bluuebunny/crossref_metadata_2025_split huggingface dataset:
IMMUNOLOGIC REJECTION OF DIETHYLNITROSAMINE-INDUCED HEPATOMAS IN STRAIN 2 GUINEA PIGS
Authors: Dvorak Harold F. , Dvorak Ann M. , Churchill Winthrop H. 
Published: June 2004

The morphologic events associated with the immunologic rejection by strain 2 guinea pigs of ascites variants of two lines of diethylnitrosamine-induced tumors have been studied by light and electron microscopy.
Tumor injection sites in the skin of control animals exhibited clusters of viable, actively mitotic tumor cells along with a modest inflammatory infiltrate composed of lymphocytes, macrophages, neutrophils, and rare basophils. In contrast, similar injections of either tumor line in specifically sensitized guinea pigs elicited typical delayed-type skin reactions associated with tumor cell necrosis and a more extensive inflammatory infiltrate including a selective increase in the number of basophilic leukocytes (12%, line 1, or 23%, line 10, of total inflammatory cells). That basophils may have a role in tumor resistance in vivo is suggested by the close anatomic associations observed between basophils and tumor cells, and by the fact that basophils were the only inflammatory cell to demonstrate a relative increase in frequency in the lesions of sensitized as compared with control animals. Moreover, intraperitoneal injection of line 1 tumor in specifically sensitized animals elicited a striking basophilia within 24 h. Unlike macrophages, basophils did not phagocytose tumor cells but did evidence occasional extrusion of granules and frequently exhibited loss of granule staining density, a change that may be related to release of mediator substances.
Electron microscope studies of line 1 tumor rejection in the peritoneal cavities of specifically sensitized guinea pigs demonstrated aggregations of "activated" macrophages, lymphocytes, basophils, and damaged or dead tumor cells. These aggregates, held together by complex interdigitations of macrophage villi, closely resembled those occurring in vitro among peritoneal exudate cells whose migration from capillary tubes was inhibited by migration inhibition factor (MIF). Moreover, cells in these aggregates, as well as macrophages inhibited by MIF in vitro, lacked a normal coating of cell surface material.
DIFFERENTIAL INHIBITORY EFFECTS OF CHOLERA TOXOIDS AND GANGLIOSIDE ON THE ENTEROTOXINS OF VIBRIO CHOLERAE AND ESCHERICHIA COLI
Authors: Pierce Nathaniel F. 
Published: June 2004

Natural cholera toxoid appears to act as a competitive inhibitor of cholera enterotoxin and is thus a useful tool for studying the interaction of cholera enterotoxin with cell membranes. Cholera enterotoxin binds to gut mucosa more rapidly than does its natural toxoid. Once binding occurs, however, it appears to be prolonged for both materials. Formalinized cholera toxoid has no inhibitory effect upon cholera enterotoxin. Enterotoxic activity, ability to bind to gut mucosa, and antitoxigenicity appear to be independent properties of cholera enterotoxin.
Natural cholera toxoid does not inhibit Escherichia coli enterotoxin, indicating that although the two enterotoxins activate the same mucosal secretory mechanism they occupy different binding sites in the mucosa. Ganglioside, which may be the mucosal receptor of cholera enterotoxin, is highly efficient in deactivating cholera enterotoxin. By contrast, ganglioside is relatively inefficient in deactivating heat-labile E. coli enterotoxin and is without effect upon the heat-stable component of E. coli enterotoxin. These findings suggest that ganglioside is not likely to be the mucosal receptor for E. coli enterotoxin. Differences in cellular binding of E. coli and cholera enterotoxins may explain, at least in part, the marked differences in the time of onset and duration of their effects upon gut secretion.
CELL INTERACTIONS BETWEEN HISTOINCOMPATIBLE T AND B LYMPHOCYTES
Authors: Katz David H. , Hamaoka Toshiyuki , Benacerraf Baruj 
Published: June 2004

Several experimental approaches, designed specifically to circumvent the possible contribution of a complicating "allogeneic effect," have been successfully used to answer the question of physiologic cooperative interactions between histoincompatible T and B lymphocytes in antibody responses to hapten-protein conjugates. This was accomplished for in vivo cell transfer studies by using an F1 hybrid host as the recipient of irradiated, carrier-primed T lymphocytes from one parent and 2,4-dinitrophenyl (DNP)-primed B lymphocytes from the opposite strain. Under these conditions, very good T-B cell cooperative interactions were observed to occur between T and B lymphocyte populations derived from syngeneic donors, whereas no cooperative response was obtained when T cells were derived from one parental strain and B cells from the other. Corroborative experiments were performed in a totally in vitro system in which DNP-primed B cells developed good secondary anti-DNP antibody responses in vitro to soluble DNP-keyhole limpet hemocyanin (KLH) when cultured in the presence of irradiated KLH-primed T cells derived from syngenic donors but not from allogeneic donors.
The failure of histoincompatible T and B lymphocytes to effect physiologic cooperative interactions has important implications for our understanding of how such interactions normally occur. The possibility that these results reflect the existence of a "block" of some sort to cell-cell interaction by virtue of the presence of a foreign major histocompatibility antigen on the surface of either cell has been definitively ruled out in the present studies. These observations demonstrate that the gene(s) that conditions the capability for physiologic T-B cell cooperation must be shared in common by the respective cell types, and suggest, furthermore, that this gene (or genes) belongs to the major histocompatibility system of the mouse. These findings, together with other relevant phenomena described previously, have led us to postulate that there exists on the B lymphocyte surface an "acceptor" molecule either for the putative active T cell product or for the T cell itself. The important genetic considerations and the possible sequence of events surrounding the actual T-B cell interaction implied by these postulates are discussed in detail.
REGULATION OF THE ANTIBODY RESPONSE TO TYPE III PNEUMOCOCCAL POLYSACCHARIDE
Authors: Baker Phillip J. , Reed Norman D. , Stashak Philip W. , Amsbaugh Diana F. , Prescott Benjamin 
Published: June 2004

The effect of treatment with antilymphocyte serum (ALS) on the magnitude of the plaque-forming cell (PFC) response to Type III pneumococcal polysaccharide (SSS-III) was assessed in athymic nude mice and thymus-bearing littermate controls. Without ALS treatment, the PFC response was slightly higher in nude than in control mice. Treatment with ALS had no effect on the response of nude mice; however, considerable enhancement was noted in thymus-bearing controls. Such enhancement was ALS dose-dependent and demonstrable under conditions in which there was substantial inactivation of thymic-derived "helper" cells required for an antibody response to erythrocyte antigens.
These findings suggest that amplifier and suppressor cells, which have been reported to regulate the magnitude of the antibody response to SSS-III, represent populations of thymic-derived cells (T cells) that are not present in nude mice. The activities of "helper" T cells and regulatory T cells appear to be independent of one another and mediated by separate subpopulations of T cells.
IN VITRO STUDIES ON STRAIN-DEPENDENT PRODUCTION OF THYMUS-SPECIFIC AUTOANTIBODIES
Authors: Fuji H. , Milgrom F. 
Published: June 2004

In vitro cultures of spleen cells (S) from normal 8–10-wk-old DBA/2J mice were shown to develop a small number of plaque-forming cells (PFC) that released antibodies lytic to syngenic and autologous thymus cells as well as to syngenic lymphoma L5178Y cells used as the target in the PFC assay. A marked increase in the number of PFC detectable on L5178Y target cells was demonstrated on day 4 in the cultures of S cells to which syngenic or autologous thymus cells had been added (S+T) at time 0, whereas the PFC detectable on thymus cells in such cultures remained at a level similar to that in S cultures. This suggested that two populations of PFC participated in the observed phenomena. No PFC developed in the culture of thymus cells (T). The addition of the cell-free supernatants of 24-h cultures of T or of L5178Y cells to syngenic S cultures also caused a specific increase in the number of the PFC detectable on L5178Y, which suggested that certain immunogenic factors released from the T cells stimulated the response observed in the S+T cultures.
Antibodies of IgM nature were detected in the supernatants of S+T cultures by means of cytolysis in agar of L5178Y cells. Although such antibodies did not cause lysis of thymus cells, they could be completely removed by absorption with normal adult or fetal thymus cells of syngenic origin. Still, the absorbing capacity of L5178Y was much higher than that of thymus cells. The absorption was more efficient at 4°C than at 22°C, and hardly any absorption occurred at 37°C. The tissue distribution of the antigen under study seemed to be restricted to thymus cells since no other murine tissue cells tested removed the antibodies.
The thymic antigen under study was not restricted to strain DBA/2J and could be demonstrated on thymus cells of all other strains tested. On the other hand, the ability of spleen cells to respond in vitro to this antigen has thus far been observed only in DBA/2J mice. Spleen cells of strains C57BL/6J and NZB/BINJ as well as (DBA/2 x NZB)F1 failed to show any significant increase in the PFC response detectable on the L5178Y target when syngenic thymus cells or DBA/2J thymus cells were added.
An intravenous injection of syngenic thymus cells to DBA/2J mice also caused the appearance in their spleens of PFC detectable on the L5178Y target.
The described in vitro system may provide a good means of studying the cellular basis of generation of self-tolerance and of its breakdown.
REGULATION OF IMMUNOGLOBULIN SYNTHESIS BY DEXTRAN
Authors: Battisto Jack R. , Pappas Frances 
Published: June 2004

Dextran, of the variety commonly used as plasma expander, markedly altered antibody synthesis to an unrelated antigenic stimulus, SRBC, in two animal species, guinea pig and mouse. The time at which dextran was administered relative to antigen was found to be most critical for increasing or decreasing the number of IgM and IgG PFC. Furthermore, these times differed for the two species studied.
Typically, when given to guinea pigs 6 h before SRBC, dextran caused a 20-fold rise in IgM-producing cells but had little effect upon IgG synthesis. However, if dextran preceded antigen by 24 h the same magnitude of increase was seen in IgG-forming cells while a decrease in IgM-producing cells occurred.
In mice, a short 2 h interval between dextran and antigen favored cells synthesizing IgG and not those producing IgM. A longer 6 to 24 h lapse between dextran and antigen resulted again in an inverted pattern, i.e., an increase in IgM and a decrease in IgG-producing cells.
In both species, if dextran was given 48 h before antigen, synthesis of IgG markedly decreased.
At the cellular level dextran activated those B cells already in the vascular compartment. In stimulating the IgM response to SRBC, dextran appears either to substitute for T cells or to amplify the effects of that small number of T cells still present in bone marrow preparations. Dextran-altered mouse B cells synthesized SRBC-specific IgG in the presence of normal T cells at an earlier time than did normal B and T cells. However, dextran was unable to cause blastogenesis in vitro of guinea pig lymph node cells or mouse B, T, and spleen cells.
The data suggest at least two effects that T cells exert upon B cells. One is to stimulate more B cells to produce IgM, a function accomplished by endotoxins, PWM, PPD, and the simple polysaccharide dextran. The other is to trigger shifts in synthesis of immunoglobulins M and G. Our observations are compatible with the view that a single cell is capable of synthesizing both of these immunoglobulins and that the stimulating factor for one may cause cessation of the other.
PRODUCTION OF A RUNTING SYNDROME AND SELECTIVE γA DEFICIENCY IN MICE BY THE ADMINISTRATION OF ANTI-HEAVY CHAIN ANTISERA
Authors: Murgita Robert A. , Mattioli Carlos A. , Tomasi Thomas B. 
Published: June 2004

Conventional Swiss mice were treated from birth with intraperitoneal injections of anti-immunoglobulins in an attempt to create an experimental dysgammaglobulinemia. Mice treated with anti-γM were immunologically suppressed in all immunoglobulin classes as determined by serum antibody titers, splenic plaque-forming cells, serum immunoglobulin levels, and immunofluorescent analysis of plasma cells in lymphoid tissues. Treatment immediately after birth with high concentrations of anti-γM leads to a developmental arrest characterized by severe immunosuppression, failure to gain weight, and premature death. The pathogenesis of anti-γM runting syndrome is unknown. Animals similarly treated with anti-γG, anti-γA, or control normal goat or rabbit γ-globulins developed normally. The frequency of occurrence and severity of anti-γM-induced runting syndrome is dependent upon the concentration of anti-γM-globulin administered.
Administration of anti-γA resulted in a selective γA deficiency that was characterized by a marked reduction in serum-γA and an absence of γA-containing cells in the spleen. However, essentially normal numbers of plasma cells were found in the gastrointestinal lamina propria of anti-γA-treated animals concomitantly with suppressed levels of γA in intestinal fluids.
DIVERSE EXPRESSION OF GROUP a ALLOTYPE SPECIFICITIES ON THE HEAVY CHAINS OF HOMOGENEOUS RABBIT ANTIBODIES
Authors: Kindt Thomas J. , Seide Rochelle K. , Tack Brian F. , Todd Charles W. 
Published: June 2004

Variations in the ability of homogeneous antibodies to absorb group a allotype antisera suggest that these VH region allotypes comprise a spectrum of specificities. While no homogeneous antibody tested would completely absorb antisera to the group a specificities, the total IgG preparations from individual rabbits was capable of doing so, including preimmune IgG from the rabbits that produced the homogeneous antibodies.
Differences in the serologic reactivities of homogeneous antibodies indicate that each possesses only a portion of the spectrum of the allotypic specificities expressed by the total IgG.
CELLULAR MEDIATORS OF ANTI-LISTERIA IMMUNITY AS AN ENLARGED POPULATION OF SHORT-LIVED, REPLICATING T CELLS
Authors: North Robert J. 
Published: June 2004

An intravenous immunizing infection with the facultative, intracellular parasite, Listeria monocytogenes results in the production in the spleen of a population of immunologically-committed lymphocytes which can adoptively immunize normal recipients against a lethal challenge infection. These cellular mediators of immunity are first produced in the spleen between days 2 and 4 of infection and reach peak production on day 6. Their production then progressively decreases until about day 20 when their presence can no longer be detected.
Increased production of cellular mediators is coincident with major increases in cell division, cellularity, and spleen weight. Decreased production of cellular mediators, on the other hand, is associated with decreases in cell division, cellularity, and spleen weight. Again, the level of delayed sensitivity to Listeria antigens expressed by the host at any one time is proportional to the number of cellular mediators in the spleen.
Increased production of cellular mediators is also associated with major increases in the total numbers of replicating T cells and B cells in the spleen. That the cellular mediators of immunity are part of the replicating T cell population, rather than the B cell population, is evidenced by their susceptibility to anti-θ serum and by their resistance to anti-Ig serum. Furthermore, they can be completely eliminated from the spleen by a brief pulse of the antimitotic drug, vinblastine. This study allows the conclusion that the cellular mediators of anti-Listeria immunity belong to an expanded population of rapidly dividing, short-lived T cells. It is suggested that they have the same properties as the T cell effectors of allograft immunity.
MUTANTS OF NONPRODUCER CELL LINES TRANSFORMED BY MURINE SARCOMA VIRUSES
Authors: Hatanaka M. , Klein R. , Toni R. , Walker J. , Gilden R. 
Published: June 2004

A variety of cell mutants were obtained by a single 5'-bromodeoxyuridine (BrdU) treatment of an nonproducer (NP) cell line transformed by the Kirsten strain of murine sarcoma virus (Ki-MSV). Isolation procedures of these cell
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mutants are described. The cell mutants obtained were classified by tumorigenic potential and shedding of Type C virus particles. The cell mutants were classified into four groups: (A) tumorigenic, without particles; (B) tumorigenic, with Type C particles; (C) nontumorigenic, without particles; and (D) nontumorigenic, with Type C particles. The tumorigenic cell lines showed variability in morphology with both flat and typical transformed appearing cell lines showing equal transplantability.
SURFACE IgE ON HUMAN BASOPHILS DURING HISTAMINE RELEASE
Authors: Becker Karl E. , Ishizaka T. , Metzger H. , Ishizaka K. , Grimley Philip M. 
Published: June 2004

The distribution of surface IgE on human basophils was studied using fluorescence microscopy and immunoferritin electronmicroscopy. Redistribution of the IgE was dose, time and temperature dependent and required divalent anti-IgE. Cells which can release histamine in vitro were indistinguishable in these respects from cells which cannot. The redistribution was unaffected by the presence or absence of Ca++.
No correlation between the conditions required for optimal histamine release and for redistribution was observed. At low doses, optimal histamine release occurred in the absence of, or before, redistribution. At higher doses redistribution occurred in the absence of histamine release. Antigen-induced histamine release was unaccompanied by gross redistribution of the surface IgE.
Since both histamine release and redistribution require bridging of IgE on basophils it is concluded that only certain kinds of cross-linking of the IgE effectively stimulates these cells.
PHYLOGENETICALLY ASSOCIATED RESIDUES WITHIN THE VHIII SUBGROUP OF SEVERAL MAMMALIAN SPECIES
Authors: Capra J. Donald , Wasserman Richard L. , Kehoe J. Michael 
Published: June 2004

Immunoglobulin heavy chains from IgG pools of several mammalian species have been subjected to Edman degradation on an automated protein sequencer. The percentage of unblocked vs. blocked heavy chains was estimated from the yield of the invariant valine in the second position. Further analysis of these unblocked polypeptides unequivocally placed them in the VHIII subgroup on the basis of homology with known human heavy chain sequences.
The mammals studied could be divided into three distinct categories on the basis of the distribution of the VHIII subgroup. In several species the VHIII subgroup could not be detected while, in others, virtually all of the heavy chains belonged to this subgroup. Several species had intermediate amounts with the level of the VHIII subgroup restricted to between 19 and 29% of the total pool. Within experimental error, all members of a given order had a similar VHIII subgroup distribution.
Further amino acid sequence studies illustrated a high degree of structural homogeneity in the heavy chains of IgG isolated from pooled sera of a number of mammalian species. The very close amino acid sequence homologies of the amino terminal 24 residues of the various pools corroborated conclusions previously obtained using several myeloma proteins from some of these same species. In particular, certain phylogenetically associated residues were identifiable at characteristic positions in the pools in confirmation of their identification in the myeloma proteins. The simplest assumptions would suggest that these findings are more compatible with a pauci-gene than a multi-gene basis for the generation of antibody diversity.
IDENTIFICATION OF HUMAN B AND T LYMPHOCYTES BY SCANNING ELECTRON MICROSCOPY
Authors: Polliack A. , Lampen N. , Clarkson B. D. , de Harven E. , Bentwich Z. , Siegal F. P. , Kunkel H. G. 
Published: June 2004

In this study a variety of human lymphocytes of known B or T cell type, obtained from multiple sources, were prepared for scanning electron microscopy (SEM) by the critical point drying method. Distinction between normal B and T lymphocytes was relatively easy in most instances, on the basis of their surface architecture. Using immunological methods, between 20 and 30% of normal peripheral blood lymphocytes (PBL) were identified as B cells and from 69 to 82% as T cells. SEM results showed that 20% of the PBL had a complex villous surface and approximately 80% of cells were smaller and had a relatively smooth surface. Comparison of the above data and enrichment of B cells from PBL, by centrifugation after T cell rosettes had formed, indicated that the "villous" cells were B lymphocytes and the "relatively smooth" cells were T lymphocytes. T cells obtained from two human thymuses were also of the generally smooth cell type.
Further evidence for the distinction of B and T lymphocytes, on the basis of surface morphology, was obtained from the examination of cultured lymphoid cell lines of known B or T cell derivation. Cells from cases of chronic lymphocytic leukemia also provided support for the above interpretations. Five of six untreated cases were clearly of B cell type by immunologic and SEM criteria. One unusual case showed the presence of T and B lymphocytes in almost equal numbers by SEM and a mixture of B and T cells by immunologic markers. An additional case that had received chemotherapy showed numerous atypical cells that were difficult to classify by SEM.
Detailed examination of the smoother T cells showed that at least half of them had a moderate number of surface digitations and a small proportion had an intermediate surface morphology with a relatively large number of surface digitations. The latter presented difficulties in classification and may correspond to different stages of differentiation and represent subpopulations of lymphocytes.
The distinction between human B and T lymphocytes on the basis of their surface architecture can be made by SEM of critical point dried samples, with relative ease in most but not all instances. The effects of stimulation, cell cycle, differentiation, intercellular contact, and density of cell population, on the surface architecture of lymphoid cells, remain to be determined.