HeLa cells was in all cases by phagocytosis. Micropseudopods were extended by the cells to envelop the attached parasites in a typical phagocytic vacuole. Apparently the toxoplasmas stimulated this response of HeLa cells and fibroblasts, cell types not usually phagocytic. No instance was seen of penetration of toxoplasmas through the cell membrane, or of parasites located free in the cytoplasm.
Essentially all of the toxoplasmas that entered HeLa cells divided with a generation time of 9 hr; the parasites formed large rosettes situated in vacuoles, eventually leading to host cell rupture. Macrophages took in larger numbers of toxoplasmas than did HeLa cells, but approximately half of the parasites inside of macrophages degenerated within a few hours. The surviving toxoplasmas in macrophages divided every 8 hr, forming rosettes and eventually rupturing the cells.
STUDIES OF GENETIC TRANSMISSION OF MURINE LEUKEMIA VIRUS BY AKR MICE
Authors: Rowe Wallace P. , Hartley Janet W. 
Published: June 2004

The transmission of murine leukemia virus (MLV) to hybrids between AKR and Fv-1b mice was studied in order to evaluate the effect of the Fv-1 gene on endogenous MLV infection and to attempt to determine if the genetic loci contributed by AKR carry viral genetic determinants. Fv-1 was shown to have a marked suppressive effect on time of appearance of detectable infectious virus and on the titers attained in vivo, but did not affect the ability of the cells to produce virus in vitro after induction with 5-iododeoxyuridine.
The host range type of the virus detected in the hybrid mice was almost always of the type carried by AKR, although the low-virus Fv-1b parents carry the genome of a different host range type. This finding provides strong, but not conclusive, evidence that the virus-inducing loci of AKR contain MLV genetic determinants.
INHIBITORY AND STIMULATORY EFFECTS OF CONCANAVALIN A ON THE RESPONSE OF MOUSE SPLEEN CELL SUSPENSIONS TO ANTIGEN
Authors: Dutton Richard W. 
Published: June 2004

The presence of concanavalin A (Con A) inhibits the immune response of mouse spleen cell suspensions to erythrocyte antigens, stimulates the incorporation of tritiated thymidine, and increases cell recovery. Con A also restores the depressed response of cell preparations treated to remove thymus-derived cells. The dose-response curve for all four effects shows peak activity at 2 µg/ml. The depressed in vitro response of spleen cell suspensions from adult thymectomized, irradiated, bone marrow-restored mice is also restored by Con A. Here the dose-response curve is quite different with activity over a much wider range of concentration. The restoration of thymus-derived cell-depleted cultures by Con A is inhibited by the addition of untreated, unirradiated, mouse spleen cell suspensions, but is not inhibited by untreated, irradiated cells.
Small numbers of spleen cells that have been preincubated with Con A and washed will inhibit the response of fresh, untreated cells to antigen. If the mouse spleen cell suspensions are incubated for 24 hr before the addition of Con A, the response to antigen is no longer inhibited but is stimulated instead.
The data are compatible with the hypothesis that there are at least two cell targets for the action of Con A. One cell, that mediates the inhibitor effect, is a short-lived, radiosensitive, thymus-derived cell. The other cell, that mediates the stimulating effect, cannot be identified from the data presented here but may also be of thymus origin on the basis of studies by other investigators.
AN ENZYMATIC FUNCTION ASSOCIATED WITH TRANSFORMATION OF FIBROBLASTS BY ONCOGENIC VIRUSES
Authors: Ossowski L. , Unkeless J. C. , Tobia A. , Quigley J. P. , Rifkin D. B. , Reich E. 
Published: June 2004

Chick, hamster, mouse, and rat embryo fibroblast cultures, transformed by either DNA or RNA viruses, show fibrinolytic activity under suitable conditions of growth and in appropriate media; normal counterpart cultures do not. The fibrinolysin is produced by the interaction of two protein factors: one of these, a cell factor, is released by transformed cells and accumulates in the medium when cultures are incubated in the absence of scrum. The second factor, the serum factor, is a specific protein that is present in sera of many avian and mammalian species, including man.
Not all sera yield fibrinolysin on interaction with any given transformed cell factor, and the spectrum of activating sera is distinctive for each cell factor. This pattern appears to be determined by the cell type, rather than by the transforming virus.
An important role for the fibrinolysin in oncogenic transformation is suggested by the following correlations. (a) The initial appearance of fibrinolysin precedes the morphological change after the transfer to permissive temperatures of chick fibroblast cultures infected with a temperature-sensitive mutant of RSV. (b) The initiation of fibrinolysis and of morphological change both require the synthesis of new protein, but not the synthesis of either DNA or rRNA. (c) The activity of the fibrinolysin is correlated with the retention of abnormal morphology in hamster cells transformed by SV-40. (d) The sera of normal chicks effectively activate fibrinolysis with the cell factor from transformed chick cells. In contrast the sera of chicks with RSV tumors do not; these contain an inhibitor of the fibrinolytic activity.