bluuebunny/crossref_metadata_2025_split huggingface dataset:
Biological Expressions of Lymphocyte Activation
Authors: Tadakuma Takushi , Kühner Alice L. , Rich Robert R. , David John R. , Pierce Carl W. 
Published: December 2022

Abstract
Supernatant fluids from murine spleen cell cultures incubated with concanavalin A for 48 hr contain a factor(s), soluble immune response suppressor (SIRS), which suppresses plaque-forming cell responses to sheep erythrocytes by murine spleen cells in vitro. In the present studies, some of the biochemical and biophysical properties of SIRS were investigated. SIRS was non-dialysable; the suppressive activity was stable at 56°C for 30 min, but was destroyed by treatment at 70°C for 30 min, 80°C for 10 min, or at pH 2. The suppressive activity was not absorbed by the stimulating antigen, SRBC, or antisera against murine IgG or µ-chain, suggesting that SIRS does not contain immunoglobulin determinants. Murine spleen and thymus, but not kidney cells, however, absorbed SIRS activity. Enzyme treatments revealed that SIRS was resistant to DNase and RNase, but was destroyed by trypsin and chymotrypsin. In gel filtration with Sephadex G-100, SIRS activity eluted in the fraction corresponding to m.w. in the range between 48,000 and 67,000. With polyacrylamide gel electrophoresis, SIRS activity migrated in the region cathodal to albumin. Isopycnic centrifugation in a cesium chloride gradient suggested that SIRS is a glycoprotein. These supernatant fluids with SIRS activity were also found to contain macrophage migration inhibitory factor (MIF). In the experiments using gel filtration, polyacrylamide gel electrophoresis, and isopycnic centrifugation to fractionate supernatant fluids, SIRS and MIF activity were found in the same fractions, and to date we have been unable to dissociate definitively SIRS activity from MIF activity.
Hybridization Kinetics of Ribonucleic Acid and Deoxyribonucleic Acid from Antigen-Stimulated Mouse Spleen Cells
Authors: Moav Neomi , Goldblatt Drora , Moav Boaz , Frensdorff Asher 
Published: December 2022

Abstract
In an attempt to explore the mechanism by which antigenic stimulation alters gene expression in lymphoid cells in vivo, three different hybridization techniques have been used to compare the complexity of the genome of lymphoid cells from normal and from immune BALB/c mice.
RNA/DNA hybridization experiments at a DNA excess of 1000 demonstrated that normal RNA and immune RNA hybridized identically with DNA extracted from mouse spleen cells before and after immunization and with liver DNA. These findings indicate that DNA sequences complementary to immune RNA or to normal RNA are represented in a number of copies not significantly different in the genome of normal lymphoid cells and in that of immune lymphoid cells.
Hybridizations of normal and of immune RNA with normal and immune pulse-labeled DNA, done at RNA excess, detected no differences between these two DNA. However, significant differences were observed in the percentage of DNA hybridized with normal and immune RNA; 3 to 4% of the DNA hybridized with normal RNA and 8 to 9% with immune RNA. This indicates that more DNA sequences are transcribed 48 hr after immunization than before immunization.
The RNA exhaustion rates caused by normal and immune DNA were found to be identical, indicating that antigenic stimulation did not induce major changes in the number of DNA base sequences complementary to the RNA tested. However, when normal and immune pulse-labeled RNA were compared by exhaustion with DNA, the immune pulse-labeled RNA obtained 48 hr after immunization displayed a slower exhaustion rate than normal RNA or RNA extracted 72 hr after immunization. These results suggest the temporary synthesis, at a higher frequency, of certain RNA species 48 hr after immunization, as compared to the RNA synthesis in normal, nonimmune cells, or that occurring 72 hr after immunization.
Thus, the three experimental approaches used lead to the conclusion that antigenic stimulation does not induce major gene amplification; it does, however, change the transcription rate of certain RNA species.
Antibodies to Guinea Pig Lymphokines
Authors: Geczy Carolyn L. , Geczy Andrew F. , de Weck Alain L. 
Published: December 2022

Abstract
A “second generation” antibody to a highly purified lymphocyte product was raised in a goat against material eluted from a rabbit anti-guinea pig lymphokine immunoadsorbent column. This anti-lymphokine serum, in contrast to anti-lymphocyte serum (ALS) did not appear to contain cytotoxic antibodies directed against membrane antigens on guinea pig lymph node lymphocytes. Furthermore, the anti-lymphokine serum did not inhibit the formation of spontaneous T rosettes nor significantly depress lymphocyte response to mitogens.
The anti-lymphokine serum totally suppressed the delayed skin reactivity to PPD and contact sensitivity to DNCB when injected intradermally around the site of antigen challenge. By contrast, intradermally injected ALS did not appear to suppress the PPD response in sensitized guinea pigs. Intravenously and i.p. administered anti-lymphokine serum was somewhat less effective in suppressing the delayed skin response to PPD. The intradermal injection of the antiserum had no effect on nonspecific inflammation evoked by turpentine-olive oil or on the extravasation of circulating Evans blue evoked by intradermally injected histamine.
Histologic examination of 24-hr DNCB-induced skin lesions from sensitized guinea pigs treated with intradermally injected anti-lymphokine serum showed marked reduction of mononuclear infiltration of the dermis and of epidermal lesions, as compared with skin sites taken from sensitized animals pretreated with normal goat serum. The anti-lymphokine serum injected i.v. also markedly reduced the perivascular infiltration of the dermis and subcutis in skin reaction sites from sensitized animals challenged with PPD. Intravenous treatment with ALS for 3 consecutive days caused extensive depletion of the paracortical areas of peripheral lymph nodes whereas treatment with normal serum and anti-lymphokine serum caused no such depletion.
It is proposed that the anti-lymphokine serum is directed against activated lymphocyte products, one of them being MIF. These products are involved in the mediation of delayed hypersensitivity reactions. This is in marked contrast to ALS, the suppressive action of which appears to be central rather than peripheral.
Cellular Immunity in Chronic Theiler's Virus Central Nervous System Infection
Authors: Rabinowitz Stanley G. , Lipton Howard L. 
Published: December 2022

Abstract
After (IC) inoculation of the DA strain of TMEV, SJL/J mice develop chronic CNS infection with marked mononuclear cell infiltration of spinal cord leptomeninges and white matter and concomitant demyelination. In the present study the temporal course of cell-mediated and humoral immune responses to virus were measured in this infection. It was shown that chronic TMEV infection is associated with the development of immunologically specific spleen cell reactivity as judged by in vitro incorporation of 3H-TdR into DNA in response to inactivated TMEV antigen. Spleen cell reactivity is first detectable about 2 months after infection, persists for at least 1 year, and correlates with the temporal development of serum-neutralizing antibody. The late development of sensitized spleen cells is not the result of an immunosuppressive effect of this virus infection since infected mice exhibit normal spleen cell proliferative responses to T cell mitogens and produce normal antibody responses to a heterologous protein antigen, sheep red blood cells. In addition, anti-viral antibody inhibits virusinduced spleen cell reactivity. Finally, the antigen-reactive lymphocyte subpopulation within the spleen responsible for proliferation to TMEV antigen are T cells and not B cells.
The Inhibitory Effect of Chemotactic Factors on Erythrophagocytosis by Human Neutrophils
Authors: Musson Robert A. , Becker Elmer L. 
Published: December 2022

Abstract
The effect of various chemotactic factors on phagocytosis of sheep erythrocytes sensitized with IgG and complement (EAC1423) by human neutrophils (PMN) was studied. The bacterial chemotactic factor, a butanol extract of an Escherichia coli culture filtrate, the pronase sensitive and insensitive chemotactic substances isolated from this extract, C5a, a chemotactic fragment of the fifth component of complement, and a chemotactic synthetic peptide, formylmethionyl-leucine all significantly reduced the initial rate of ingestion at concentrations that are chemotactic for PMN. The bacterial chemotactic factor produced a 45 to 75% decrease in the initial rate of ingestion, but did not affect adherence of the EAC1423 and PMN. This same substance had no consistent effect on the total number of EAC1423 ingested at 90 min or longer or on the time interval from the addition of the EAC1423 to the start of ingestion. The inhibitory effect of the bacterial factor increased as the amount of bacterial factor was increased and the inhibitory effect was reversible. Inhibition by bacterial factor could be decreased by increasing the concentration of EAC1423; and if the concentration was increased 3-fold, the inhibition was abolished. These results suggest that inhibition by bacterial factor is competitive in nature.
Requirements for Induction of T Cell Tolerance to Dnfb: Efficiency of Membrane-Associated DNFB
Authors: Claman Henry N. , Miller Stephen D. 
Published: December 2022

Abstract
Tolerance to contact sensitization with DNFB,3 a T cell-dependent phenomenon, was induced in mice by preparations of DNFB coupled to mouse RBC or spleen cells. Such tolerance is dose related, wanes with time, and can be transferred to normal animals with lymphoid cells (presumably containing suppressors). Tolerance to DNFB-RBC can be produced by whole DNFB-RBC, by ghosts of these cells, by sonicates of the ghosts, and by detergenttreated DNFB-RBC ghosts. Tolerance cannot be produced by larger amounts of DNFB-RBC components not associated with membrane. The ability of various DNP compounds to stimulate DNA synthesis in DNFB-sensitized cells also correlates with their ability to bind to protein components; i.e., DNFB is a far more efficient stimulator than DNBSO3, whereas DNP-lysine does not stimulate at all. Thus, the ability to sensitize or to tolerize with DNFB congeners is related to their ability to couple to proteins. It appears that the active induction of T cell tolerance requires that tolerogen be coupled to cell membranes. Since both T cell sensitization and tolerance to DNFB are best produced by DNFB-membrane, the actual occurrence of one state or the other must depend on the molecular method of “presentation” of DNFB-membrane.
Isolation of a Murine Leukemia Fc Receptor by Selective Release Induced by Surface Redistribution
Authors: Cooper Sheldon M. , Sambray Yugalkishore 
Published: December 2022

Abstract
A protein which binds to the Fc region of IgG has been isolated from the murine leukemia L1210. The isolation technique involves surface cross-linking of the cell's Fc receptors with the use of aggregated human IgG and anti-human IgG. This results in the redistribution (patch formation and capping) of the cell's Fc receptors. Lactoperoxidase-catalyzed radioiodination of the cells before complex binding indicates that Fc receptor redistribution results in the selective release of surface proteins. SDS-PAGE analyses of the supernatants from cells thus treated reveals a major peak corresponding to a molecular weight of 45,000 daltons. This protein has been purified from the cell supernatants by immunoprecipitation and chromatography of the percipitates on Sephadex G-200 under dissociating conditions. After separation from the immune complex this protein can be bound to heat-aggregated IgG, but not aggregated F(ab′)2 fragments. The 45,000 dalton protein appears to be the Fc receptor which has been released from the cell surface in association with the complex.
Mechanisms Involved in Elimination of Organisms from Experimental Cutaneous Candida Albicans Infections in Guinea Pigs
Authors: Sohnle Peter G. , Frank Michael M. , Kirkpatrick Charles H. 
Published: December 2022

Abstract
Experimental cutaneous Candida albicans infections were produced in guinea pigs either by using occlusive dressings over the organisms or by applying them to the shaved skin directly without occlusive dressings. In either model there was clearance of the infecting organisms from the skin by a process involving profuse scaling of the keratinized layer in which they were confined. However, for each type of infection the mechanisms producing this scaling seemed to involve different parts of the host defense system.
Infections produced under occlusive dressings were characterized by a rapid accumulation of polymorphonuclear leukocytes (PMN) in the epidermis and formation of thick crusts in which organisms were trapped. Sloughing of the crust removed the organisms. In this model, evolution of the lesions and the rate of clearance of the organisms did not depend on prior immunity to Candida. Two possible mechanisms for attraction of PMN into the lesions were direct activation of the alternative complement pathway by the organisms in the lesions and direct chemotactic activity in components of Candida albicans.
In contrast, infections produced without occlusive dressings showed only minimal epidermal PMN infiltration, but also underwent profuse scaling of the keratinized layer. This response appeared to depend on cell-mediated immunity. Only animals with previously-acquired delayed hypersensitivity to Candida antigens could undergo this type of scaling, and, indeed, this response was transferable to nonimmune animals with peritoneal exudate cells from Candida-immune animals. Clearance of the infecting organisms from this type of infection was significantly faster in immune than in nonimmune animals. It is postulated that a lymphokine released from lymphocytes in the upper epidermis acts on epidermal cells to increase the rate of keratin turnover either by increasing the mitotic rate of the germinal cells or by increasing their rate of keratinization.
Cellular Specificity of Plasmacytoma-Induced Immunosuppression
Authors: Zolla-Pazner Susan , Sullivan Bessie , Richardson Deborah 
Published: December 2022

Abstract
The pattern of immunodeficiency in plasmacytoma-bearing mice appears to be unique. Mice bearing these tumors exhibit a severe impairment in their ability to mount a primary immune response to thymus-dependent and -independent antigens. However, cell-mediated immune functions in these mice apparently remain intact. Thus, when T cell activity of lymph node cells from plasmacytomabearing mice was tested in vivo by sensitization with dinitrofluorobenzene and in vitro by responsiveness to phytohemagglutinin, allogeneic cells, and dinitrobenzene sulfonate, cell-mediated immunity was found to be normal.
Histamine Release by Chemotactic, Formyl Methionine-Containing Peptides
Authors: Hook William A. , Schiffmann Elliott , Aswanikumar Srinivasabhat , Siraganian Reuben P. 
Published: December 2022

Abstract
Certain formyl dipeptides and tripeptides containing methionine released histamine from human basophils at concentrations of 10-4 to 10-7 M. However, N-formyl amino acids did not release histamine. Tripeptides, in general, were more active than dipeptides. An acyl group was required for histamine release although an N-terminal position for Met was not essential. Histamine release from human basophils by these peptides correlated well with their chemotactic activity for rabbit leukocytes.
Altered Lymphocyte Functions in Rats Bearing Syngeneic Moloney Sarcoma Tumors
Authors: Veit Bruce C. , Feldman Joseph D. 
Published: December 2022

Abstract
Impairment of mitogen responses to Con A and LPS and of MLR and MLTR was detected in the spleens of rats bearing syngeneic Moloney sarcoma tumors. Depressed responses of both T cell and Ig+ cell populations were observed. During the observation period of 6 to 10 days post-tumor inoculation when maximal T cell-mediated cytotoxicity was observed in spleen and draining lymph node cells, spleen cells showed marked impairment in response to stimuli mentioned above. By contrast, draining lymph node cell activity was either unaltered or somewhat elevated above the level of activity measured in normal control populations. Data presented in this and an accompanying paper strongly indicate that macrophages are activated as immunosuppressor cells in tumor-bearing rats.
Altered Lymphocyte Functions in Rats Bearing Syngeneic Moloney Sarcoma Tumors
Authors: Veit Bruce C. , Feldman Joseph D. 
Published: December 2022

Abstract
Spleens from tumor-bearing rats contained a population of adherent cells that suppressed lymphocyte responses to Con A and LPS and cell-mediated cytotoxicity (CMC). By use of various fractionation procedures, Ig+ cells, T cells, and null cells were excluded as candidates for the suppressor cell activity. Procedures that removed macrophages abolished the suppressive activity whereas those procedures that enriched for or involved direct addition of macrophages resulted in augmented suppression. On the basis of these results, we conclude that the suppressor elements in spleens of tumor-bearing rats were macrophages.
The Homologues of Rabbit b-Allotypes on Hare Immunoglobulin Light Chains: An Evolutionary Puzzle
Authors: Tosi Simonetta Landucci , Mage Rose G. , Tosi Roberto M. 
Published: December 2022

Abstract
Most alloantisera directed against the rabbit allotypes b4, b5, and b6 cross-reacted with hare IgG. The determinants recognized by antisera against the three allotypes were shown to reside on the same hare L chains. Hare immunoglobulins, when injected into b4, b5, or b9 rabbits, elicited the formation of antibodies which reacted with hare IgG and cross-reacted with those rabbit allotypes (except b9) absent from the recipient. The anti-b9 antisera tested lacked reactivity with hare IgG.
Deficient Production of a Thymus-Dependent High Affinity Antibody Subset in Mice (CBA/N) with an X-linked B Lymphocyte Defect
Authors: Gershon Richard K. , Kondo Kazunari 
Published: December 2022

Abstract
Since the original demonstration by Amsbaugh et al. (1) that a sub-line of CBA/H (CBA/N) mice has a recessive X-linked genetic defect which prevents them from responding to type III pneumococcal polysaccharide this sub-line of mice has come under intensive study, particularly by Scher and his colleagues (2–9). These workers have established that the X-linked defect is expressed in B cells (4) and that by a number of criteria the T cells of the mice with the defect are indistinguishable from those of appropriate control mice (4). They have further shown that the defect preferentially inhibits the response to so called “thymus-independent antigens” (1, 2, 5, 9); it leads to a much smaller deficit in the response to “thymus-dependent antigens”. CBA/N B cells are intrinsically defective and are not influenced by the environment in which they reside (4, 9). The defect can best be explained as a failure of maturation or differentiation in that it has been shown that adult CBA/N mice lack a population of B cells which is also lacking in young (but not mature) normal mice (6, 7).
Genetic Control of the Immune Response in Guinea Pigs to the Known Sequence Polymer (Tyr-Ala-Glu-Gly)n
Authors: Zeiger Allen R. , Maurer Paul H. 
Published: December 2022

Abstract
The genetic control of the immune response to randomly polymerized polypeptides containing amino acids such as glutamic acid, alanine, and tyrosine is now well established in inbred guinea pigs (1, 2). Recent advances in the field of peptide chemistry now make possible the synthesis of polypeptides of similar amino acid composition but with defined amino acid sequences. Studies with these polymers may yield information on the specificity of the genetic control at the molecular level.
We have reported the synthesis of (Tyr-Glu-Ala-Gly)n of 53,000 m.w. (3). Under physiologic conditions, it exists primarily in the α-helical configuration and is immunogenic in some Hartley guinea pigs and in inbred strain 13 guinea pigs, but not in strain 2 guinea pigs (4).
We have recently synthesized a polymer of similar amino acid composition but with a different sequence, (Tyr-Ala-Glu-Gly)n, of 33,000 m.w. and have shown that it too is α-helical under physiologic conditions (Zeiger and Maurer, manuscript in preparation).
Bence Jones Proteins and Light Chains of Immunoglobulins
Authors: Solomon Alan , Schmidt Wilhelm , Havemann Klaus 
Published: December 2022

Abstract
Bence Jones proteins can be cleaved specifically by several types of endopeptidases into fragments corresponding to the amino-terminal, variant (VL) portion and to the carboxyl-terminal, constant (CL) portion of the light polypeptide chain. Two types of neutral proteases, designated elastase-like (ELP) and chymotrypsin-like (CLP), have been isolated and purified from human polymorphonuclear leukocytes. Because these proteases have defined proteolytic activity under physiologic conditions for several types of human proteins, we investigated their effect on human Bence Jones proteins. Incubation of κ-type or λ-type Bence Jones proteins with ELP or CLP under appropriate conditions resulted in cleavage of both types of light chains as evident by immunochemical and electrophoretic analyses. Treatment with ELP or CLP of one κ Bence Jones protein resulted in the formation of a single component that had antigenic and electrophoretic properties similar to the VL fragment derived from pepsin digestion of the native protein. No component corresponding to the CL could be detected immunochemically or electrophoretically. Studies of isolated pepsin-labile (37°C) and pepsin-stable (55°C) CL fragments demonstrated the marked susceptibility of the carboxyl-terminal half of the light chain to proteolysis by the leukocyte-derived neutral proteases. Incubation with ELP of three other κ Bence Jones proteins and three reduced-alkylated λ Bence Jones proteins resulted, in each case, in the formation of a homogeneous component which was electrophoretically and immunochemically distinct from the pepsin-derived VL fragment. An identical component could also be formed by incubating a pepsin-derived VL fragment with ELP. In the ELP-treated samples, no CL-related material was detected electrophoretically or immunochemically with antisera possessing specificity for CL antigenic determinants present on the unfolded light polypeptide chain or on the isolated CL. The component formed by ELP or CLP treatment of certain Bence Jones proteins thus appears to be VL-related, but lacks the idiotypic antigenic determinant present on the native protein. In this respect, these neutral protease-derived light chain components are similar to the amyloid-like VL fragments generated in vitro from certain endopeptidase-treated Bence Jones proteins.