bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cross-reactive cellular and humoral immunity to carcinogen-induced chicken fibrosarcomas. I. Protective cross-immunity between transplantable tumor lines.
Authors: Edelman A S , Xue B , Sanchez P , Thorbecke G J 
Published: December 2022

Abstract
Dimethylbenz[a]anthracene (DMBA)-induced transplantable fibrosarcomas in B2 homozygous chickens (SC line) grow progressively in normal chickens, but are rejected by chickens immunized previously with irradiated tumor cells and Corynebacterium parvum. Tumor-immune chickens resist challenge by the immunizing tumor lines as well as by some, but not all, fibrosarcoma lines. The pattern of cross-reactivity between four DMBA-induced transplantable tumor lines was examined in detail. Ability to reject a tumor challenge correlated very well (p less than 0.001) with the presence of delayed-type hypersensitivity (DTH) to that tumor. Immunization with one of two of the DMBA-induced lines tested also caused rejection of transplantable tumors developed from methylcholanthrene-induced and benzo(a)pyrene-induced primary fibrosarcomas. Although immunization with tumor caused DTH to chicken embryo fibroblasts (CEF), immunization with CEF failed to cause protective immunity or DTH to tumors. Presence of protective immunity, where tested, also correlated with the ability of spleen cells from immune donors to inhibit tumor growth in Winn tests. Humoral immunity exhibited even greater cross-reactivity than did cellular immunity. Distinct patterns of cross-reactivity were nevertheless observed with respect to the serum antibodies as detected in ELISA. Two of these patterns were also observed in several sera from primary tumor-bearing chickens, both including reactivity with CEF. Such reactivity was absent from normal chicken sera.
Regulatory role of a monomorphic determinant of HLA Class I antigens in T cell proliferation.
Authors: Turco M C , De Felice M , Corbo L , Morrone G , Mertelsmann R , Ferrone S , Venuta S 
Published: December 2022

Abstract
The role of HLA Class I antigens in T cell proliferation was investigated by using the anti-HLA Class I monoclonal antibodies (MoAb) CR10-215, CR10-325, and CR11-115. MoAb CR10-215 and CR11-115 recognize the same (or spatially close) monomorphic determinant, which is distinct and spatially distant from that reacting with MoAb CR10-325. Addition of MoAb CR10-215 and CR11-115 to cultures of peripheral blood mononuclear cells stimulated with MoAb OKT3, MoAb Pan T2, PHA, or PPD inhibited cell proliferation. The blocking is specific in that the anti-HLA Class I MoAb CR10-325 and the Pan T MoAb Pan T1 had no effect on the proliferation. The inhibitory activity of MoAb CR10-215 and CR11-115 does not reflect i) toxic effects, ii) induction of suppressor cells and factors, iii) blocking of the binding of mitogens to lymphocytes, iv) inhibition of the production of interleukin 1 (IL 1) and interleukin 2 (IL 2), or v) function of IL 2 receptor. Anti-HLA Class I MoAb were able to inhibit the proliferation of purified, Tac-, T cells. The inhibited cells did not express Tac antigen, as assayed by direct immunofluorescence, with MoAb anti-Tac, but released a normal amount of IL 2 in culture medium. These results indicate that monomorphic determinants of the HLA Class I complex are involved in the regulation of T cell proliferation. The effect appears to occur at the level of IL 2 receptor expression.
Antibodies to Tp67 and Tp44 augment and sustain proliferative responses of activated T cells.
Authors: Ledbetter J A , Martin P J , Spooner C E , Wofsy D , Tsu T T , Beatty P G , Gladstone P 
Published: December 2022

Abstract
We have shown previously that binding of a monoclonal antibody (MAb) to Tp44 molecules increased the proliferation of anti-CD3-activated T cells by causing enhanced IL 2 receptor expression and IL 2 release. We now show that anti-CD5 (Tp67) antibodies have a similar effect under conditions in which monocytes are suboptimally activated or where monocytes are not present. The activity did not depend on antibody isotype or on the precise CD5 epitope recognized. Functional experiments indicated that both IL 2 production and IL 2 receptor expression were enhanced by antibody binding. Anti-Tp67 and anti-Tp44 appear to augment proliferation through distinct mechanisms, because both antibodies together had greater activity than either antibody alone. In neither system is the Fc portion of the antibody required, because F(ab')2 fragments had activity equivalent to that of the intact antibody and were effective at concentrations as low as 10 ng/ml. Fab fragments of anti-Tp67 were active, but Fab fragments of anti-Tp44 had no effect. Anti-Tp67 and anti-Tp44 were able to sustain continuous proliferation of anti-CD3-Sepharose-stimulated T cells for up to 2.5 wk without exogenous IL 2 or feeder cells. These experiments suggest that Tp67 and Tp44 are receptors that play a critical regulatory role in the control of T cell proliferation.
Cutaneous mast cell depletion results from topical corticosteroid usage.
Authors: Lavker R M , Schechter N M 
Published: December 2022

Abstract
The effect of long-term topical application of corticosteroids on human cutaneous mast cells was examined. Two potent corticosteroids, clobetasol-17-propionate and fluocinonide, produced a greater than 85% decrease in histamine content over a 6-wk treatment period, whereas betamethasone valerate, a less potent corticosteroid, produced a 66% decrease. Electron microscopic examination of the biopsies taken from sites after 6 wk of treatment indicate that the reduced levels of histamine were caused by the depletion of mast cells, as evidenced by: the inability to identify any cells representative of mast cells by detailed electron microscopy of the biopsies; and the marked acellularity around the vasculature where mast cells are certain to be detected. Histamine levels did not begin to decline until after 3 wk of corticosteroid treatment, indicating that corticosteroids are not immediately harmful to mast cells. Electron microscopic examination of biopsies taken at the beginning of treatment and 1 wk later showed normal-appearing mast cells, whereas at 3 wk, a small population of mast cells was detected with features usually associated with degenerating or dying cells. These observations suggest that protracted application of corticosteroids to skin is toxic to mast cells. After discontinuation of treatment, the drug-related atrophy associated with chronic application of potent corticosteroids to skin is rapidly reversed, and skin structure returns to near normal by 14 days. Over this time period, however, histamine levels did not increase and mature mast cells could not be observed by electron microscopy. At 14 days post-steroid treatment, the first signs of cells containing sparse amounts of granules having the characteristics of mast cell granules were seen. We interpret this to represent new mast cells beginning to mature in the skin. By 3 mo, histamine levels returned to normal, demonstrating the reversibility of the steroid-induced mast cell depletion. The studies presented here establish the deleterious effects of long-term topical corticosteroid treatment on cutaneous mast cells, and begin to establish a system in which the development of mast cells in tissue can be investigated.
Activation of tissue macrophages from AIDS patients: in vitro response of AIDS alveolar macrophages to lymphokines and interferon-gamma.
Authors: Murray H W , Gellene R A , Libby D M , Rothermel C D , Rubin B Y 
Published: December 2022

Abstract
To test the hypothesis that tissue macrophages from AIDS patients have no intrinsic defects in either antimicrobial activity or in the capacity to respond to T cell-derived activating stimuli, alveolar macrophages from 11 patients were treated with crude lymphokines produced by healthy donors. After 72 hr of pretreatment with 10% mitogen- or antigen-induced crude lymphokines (which contained 300 U/ml of interferon-gamma [IFN-gamma]), AIDS alveolar macrophages generated twofold to threefold more H2O2 and readily inhibited the replication of the intracellular pathogens Toxoplasma gondii and Chlamydia psittaci. These responses were indistinguishable from those displayed by activated alveolar cells from 12 non-AIDS patients and three healthy volunteers. As judged by the abrogating effects of a neutralizing anti-human IFN-gamma monoclonal antibody, lymphokine-induced alveolar macrophage activation appeared to be largely IFN-gamma-dependent; thus, macrophages were also stimulated with recombinant (r)IFN-gamma alone. Seventy-two hours of treatment with 300 U/ml of rIFN-gamma resulted in both enhanced oxidative and antimicrobial activity comparable to that achieved by crude lymphokines, and the responsiveness of AIDS alveolar macrophages to rIFN-gamma was identical to control cells. These in vitro results suggest that tissue mononuclear phagocytes from AIDS patients a) are free of apparent defects in intracellular antimicrobial activity, b) are fully responsive to activating T cell products, and c) support the use of IFN-gamma as a potential macrophage-activating immunotherapeutic agent in AIDS-related opportunistic infections.
Identification of ribosomal protein autoantigens.
Authors: Francoeur A M , Peebles C L , Heckman K J , Lee J C , Tan E M 
Published: December 2022

Abstract
Approximately 20% of patients with systemic lupus erythematosus and with anti-Sm autoantibodies synthesize autoantibodies, called anti-rRNP, to components of the ribosome. We found that anti-rRNP sera reacted predominantly with three ribosomal phosphoproteins of approximate Mr = 38,000, 16,000 and 15,000, both by immunoprecipitation and by immunoblotting. The human autoantibodies cross-reacted with similar antigens present in rodent, brine shrimp, and yeast cells but reacted weakly if at all with proteins of bacteria. Thus the human autoantibodies recognize epitopes that are widely conserved in evolution. Purified ribosomal proteins together with specific rabbit antisera were used to identify the two smaller rRNP antigens as the acidic phosphoproteins of the large ribosomal subunit, designated P1/P2(L40/L41) (rat), eL7/eL12 (Artemia, brine shrimp), and A1/A2 (yeast). These proteins function in the elongation step of protein synthesis in an analogous fashion to the L7/L12 ribosomal proteins of E. coli. The 38,000-dalton rRNP antigen corresponds to a nonacidic protein also associated with the large ribosomal subunit. The human autoantibodies appear to have a specificity similar to that of a previously described mouse monoclonal antibody obtained from mice injected with heterologous (chick) ribosomes, suggesting that both the human polyclonal autoantibodies and the mouse monoclonal recognize a class of epitope(s) that is common in all three ribosomal proteins. In addition, we found that many of the anti-ribosomal sera contained a further class of autoantibodies reactive with naked RNA. These may be similar to the anti-RNA antibodies previously described in both humans and mice with autoimmune disease.
Allogeneic leukocyte and germ cell-induced murine immunodeficiency.
Authors: Raghunathan R , Mundy T M , Faust J , Misra S 
Published: December 2022

Abstract
Immune deficiency, as defined by significant decreases in lymphocyte Con A and allo-reactivity and in natural killer (NK) function, was induced in normal adult mice by i.p. injections of combinations of allogeneic testicular germ cells and splenic leukocytes over 3 wk. This immune deficiency was evident at 8 wk after initial injection, and profound by 12 wk. Neither leukocytes nor testicular cells, given alone, were able to induce similar immune deficiency. These findings suggest the possibility that allogeneic germ cells and leukocytes of semen, on repeated administration, may induce immune deficiency and may act as co-factors to viral agents in the development of clinical AIDS in humans.
Type II collagen-induced arthritis in mice. IV. Variations in immunogenetic regulation provide evidence for multiple arthritogenic epitopes on the collagen molecule.
Authors: Wooley P H , Luthra H S , Griffiths M M , Stuart J M , Huse A , David C S 
Published: December 2022

Abstract
Type II collagen from six mammalian species was investigated for the capacity to induce an immune response and collagen-induced arthritis (CIA) in C57/B10 congenic mouse strains. H-2q haplotype mice were susceptible to chick, bovine, deer, rat, and human type II collagen, but were resistant to arthritis induced by porcine type II collagen. H-2r haplotype mice only developed CIA in response to bovine, deer, and porcine collagen. High antibody responses in the absence of disease, directed against a specific type II collagen, were observed in many independent haplotypes. The cross-reactive capacity of different antisera to the various collagen species was studied. The data support the existence of two arthritogenic and multiple nonarthritogenic epitopes on the type II collagen molecule.
Monoclonal antibody OKT11A inhibits and recombinant interleukin 2 (IL 2) augments expression of IL 2 receptors at a pretranslational level.
Authors: Reed J C , Greene W C , Hoover R G , Nowell P C 
Published: December 2022

Abstract
The expression of receptors for interleukin 2 (IL 2) represents a critical event regulating the growth of normal T lymphocytes. We investigated the effects of the inhibitory monoclonal antibody OKT11A (anti-sheep erythrocyte receptor) and of purified recombinant IL 2 (rIL 2) on the expression of IL 2 receptors by activated T cells at both the protein and the mRNA levels. Adding OKT11A antibody (0.5 microgram/ml) to phytohemagglutinin (PHA)-stimulated cultures of human peripheral blood mononuclear cells (PBMC) markedly suppressed cellular proliferation (assessed by [3H]thymidine incorporation) and IL 2 receptor expression (determined by immunofluorescence assay by using the anti-IL 2-receptor antibody, anti-Tac). Northern blot analysis performed with the use of a cDNA probe specific for the human IL 2 receptor gene demonstrated that OKT11A antibody also decreased the accumulation of IL 2 receptor mRNA induced by PHA in PBMC. Purified rIL 2 (10 U/ml) alone had little effect on the expression of IL 2 receptors in unstimulated PBMC cultures. In combination with PHA or with PHA plus OKT11A, however, rIL 2 augmented both the expression of IL 2 receptor protein on PBMC and the accumulation of IL 2 receptor mRNA in PBMC. Adding anti-Tac antibody to PBMC cultures to block the interaction of IL 2 with its receptor diminished the accumulation of IL 2 receptor mRNA induced by PHA. Taken together, these data demonstrate that OKT11A antibody inhibits and IL 2 augments expression of IL 2 receptors on PHA-stimulated T cells, at least in part, at a pretranslational level.
Regulation of mediator release from mouse bone marrow-derived mast cells by glucocorticoids.
Authors: Robin J L , Seldin D C , Austen K F , Lewis R A 
Published: December 2022

Abstract
Mouse bone marrow-derived mast cells (BMMC), which were differentiated from their bone marrow precursors during 14 days of culture in the presence of a T cell lymphokine, were cultured in the absence or in the presence of 0.01 to 5 microM dexamethasone (DEX) for periods of 6 to 96 hr to assess the effects of steroid treatment on stimulus-dependent mediator release. Preincubation of the BMMC for 24 hr with DEX inhibited the subsequent immunoglobulin (Ig) E-dependent release of beta-hexosaminidase in a dose-dependent manner by up to 38% (mean, n = 7) at 1 microM DEX, and the decrease was statistically significant at DEX concentrations greater than or equal to 0.5 microM. DEX (1 microM) inhibited granule secretion from BMMC in a time-dependent manner; the decrease was statistically significant after a preincubation period of 6 hr, was maximal after preincubation times greater than or equal to 24 hr, and was reversible by 24 hr of incubation in medium lacking the steroid. Preincubation for 24 hr with DEX also inhibited the IgE-dependent biosynthesis and release of the immunoreactive leukotrienes (LT)C4 and LTB4 in a dose-dependent manner by up to 56% (n = 7) and 54% (n = 7), respectively, at 1 microM DEX, and the decrease was statistically significant for each product at DEX concentrations greater than or equal to 0.1 microM. In contrast, BMMC preincubated with DEX for 24 hr before sensitization and antigen challenge demonstrated a statistically significant increase in the release of immunoreactive prostaglandin (PG) D2 at DEX concentrations greater than or equal to 0.1 microM and a maximal enhancement of 188% (n = 3) at 1 microM DEX. The effect of 1 microM DEX on the enhancement of IgE-dependent PGD2 generation was significant after 6 hr, and was maximal by 72 hr. The inhibitory effects of DEX on the antigen-induced release of 5-lipoxygenase pathway products were confirmed by the physical measurements of 5-hydroxy-eicosatetraenoic acid (5-HETE) and LTC4, and by isotopic measurement of [3H]LTC4 after reverse-phase high performance liquid chromatography (RP-HPLC). As assessed by fluorescence cytofluorography of IgE-sensitized BMMC that were interacted with F(ab')2 rabbit anti-mouse epsilon and fluorescein isothiocyanate-labeled F(ab')2 goat anti-rabbit IgG-F(ab')2, the number of IgE-Fc receptors on the cell surface decreased by more than 55% after treatment for 24 hr with 1 microM DEX.+
The fibrinogenolytic activity of purified tryptase from human lung mast cells.
Authors: Schwartz L B , Bradford T R , Littman B H , Wintroub B U 
Published: December 2022

Abstract
The capacity of purified tryptase from human lung mast cells to metabolize human fibrinogen, fibrin, and plasminogen was evaluated. Tryptase (5 micrograms/ml) inactivated the thrombin-induced clotting activity of fibrinogen (100 micrograms/ml) with essentially similar t 1/2 values of 4.6 min in the absence of heparin and 5.8 min in the presence of heparin (20 micrograms/ml) that were not appreciably different than with lysine-Sepharose-purified plasmin (5 micrograms/ml). Fibrinogen treated with tryptase together with heparin lost all detectable clotting activity by 4 hr at 37 degrees C, whereas fibrinogen treated with tryptase alone resulted in destruction of only 80% of fibrinogen clotting equivalents after 16 hr. Tryptase alone was observed to cleave only the alpha-chains of fibrinogen by electrophoresis of tryptase-treated, denatured, and reduced fibrinogen in polyacrylamide gradient gels. Tryptase together with heparin cleaved first the alpha-chain and then the beta-chain, the latter cleavage corresponding to complete loss of fibrinogen clotting activity by 4 hr. No fibrinogen fragments with anticoagulant activity were generated by tryptase. In contrast, plasmin left no residual clotting activity after 4 hr of incubation and generated fibrinogen fragments with anticoagulant activity. Plasmin sequentially cleaved the alpha, beta, and gamma subunits of fibrinogen. Tryptase alone (6 micrograms/ml) or together with heparin (20 micrograms/ml) failed to activate plasminogen (0.6 mg/ml) after a 60-min incubation at 37 degrees C. Addition of urokinase to tryptase-treated or untreated plasminogen resulted in essentially identical plasmin activities (0.32 and 0.34 U/ml, respectively), indicating that tryptase neither activates nor destroys plasminogen. Tryptase (700 ng) also failed to substantially solubilize cross-linked fibrin (2.6 micrograms) or the corresponding amount of fibrinogen bound to plastic microtiter plates with or without heparin. The failure to solubilize fibrinogen and, possibly, fibrin is consistent with the observation that the apparent m.w. by SDS polyacrylamide gel electrophoresis of unreduced fibrinogen is not appreciably altered by prior treatment with tryptase, even though cleavage of alpha-and beta-chains is revealed after reduction. Fibrinogenolysis by tryptase complements other mast cell mediators with anticoagulant properties such as heparin and suggests a significant prevention of coagulation by activated mast cells.
Recognition of viral antigens by human influenza A virus-specific T lymphocyte clones.
Authors: Fleischer B , Becht H , Rott R 
Published: December 2022

Abstract
The nature of the viral antigens recognized by influenza A virus-immune cytotoxic T lymphocytes (CTL) is still a matter of debate. We have used four human influenza A virus-specific T lymphocyte clones with antigen-specific cytotoxic and proliferative activity to investigate the requirements for recognition of viral antigens on infected cells. One clone recognized a cross-reactive determinant on the viral hemagglutinin, and two clones were specific for different epitopes on the viral nucleoprotein (NP). A fourth clone seemed to be specific for the viral M protein. Target cell recognition was abrogated by the addition, during infection, of the lysosomotropic drug chloroquine, known to inhibit antigen processing. Furthermore, target cells that had been pulsed with soluble purified NP were recognized and were lysed by the NP-specific clone. This reaction could also be abrogated by the addition of chloroquine during pulsing. These results were obtained irrespective of whether EBV-transformed B lymphoblastoid cells or Ia antigen-expressing T cell blasts were used as target cells. It is concluded that CTL can recognize internal viral proteins that are actively presented at the surface of the target cell. These data indicate that probably every viral protein can function as a target molecule for virus-immune CTL.
Allograft rejection-defined antigens of the B2m,H-3 region.
Authors: Graff R J , Martin-Morgan D , Kurtz M E 
Published: December 2022

Abstract
In this report we delineate the production and histocompatibility characteristics of two new B2m, H-3 region congenic strains, B10.SM-a and B10.FS-a, and further characterize previously described strains. Strains C57BL/10 and B10-we are shown to be histocompatible by the exchange of skin grafts, as are strains B10.UW-we,un at, B10.UW we un a, B10.UW-we + a, B10.UW-+ + a and B10.LP-a. (The latter group will be called B10-H-3b when referred to collectively). C57BL/10, B10-H-3b, B10.C-a, B10.KR-a, B10-pa at, B10.SM-a, and B10.FS-a are shown to be histoincompatible by the rejection of exchanged skin grafts, and histoincompatibility between these strains has been localized to the B2m, H-3 region. The histoincompatibility between C57BL/10 and B10.FS-a is of particular significance because of the identity of these strains at the B2m, H-3 region loci B2m and H-3. Thus the B2m, H-3 region histoincompatibility herein described defines a new locus, which we have called H-42, the a allele being assigned to C57BL/10 and the b allele to B10.FS-a. By using cross-immunization techniques, four allograft rejection-defined reactivity patterns (ADR) have been defined that show concordant strain distribution patterns with the CTL-defined reactivity patterns described elsewhere. On the basis of data presented in this report indicating C57BL/10 and B10.FS-a to differ by a histocompatibility gene in the B2m, H-3 region, and data presented by Kurtz et al. elsewhere indicating C57BL/10 and B10.FS-a to possess the same alleles at the B2m and H-3 loci, the presence of at least three B2m, H-3 region loci-defining cell membrane antigens is established.