bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhancement of Human Eosinophil Complement Receptors by Pharmacologic Mediators
Authors: Anwar A. R. E. , Kay A. B. 
Published: December 2022

Abstract
With the rosette technique, the ECF-A tetrapeptides (Val-Gly-Ser-Glu and Ala-Gly-Ser-Glu) and histamine, agents previously shown to be preferentially chemotactic for the eosinophil, markedly enhanced the expression of human eosinophil receptors for C3b. The enhancement was both dose- and time-dependent, and highly selective for the eosinophil since there was no evidence that C3b receptors on neutrophils or monocytes were altered by these pharmacologic agents even when varying concentrations of C3 were added to the indicator red cells. The agents similarly enhanced receptors for C4, but under the same conditions C3d and IgG (Fc) receptors were unaffected.
A number of other pharmacologic mediators including bradykinin and the prostaglandins PGE1, E2, and F2α had no apparent effect on eosinophil C3b receptors at the same molar concentrations (5 × 10-5 to 5 × 10-7 moles 1-1). However, a major histamine catabolite, imidazoleacetic acid, also recognized as an anaphylaxis-associated eosinophilotactic agent, enhanced eosinophil C3b receptors to a degree comparable to that of histamine. In contrast, l-histidine and the histamine catabolites, N-acetylhistamine, 1,4-methylhistamine, and 1-methyl-4-imidazoleacetic acid, had no eosinophil C3b receptor-enhancing effect. 5-hydroxytryptamine at the highest concentration tested (5 × 10-5 moles 1-1) gave enhancment of eosinophil C3b receptors which was approximately one-third of that achieved with the same concentration of the ECF-A peptides, histamine, or imidazoleacetic acid.
A human lung anaphylactic diffusate also enhanced eosinophil C3b receptors. Approximately 10 times more synthetic histamine than that contained in the lung-derived material was required for comparable enhancement, indicating that the histamine and ECF-A peptides present in the diffusate may have combined to give optimal enhancing effect. However, when synthetic histamine and the valyl- or alanyl-peptide, were mixed in various proportions, the enhancement was no greater than that achieved when each agent was tested alone.
These results suggest that pharmacologic mediators of hypersensitivity may regulate certain eosinophil-dependent biologic reactions and that there may be a direct relationship between the cell surface “recognition unit” for eosinophil locomotion and some of the membrane receptors that promote the adhesion of eosinophils to opsonized particles.
Regulation of Human Lymphocyte Function by a Soluble Extract from Normal Human Liver
Authors: Chisari Francis V. 
Published: December 2022

Abstract
The blastogenic and DNA synthetic response of human peripheral blood lymphocytes (PBL) to phytohemagglutinin (PHA) and allogeneic cells can be inhibited by a nontoxic aqueous extract (LEx) of normal human liver. LEx reversibly inhibits the activation of PBL by PHA, arrests ongoing DNA synthesis, and limits the duration of the DNA synthetic response to PHA at concentrations as low as 0.7 to 1.5 µg LEx protein/culture. In contrast, human T lymphocyte E rosette formation is unaffected by LEx concentrations in excess of 900 µg/culture. LEx has been partially purified by ultracentrifugation, ammonium sulfate precipitation, and molecular exclusion chromatography and appears to be a heat labile protein with a m.w. of approximately 65,000 and an isoelectric point of approximately 4.08. LEx is distinct from other previously described human immunoregulatory molecules and is potentially releasable in vivo from injured or necrotic liver cells. Because of its potency and anatomic distribution LEx may potentially modulate immunopathogenetic events responsible for assorted inflammatory and neoplastic liver diseases.
Estimates of the Precursor Frequency of Cytotoxic T Lymphocytes against Antigens Controlled by Defined Regions of the H-2 Gene Complex: Comparison of the Effect of H-2 Differences Due to Intra-H-2 Recombination VS Mutation
Authors: Pimsler Meade , Forman James 
Published: December 2022

Abstract
Lymph node cells were sensitized in a limiting dilution assay against B10.D2 (H-2d) and the frequency of cytotoxic T lymphocyte (CTL.P) precursors was determined. A mean CTL.P frequency of 0.047% was observed when responding strains differed from the stimulators at the entire H-2 gene complex. When intra-H-2 recombinant strains were sensitized against B10.D2, lower frequencies of CTL.P were observed. Responding strains that differed from the stimulators at the H-2K-end only had 2- to 6-fold more CTL.P compared to strains sensitized against the D-end only.
In order to study the CTL.P frequency against minor antigenic differences, the B10.D2 (M504-H-2da) mutant strain, which carries a mutation with an antigenic gainloss in the D-region of H-2d, was examined. This mutant showed an identical CTL.P frequency against H-2d as H-2D-end recombinant strains. Therefore, this H-2 mutant (M504) has either undergone extensive mutation or the qualitative nature of the antigenic loss in this strain results in a high CTL.P frequency against the strain of origin.
IgG Antibodies Produced by Heterozygous a1a3 Rabbits Responding to Acidic Azohaptens Are Predominantly of Allotype a1
Authors: Chien Chau-Chun , Ingraham Joseph S. 
Published: December 2022

Abstract
Rabbits of allotype a1a3 were immunized with one of three acidic hapten-bovine serum albumin (BSA) conjugates: p-azophenyl arsonate (AA)-, p-azophenyl sulfonate (SA)-, or p-azobenzoate (CA)-BSA; all animals also received the basic conjugate, p-azophenyl-N-trimethyl-ammonium (TMA)-BSA. After 6 to 12 months, each animal was challenged with the same combination of BSA conjugates as given originally. The allotype of the plaque-forming cells (PFC) from lymph nodes and spleen was determined by enhancement with anti-allotype antisera. PFC detected upon addition of anti-a1 were designated a1-PFC and those detected with anti-a3 were designated a3-PFC. Results were expressed as the ratio of a1-PFC to a3-PFC. For the basic hapten, TMA, this ratio was 0.2 to 1.0 for nine lymph nodes and 0.3 to 1.6 for seven spleens. In contrast, the ratio for the acidic haptens was much higher: for AA, from 4 to 16 in three lymph nodes and 24 to 87 in two spleens; for SA, from 4 to 114 in three nodes and 38 to 59 in two spleens; for CA from 13 to 130 in two nodes and 4 to 33 in three spleens. Analogous use of anti-allotype sera for enhancement of anti-acidic hapten hemolytic serum titers showed that anti-a1 gave 8 to 16 times the enhancement given with anti-a3. Thus, the results indicate that the a1a3 rabbits made little or no antibody of allotype a3 during the secondary response to these acid haptens.
Kinetic Analysis of Antibody-Dependent Cellular Cytotoxicity: Evidence for Noncompetitive Inhibition by Autologous Lymphoid Cells
Authors: Herrick Michael V. , Pollack Sylvia B. 
Published: December 2022

Abstract
Inhibition of antibody-dependent cellular cytotoxicity (ADCC) by autologous lymphocytes was analyzed by using classical techniques for enzyme-substrate interactions. We determined empirically that the interaction of murine spleen cells with antibody-coated targets to produce lysis was analogous to the interactions that have been described for an enzyme with its substrate. Varying numbers of antibody-coated target cells (“substrate”) were mixed with a constant number of spleen cells (“enzyme”) and the number of target cells killed (“product”) was measured as a function of time. By analogy with Michaelis-Menten enzyme kinetics, two parameters of the reaction were determined: Vmax, the maximum velocity of lysis that is proportional to the number of killer cells present, and K½, an intrinsic property of the killer cells. These parameters were found to be independent variables. Addition of autologous lymph node cells produced a dose-dependent decrease in Vmax whereas K½ was not significantly changed. By analogy with enzyme kinetics, this inhibition is noncompetitive, suggesting that the autologous lymphocytes inactivate the killer cells rather than competing for the cell-cell binding sites.
Liposomes As Model Membrane Systems for Immune Attack
Authors: Ozato Keiko , Ziegler H. Kirk , Henney Christopher S. 
Published: December 2022

Abstract
The interaction of human peripheral blood lymphocytes with liposomes containing DNP-aminocaproylphosphatidylethanolamine together with either egg yolk or dipalmitoylphosphatidylcholine has been investigated. When lymphocytes were incubated with liposomes at 37°C, the aqueous compartment (86Rb+) and the lipid portion (3H-lipid) of the liposomes became cell associated to an equivalent extent. At 0°C, however, the incorporation of 3H-lipid exceeded that of 86Rb+. Lymphocyte-liposome interactions were accompanied by the transfer of DNP to the surface of the lymphoid cell as measured by susceptibility to complement in the presence of anti-DNP antibody. Hapten transfer was not limited to liposome interactions with lymphocytes, but occurred also with other cells (e.g., Chang cells). Hapten transfer could also be demonstrated by susceptiblity to K cell-mediated lysis. These findings suggest that liposomes may prove to be a useful vehicle for the transfer of new antigenic determinants onto cell surfaces. The implications of these findings are discussed in the context of using liposomes as targets for cell-mediated cytotoxic attack.
The Importance of an Intact Complement Pathway in Recovery from a Primary Viral Infection: Influenza in Decomplemented and in C5-Deficient Mice
Authors: Hicks John T. , Ennis Francis A. , Kim Elizabeth , Verbonitz Martha 
Published: December 2022

Abstract
To investigate the role of complement (C) in the recovery from a primary viral infection in vivo, the course of influenza infection in decomplemented BALB/c mice and in C5-deficient B10.D2/OSN mice was examined. BALB/c male mice decomplemented with cobra venom factor demonstrated a prolonged viral infection, an increased degree of pulmonary consolidation, and a higher rate of morbidity and mortality than did nondecomplemented mice for each dose of virus administered. This deleterious effect occurred in mice decomplemented before infection and immunologic induction, as well as in mice decomplemented after infection and immunologic induction, provided the C3 levels remained depressed at the time of viral clearance (days 7 to 9). The time of appearance and the levels of serum neutralizing antibodies and viral-specific cytotoxic T cells were equivalent in decomplemented and nondecomplemented BALB/c mice infected with influenza. Similarly, C5-deficient B10.D2/OSN male mice, infected with influenza, demonstrated a prolonged viral infection, an increased degree of pulmonary consolidation and a higher rate of mortality than did C5-sufficient B10.D2/NSN agematched mice for each dose of virus administered. These results suggest than an intact complement pathway plays an adjunctive role in host recovery from primary influenza infection.
Mechanisms of Regulation of Cell-Mediated Immunity
Authors: Bach Bruce Allen , Sherman Linda , Benacerraf Baruj , Greene Mark Irwin 
Published: December 2022

Abstract
We have investigated the induction, transfer, and suppression of delayed-type hypersensitivity (DTH) to the hapten azobenzenearsonate (ABA), using ABA-derivatized spleen cells in mice. It was found that ABA-derivatized syngeneic cells administered subcutaneously induced hapten-specific DTH responses detected by footpad swelling upon challenge with similarly ABA-modified syngeneic cells, but not with syngeneic cells modified with an irrelevant hapten. The footpad response was determined to be a manifestation of cell-mediated immunity (CMI) from the time course of the reactivity, the characteristic histology, and the results of adoptive transfer experiments. Negative selection experiments with anti-Thy 1.2 antiserum and complement demonstrated that the response was thymic dependent (T) and was transferable to naive recipients by immune T cells but not by immune sera. The induction and elicitation of the response required, minimally, identity at the I-A region of the H-2 major histocompatibility complex (MHC) between the immunizing hapten-modified cell and the recipient. Further studies revealed that syngeneic ABA-modified adherent cells were more capable of inducing ABA-specific DTH responses than similarly derivatized nonadherent cells. Studies dealing with the presentation of hapten with (BALB/c × A/J)F1 derivatized cells as immunogens indicated that F1 immune mice appeared to respond preferentially to BALB/c hapten cell surface conjugates rather than A/J cell surface as assessed by challenge of F1 immune mice with modified parental cells of either type.
In adoptive transfer experiments it was found that immune T cells could transfer reactivity if, and only if, the immune T cells, the recipient, and the challenging modified cell were syngeneic or semisyngeneic. Allogeneic transfers were unsuccessful, even when the priming cells, the immune T cells, and challenge were syngeneic, but the recipient was not. The apparent failure of allogeneic transfer was not due to the presence of suppressor cells.
Finally, we were able to elicit suppressor T cells by the i.v. administration of ABA-modified syngeneic cells. ABA-specific suppressor T cells limit the generation of DTH to ABA-modified cells, but do not decrease DTH to cells modified with an irrelevant hapten.
Cellular and Genetic Control of Antibody Responses in Vitro
Authors: Hodes Richard J. , Ahmann Gerald B. , Hathcock Karen S. , Dickler Howard B. , Singer Alfred 
Published: December 2022

Abstract
The expression of Ia antigens by accessory cells participating in in vitro primary antibody responses, including responses under Ir gene control, has been investigated. The ability of radiationresistant, non-T, non-B, spleen-adherent cells to function as accessory cells has been demonstrated both for the Ir gene-controlled response to TNP-(T,G)-A--L and for the response to TNP-KLH, for which no Ir gene control has been demonstrated. Pretreatment of these adherent accessory cells with anti-Ia reagents and complement totally abrogated the accessory function of this population for responses to both antigens. This abrogation of accessory function resulted from the elimination of accessory cells, rather than from any active suppression of responsiveness, either by carry-over of anti-Ia antibody or antigen-antibody complexes. By using appropriate recombinant strains and specific anti-Ia reagents, it has further been demonstrated that Ia determinants encoded in at least two I subregions, I-A and I-E/C, are expressed on accessory cells for responses to TNP-KLH and TNP-('T,G)-A--L; and that determinants encoded in at least two I subregions are expressed simultaneously on the same cells. The data presented also suggest that the functionally active Ia-positive accessory cell is itself either nonphagocytic or constitutes a subpopulation of phagocytes expressing Ia antigens encoded in at least two I subregions.
In Vitro Studies of the Rabbit Immune System
Authors: Redelman Doug , Trefts Park E. 
Published: December 2022

Abstract
Xenogeneic rabbit anti-mouse cell-mediated cytotoxic activity could be generated by culturing lymphoid cells from mesenteric lymph nodes (MLN), spleen, or peripheral blood of rabbits primed 2 to 8 weeks earlier with mouse tumor or spleen cells. MLN cells, which provided the best source of activity after being cultured with 5 to 10 × 106 mitomycin C-treated mouse spleen cells for 4 to 6 days, produced 30 to 90% specific isotope release after 4 to 7 hr incubation with 15Cr-labeled tumor target cells. Xenogeneic cytotoxic activity was primarily H-2 specific and could not be blocked by immune complexes but was abrogated by treatment with goat anti-rabbit thymocyte serum plus complement (ATS + C) before or after culture. Therefore, the activity appeared to be mediated by cytotoxic T lymphocytes (CTL). Furthermore, ATS without C abrogated cytotoxic activity when included in the CTL assay at concentrations of 5 to 15 µl/107 effector cells. The inhibitory activity of ATS was directed to the rabbit effector population and could be adsorbed completely by rabbit thymocytes. Antisera to mouse T cells with comparable cytolytic activity in the presence of C did not inhibit murine allogeneic CTL.
Studies on the Mechanism of Lymphocyte-Mediated Cytolysis
Authors: Green William R. , Ballas Zuhair K. , Henney Christopher S. 
Published: December 2022

Abstract
The role of lectin in lectin-dependent cell-mediated cytolysis has been pursued by using alloimmune C57BL/6 spleen cells as a source of effector cells and EL4 lymphoma cells, syngeneic to the effector, as targets. Of a variety of lectins studied, in this system, only the T cell mitogens concanavalin A (Con A), Lens culinaris hemagglutinin A, and leucoagglutinin derived from phytohemagglutinin were able to support cytolysis. Agglutinating agents that were not mitogenic, such as wheat germ agglutinin or antisera against the interacting cells, did not promote cytolysis. B cell mitogens were similarly unable to support lysis even when co-incubated with agglutinating agents.
The role of the T cell mitogens in lectin-dependent cytolysis appeared to be 2-fold: “activation” of the effector cell to express its cytotoxic potential and “bridging” of the effector cell to its target. These conclusions were based on the findings that: a) agglutination of target cells to T effector cells, although necessary to elicit cytolysis, was in itself insufficient, and b) T cells “activated” by mitogen under conditions which precluded cell-cell bridging did not lead to lysis.
Furthermore, we could find no evidence that the bridging function of the lectin during cytolysis could be served by agents other than T cell mitogens. This might explain our finding that the Ca++ ionophore A23187, which others have shown to substitute for Con A in the early stages of a mitogenic response, but which does not cause cell agglutination, did not mediate cytolysis, even in the presence of nonmitogenic agglutinins.
These findings of stringent requirements for both the “activating” and “bridging” roles of lectin during cytolysis necessitate radical revision of previous notions that the lectins serve merely as a “glue.”
Biosynthesis of the First Component of Complement by Human and Guinea Pig Peritoneal Macrophages: Evidence for an Independent Production of the C1 Subunits
Authors: Müller Wolfgang , Hanauske-Abel Hartmut , Loos Michael 
Published: December 2022

Abstract
The first component of complement, C1, was produced by human as well as guinea pig macrophages. Supernatants from serum-free cultured macrophage monolayers, tested separately for C1q and C1 activity, showed a ratio of 15:1, respectively, and a different time course of C1q and C1 production, indicating that the subcomponents of C1 are synthesized independently. Heat-inactivated fetal calf or guinea pig serum (2 hr, 56°C), added to the culture medium, were found to be inhibitory for C1 but not for C1q activity, obviously due to still active C1 inhibitor in these sera. De novo synthesis was confirmed by reversible inhibition of C1 and C1q production by cycloheximide (0.5 µg/ml) and puromycin (1 µg/ml), by incorporation of radiolabeled amino acids into the C1s subcomponent, and by uptake of incorporated radioactivity by EA, which was sensitive to EDTA. In additional experiments, 2,2′-dipyridyl markedly reduced C1q and also C1 secretion in the supernatants. Inhibition of the prolyl and lysyl hydroxylation and, as a consequence, structural instability of the collagenous region in the C1q molecule, is discussed as the cause of this effect which is analogous to collagen biosynthesis.
Immunologic Characterization of Tumor-Associated Transplantation Antigens on MM102 Mammary Tumor Eliciting Preferentially Helper T Cell Activity
Authors: Fujiwara Hiromi , Aoki Hisakazu , Tsuchida Tetsuo , Hamaoka Toshiyuki 
Published: December 2022

Abstract
The immunologic nature of tumor-associated transplantation antigens (TATA) of MM102 mammary tumor that originated spontaneously in C3H/He (H-2k) mice was analyzed. The TATA of MM102 tumor have been demonstrated in our laboratory to induce preferential generation of helper T cell activity without any significant killer T cell generation. The helper T cells that were generated by the immunization of syngeneic C3H/He mice with MM102 tumor and specifically reactive to the TATA of MM102 tumor were also reactive with the cellsurface antigens present on the normal or malignant lymphoid cells of allogeneic C57BL/6 (B6) and C57BL/10 (B10) mice. The reactivities of such TATA-reactive helper T cells were eventually the same irrespective of whether those lymphoid cells are derived from B10 (H-2b) mice or B10.BR (H-2k), the congenic strain of the same B10 background. Furthermore, in addition to the fact that the immunization of C3H/He mice with those lymphoid cells could induce the resistance against the challenge with viable MM102 cells, C3H/He mice that had been neonatally rendered tolerant to B10.BR could not develop the immune resistance against MM102 tumor.
These results clearly indicate that TATA of MM102 tumor are closely similar or identical to the non-H-2 antigens of allogeneic B10 mice on the level of helper T cell recognition, and that those non-H-2 alloantigens are capable of acting as the adequate transplantation antigens required for the effective induction of immune resistance against MM102 tumor.
Heterogeneity of I-J Subregion Gene Products: Their Expression on Functionally Different Subsets of T Cells
Authors: Tada Tomio , Okumura Ko , Tokuhisa Takeshi , Nonaka Makoto , Taniguchi Masaru 
Published: December 2022

Abstract
I-J subregion was originally identified by a locus, Ia-4, which controls a cell surface molecule on suppressor T cells (Ts). By the occurrence of two pairs of recombinants, B10.A(3R) and B10.A(5R), and B10.S(9R) and B10.HTT, which differ in the haplotype origin of Ia-4, I-J subregion was defined as a segment intercalated between I-B and I-E subregions. It has been shown that the suppressive T cell factor (TsF) is derived from Lyt-2+, 3+ T cells and can be absorbed by anti-I-J antisera. The acceptor site for the TsF on Lyt-1+, 2+, 3+ cells is also blocked by anti-I-J. A question remains to be solved as to whether or not the TsF and acceptor are coded for by the same locus. Moreover, we have recently shown that some but not all helper T cells carry determinants coded for by genes in I-J subregion.
Chemical Characterization of Rat Ia Antigens
Authors: Blankenhorn Elizabeth P. , Cecka Michael , Götze Dietrich , Hood Lee 
Published: December 2022

Abstract
Ia antigens from two inbred strains of rats have been characterized by two-dimensional gel (IEF/SDS PAGE) and microsequence analysis. Rat Ia antigens are isolated from biosynthetically radiolabeled spleen cells using semicongenic alloantisera. Rat Ia antigens are composed of two components on SDS-PAGE as are their mouse, human, and guinea pig counterparts. The larger polypeptide (α) has an apparent molecular weight of 33,000. The α polypeptides of AgB3 and AgB4 haplotypes show striking homology in their partial N-terminal amino acid sequences to the mouse ECαk and ECαd polypeptides and to human P34. The rat B3 and B4 α polypeptides are identical at six of eight positions which can be compared. The smaller polypeptide (β) has an apparent molecular weight of 28,000. Preliminary data on the β polypeptides suggest the existence of multiple molecular species for each haplotype. Sequences resembling mouse IA-β and I-EC-β polypeptides may be present.