bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multiple splenic lymphoid cell subpopulations regulate H-2 antigen expression on teratocarcinoma cells in vivo.
Authors: Ostrand-Rosenberg S , Cohn A L , Sandoz J W 
Published: December 2022

Abstract
Undifferentiated murine 402AX teratocarcinoma cells do not express MHC antigens when passaged in vitro or in vivo in genetically susceptible host mice. When passaged in vivo in genetically resistant mice, however, the tumor cells become H-2b antigen positive regardless of the H-2 haplotype of the resistant host mouse. The present studies use monoclonal anti-H-2b antibodies to corroborate these earlier findings, which were performed with conventional antisera. Previous studies have established that host bone marrow plus lymphoid cells from resistant primed donors regulate tumor cell H-2b antigen expression. Using bone marrow and mature lymphoid cell reconstitution techniques, the present studies indicate that splenic Ig- cells from genetically resistant host mice are the most efficient lymphoid cell subpopulation in tumor cell H-2b antigen induction. Ig+ spleen cells also reconstitute the capacity to induce teratocarcinoma cell H-2 antigens but are less effective than Ig- spleen cells. Tumor cell H-2 antigen induction in C57BL/6 beige mice is impaired compared to C57BL/6 hosts, which suggests that host NK cells may also be involved in tumor cell H-2 antigen induction. Reconstitution of lethally irradiated resistant hosts for teratocarcinoma cell H-2 antigen expression requires bone marrow plus resistant primed lymphoid cell subpopulations; bone marrow alone is insufficient. These results indicate that multiple splenic lymphoid cell subpopulations requiring a radiosensitive host environment and/or factor for differentiation regulate teratocarcinoma 402AX H-2b antigen expression in vivo in genetically resistant mice.
Immunoperoxidase localization of large granular lymphocytes in normal tissues and lesions of athymic nude rats.
Authors: Ward J M , Argilan F , Reynolds C W 
Published: December 2022

Abstract
The immunocytochemical localization of cells reacting with the OX-8 monoclonal antibody was studied in athymic nude rats by the avidin-biotin-peroxidase complex (ABC) immunoperoxidase technique. By a number of criteria, including morphology and tissue distribution of OX-8-positive cells, it is postulated that the majority of lymphocytes reacting with OX-8 antibody in nude rats are LGL. The cell surface of large lymphocytes reacted with the OX-8 antibody in fixed tissue sections. The tissues with the greatest density and percentages of these reactive cells included the paracortex of lymph nodes in association with interdigitating cell (IDC) hyperplasia, bronchial-associated lymphoid tissue (BALT), the medullary cords and sinuses of lymph nodes, and intestinal epithelium. Ultrastructure of the paracortical areas of IDC hyperplasia revealed granular lymphocytes in close association with IDC. Tissues with the fewest positive cells included bone marrow, B cell areas of lymphoid tissues, and parenchymal epithelial organs. In healthy and cachectic nude rats, various incidental and pathologic lesions contained a significant number of OX-8-positive cells. Large numbers of positive lymphocytes were seen in suppurative pneumonic lesions, enteritis, focal ulcerative epithelial lesions, and papovaviral sialoadenitis. The observation of a large number of OX-8-positive lymphocytes in nonlymphoid organs supports the hypothesis that these cells play a major role in the first line of defense against not only tumors but also infectious agents.
Alteration of T cell subsets and induction of suppressor T cell activity in normal subjects after exposure to sunlight.
Authors: Hersey P , Haran G , Hasic E , Edwards A 
Published: December 2022

Abstract
The effects of exposure to natural sunlight on the immune system were studied in 15 normal human subjects. Exposure was for 1 hr each day for 12 days over 2 wk and tests were carried out before, on completion, and 2 wk after completion. In comparison to concurrent studies on 13 age- and sex-matched controls, sun-exposed subjects had a significant increase in their circulation of T cells recognized by OKT8 monoclonal antibodies and a decrease in OKT4 positive T cells. Suppressor T cell activity measured in pokeweed mitogen-stimulated cultures of T and B cells was significantly increased against IgG and IgM production. These changes were still evident in many of the subjects 2 weeks after completion of the sun exposure. A trend for depression of natural killer cell activity against a melanoma target cell was noted in the present study, but this did not appear as marked as that noted previously in subjects exposed to radiation in solariums. The differences between the effect of radiation from solariums and natural sunlight on the immune system may result from the higher dosage of UV-A in radiation from solariums. The results suggest that exposure to sunlight may favor the induction of suppressor pathways in response to antigenic stimuli and that this may limit immune responses against tumor cells such as melanoma. They support the idea from animal studies that systemic changes in the immune system may be an important factor in the association of UV radiation with malignancy.
Decreased Fc receptor avidity and degradative function of monocytes from patients with systemic lupus erythematosus.
Authors: Katayama S , Chia D , Knutson D W , Barnett E V 
Published: December 2022

Abstract
We studied the binding and degradation of stable, soluble heat aggregates of 125I-IgG (A-IgG) by monocytes from 30 patients with systemic lupus erythematosus (SLE) and 30 normals. Relative avidities (KE) for Fc receptor (FcR) binding of A-IgG and maximal binding of A-IgG by monocytes were determined from Scatchard plots of binding data obtained at 4 degrees C. Rates of degradation (Vmax) of A-IgG at 37 degrees C were calculated from Lineweaver-Burke plots of the Michaelis-Menton equation. KE were decreased in SLE monocytes (15.5 X 10(-9) L/M) as compared with normals (20.1 X 10(-9) L/M, p less than 0.005) and Vmax were decreased for SLE (0.89 ng/hr) as compared with normals (1.11 ng/hr, p less than 0.005). The maximal FcR binding by SLE monocytes was not statistically different in SLE patients and normals, but monocytes from SLE patients with active disease showed a lower maximal binding capacity for A-IgG (4.9 ng/10(5) cells) than normals (5.4 ng/10(5) cells, p less than 0.05). KE and Vmax in SLE were also lower for patients with active disease than for normal subjects. KE in patients whose anti-ssDNA binding was greater than 20% were lower than for those with DNA binding of less than 20% (p less than 0.005). These data suggest that patients with active SLE have diminished numbers of available FcR on their circulating monocytes, possibly due to interiorization of FcR during endocytosis of endogenous circulating immune complexes.
Autoimmunity and immune complex disease after neonatal induction of transplantation tolerance in mice.
Authors: Goldman M , Feng H M , Engers H , Hochman A , Louis J , Lambert P H 
Published: December 2022

Abstract
Mice made neonatally tolerant to alloantigens were found to develop an immunologic disease resembling systemic lupus erythematosus. In BALB/c mice neonatally injected with C57BL/6 X BALB/c F1 hybrid spleen cells, features of autoimmunity were observed first. After 5-24 wk, antinuclear, anti-SS DNA, thymocytotoxic, and rheumatoid factor-like antibodies were detected in association with hypergammaglobulinemia and with the occurrence of circulating immune complexes and cryoglobulins. Some of the antinuclear antibodies were found to be produced by F1 donor B cells persisting in the host. Second, immunopathologic changes were detected in tolerant mice. In the kidneys, an immune complex glomerulonephritis of the membranous type was observed. Immunoglobulin deposits were also found in the choroid plexus and at the dermoepidermal junction. In addition, thrombocytopenia was a common finding, and a positive direct Coomb's test occasionally was detected. Features of autoimmune disease were closely associated with the effective induction of transplantation tolerance, as revealed by the inability of spleen cells to generate in vitro cytolytic responses against C57BL/6 alloantigens. It is suggested that, although transplantation tolerance is associated with a lack of cytolytic reaction of the host against F1 hybrid donor alloantigens, other types of allogeneic interactions could lead in this model to the development of autoimmunity and immunopathology.
Immunologic and biochemical properties of several retinal proteins bound by antibodies in sera from animals with experimental autoimmune uveitis and uveitis patients.
Authors: Gregerson D S , Abrahams I W 
Published: December 2022

Abstract
Sera from guinea pigs and rabbits with and without experimental autoimmune uveitis (EAU) induced by immunization with retina, choroid, optic nerve, retinal rod outer segments (ROS) and purified bovine S-antigen were tested for the ability to immunoprecipitate 125I-labeled, detergent-solubilized bovine retinal proteins. The results demonstrate that three major protein antigens with m.w. of 50,000 (p50), 35,000 (p35) and 27,000 (p27) and several minor activities between 30,000 and 60,000 m.w. are recognized by antibodies from these animals. The p50 component was immunoprecipitated by sera from animals immunized with whole retina homogenate, the high speed supernatant of whole retina homogenate, ROS, and S-antigen, and has been identified as S-antigen in competition experiments. The p35 band appeared when sera were used that were raised against antigen preparations containing membrane-bound retinal protein, i.e., whole retina homogenate, ROS, and washed ROS, and thus appears to be an ROS membrane protein. The p27 band was found when sera raised against ROS, washed ROS, optic nerve and whole retina homogenate were used, suggesting it is a membrane-bound antigen common to ROS and optic nerve. Serum from animals immunized with homologous choroid did not immunoprecipitate a detectable product. S-antigen and p35 were also precipitated by some uveitis patient sera. Because S-antigen is also an ROS protein as is rhodopsin, a putative uveitogenic retinal antigen, ROS appear to be an unusually rich source of autoantigenic proteins. S-antigen was also shown to be synthesized in the retina, and the primary translation product was indistinguishable from purified S-antigen by SDS-PAGE, thus eliminating the possibility that it is derived from or is cross-reactive with the 67,000 m.w. rhodopsin kinase.
The cellular basis for immune interferon production in autoimmune MRL-Ipr/Ipr mice.
Authors: Santoro T J , Benjamin W R , Oppenheim J J , Steinberg A D 
Published: December 2022

Abstract
Disturbances in immune interferon (IFN gamma) activity have been implicated in the development of human systemic lupus erythematosus (SLE) and the spontaneous disease sustained by autoimmune-prone mice. We therefore investigated the cellular basis for IFN gamma production in MRL-Ipr/Ipr mice and examined the relationship between synthesis of interleukin 2 (IL 2) and IFN gamma. In vitro IL 2 and IFN gamma production in 3 to 6-mo-old, autoimmune MRL-Ipr/Ipr and MRL-+/+ mice was compared with that seen in age- and sex-matched, immunologically normal CBA/J mice. 5 X 10(6) spleen cells were pulsed with 5 micrograms of concanavalin A (Con A), and the cellfree supernatant was assayed for IL 2 and IFN gamma activity at various times up to 72 hr. We found that peak levels of IL 2 in MRL mice were less than 10% of those in the CBA/J. Yet, production of IFN gamma by cells from the autoimmune and normal strains was quite comparable. The addition of murine IL 2 to optimally Con A-stimulated cells from the MRL-Ipr/Ipr or normal mice did not affect the subsequent peak production of IFN gamma. Although the primary producers of IFN gamma in cultures of normal mice bear the Lyt-2+ phenotype, the Lyt-1+2- T-cell subset was found to be the principal source of IFN gamma in the aged MRL-Ipr/Ipr. These data suggest that Lyt-1+ cells from MRL-Ipr/Ipr mice may be differentially responsive to the signal delivered by the same mitogenic lectin with respect to lymphokine production and may indicate a distorted commitment of such cells toward production of IFN gamma and repression of IL 2 synthesis. The relationship between hypoproduction of IL 2, this usual source of IFN gamma, and the autoimmune disease sustained by MRL-Ipr/Ipr mice remains unclear.
Interleukin 2 induces gamma-interferon production: participation of macrophages and NK-like cells.
Authors: Kawase I , Brooks C G , Kuribayashi K , Olabuenaga S , Newman W , Gillis S , Henney C S 
Published: December 2022

Abstract
Interleukin 2 (IL 2) has been shown to be a potent stimulator of natural killer (NK) cells. In the present studies, partially purified mouse and human IL 2 preparations were also found to induce interferon (IFN) from mouse spleen cells. By the criteria of sensitivity to treatment at pH 2 and failure to be neutralized by a potent anti-alpha, beta IFN serum, the species of IFN produced was of type gamma. Cooperation between two types of cell, a macrophage and an NK-like cell, was required for IFN production by murine spleen cells treated with IL 2. The requirement for macrophages could be replaced with supernatant obtained by incubating macrophages for 24 hr with lymphokine preparations containing IL 2. Interestingly, mature T cells apparently played no role in the process. Furthermore, the beige (bg/bg) mutation, which severely impairs NK cell lytic activity, had no effect on the ability of NK-like cells to participate in IFN production. Cell fractionation experiments revealed no dissociation between the requirements for augmentation of NK cytotoxic activity and for IFN production, and it is concluded that at least a portion of the NK boosting induced by IL 2-containing preparations is mediated through gamma-IFN.
Effect of vesicular stomatitis virus (VSV) infection on the development and regulation of T cell-mediated immune responses.
Authors: Sy M S , Tsurufuji M , Finberg R , Benacerraf B 
Published: December 2022

Abstract
Infection of mice with vesicular stomatitis virus (VSV) at the time of immunization failed to enhance T cell-mediated immune response to azobenzenearsonate-(ABA) conjugated spleen cells as measured by delayed-type hypersensitivity and by in vitro proliferation and in vitro generation of ABA-specific cytotoxic T cells. However, mice infected with VSV are incapable of responding to signals from suppressor T cells or their soluble factors. Further analysis revealed that VSV infection does not interfere with the induction of Ts-1 or Ts-2 cells. Because infection of Ts-1 or Ts-2 donors had no effect on the subsequent response seen in the recipients of antigen and suppressor T cells, the most likely candidate for the target of VSV infection is therefore the Ts-3 cell or another T cell interacting with Ts-3. This is supported by our observation that it is possible to bypass the VSV effect by providing the recipients of VSV with normal Lyt-2+-bearing T cells.
Isolation of intact Sm/RNP antigens from rabbit thymus.
Authors: Billings P B , Hoch S O 
Published: December 2022

Abstract
A comparison of the immunologically reactive components of the highly conserved Sm and RNP autoantigens from various mammalian tissue sources suggested the complete absence of a major 26K to 27K Sm-specific polypeptide in rabbit thymus extracts prepared by conventional procedures. A simple modification of the solubilization protocol, achieved by sonicating a suspension of commercial rabbit thymus acetone powder in 0.35 M NaCI, gave an extract containing the full complement of immunologically reactive Sm and RNP proteins detectable in other mammalian species. Without further manipulation, extracts were immediately passed through an immunoaffinity column constructed from human SLE IgG with both anti-Sm and anti-RNP reactivities. The proteins of the purified Sm/RNP were recovered in sufficient quantities for direct analysis by protein staining or immunoblot assays. The antigenic polypeptides were recovered intact and consisted of a single 73K RNP-specific species together with Sm-specific proteins of 26K to 27K (a doublet) and 13K. These proteins were easily visible by protein stain as were nonantigenic components of 35K, 32K, 11K, and less than 10K. The same polypeptides were present in affinity-purified Sm/RNP from HeLa cells, although the RNP protein was slightly smaller. The resolution and integrity of the complexes isolated by this simple two-step procedure, requiring less than 4 hr for completion, is remarkable, and the protein composition of the product compares quite favorably with antigens isolated from other sources by considerably more lengthy and laborious procedures.
Human monocytes, B lymphocytes, and non-B lymphocytes each have structurally unique Fc gamma receptors.
Authors: Cohen L , Sharp S , Kulczycki A 
Published: December 2022

Abstract
Human Fc gamma-binding macromolecules were isolated from subpopulations of mononuclear cells by repetitive affinity chromatography. Mononuclear cells, nylon wool-filtered cells, plastic-nonadherent cells, and plastic-adherent cells from normal donors were radiolabeled by using 125I and lactoperoxidase. Washed cells were solubilized in 1% NP-40 buffer containing proteinase inhibitors at 0 degrees C. Fc gamma receptors were purified on human IgG-Sepharose columns by use of the repetitive affinity chromatography procedure. Analysis by SDS-polyacrylamide gel electrophoresis demonstrated only a 52,000 to 58,000 Mr Fc gamma receptor from nonadherent cell populations. Both rosetting and nonrosetting subpopulations of non-B lymphocytes expressed the 52,000 to 58,000 Mr receptor. The predominant Fc gamma receptor isolated from plastic-adherent cells was a 60,000 to 68,000 Mr macromolecule. Cell preparations enriched in B lymphocytes yielded prominent 43,000 Mr Fc gamma receptors. Thus human monocytes, B lymphocytes, and non-B lymphocytes each appear to have structurally distinct and unique Fc gamma receptors.
Generation of biologically active, complement-(C5) derived peptides by cathepsin H.
Authors: Perez H D , Ohtani O , Banda D , Ong R , Fukuyama K , Goldstein I M 
Published: December 2022

Abstract
The thiol proteinase cathepsin H, isolated and purified from rat liver lysosomes, provokes acute inflammation characterized by the accumulation of polymorphonuclear leukocytes (PMN) when injected intracutaneously into newborn rats. We have examined the possibility that the accumulation of PMN at skin sites injected with cathepsin H is due, in part, to generation locally of C-derived chemotactic factors. We have found that cathepsin H acts in a concentration- and time-dependent fashion in whole human (and rat) EDTA-plasma to generate C5-derived peptides with chemotactic activity for PMN. Chemotactic activity was not generated in EDTA-plasma by either heat-inactivated cathepsin H or by a combination of active enzyme and a thiol proteinase inhibitor isolated from rat epidermis. Cathepsin H also acted in a concentration- and time-dependent fashion on isolated (functionally pure) human C5 to yield chemotactic activity for PMN as well as PMN lysosomal enzyme-releasing activity. Whereas 10 ng/ml cathepsin H generated significant chemotactic activity from isolated C5 (1000 CH50 U/ml), 7 to 10 micrograms/ml were required to generate chemotactic activity in whole EDTA-plasma. Cathepsin H not only was capable of generating biologically active, C5-derived peptides, but also was capable of degrading these peptides. Incubation of either whole EDTA-plasma or isolated C5 with high concentrations of cathepsin H (e.g., 25 micrograms/ml and 100 ng/ml, respectively) caused the rapid appearance of chemotactic activity followed by an equally rapid disappearance. PMN accumulated more rapidly in the skin of newborn rats injected with cathepsin H-treated C5 than in the skin of animals injected with cathepsin H alone. These data suggest that generation by cathepsin H of C-derived chemotactic activity contributes to the ability of this enzyme to induce dermal inflammation.
Erythromyeloid tumor cells (K562) induce PGE synthesis in human peripheral blood monocytes.
Authors: Leung K H , Fischer D G , Koren H S 
Published: December 2022

Abstract
Human peripheral blood monocytes were found to spontaneously produce prostaglandin of the E series (PGE) in culture medium (0.5 ng to 3.0 ng/7.5 X 10(5) cells), and the addition of K562 tumor cells enhanced the production by five- to 15-fold after 18 hr of incubation. PGE2 (10(-6) M) inhibited the cytolytic activity of freshly isolated peripheral blood monocytes against K562 target cells by 50%. The PGE production was inhibited by inhibitors of cyclo-oxygenase (indomethacin, aspirin, and ETYA) when present during the incubation. However, pretreatment of monocytes with these cyclo-oxygenase inhibitors was ineffective in preventing PGE production. Kinetic experiments showed that appreciable stimulation of PGE production occurred only after 6 hr of co-culture. Other human tumor cell lines (HSB, SB, and CEM) enhanced PGE production upon co-culture with monocytes but to a lesser extent (twofold to threefold). Monocytes treated with 0.4% formaldehyde or heat (56 degrees C) were not capable of producing PGE when cultured alone or with K526 tumor cells. In contrast, formaldehyde-treated, but not heat-treated, K562 tumor cells were able to induce monocytes to produce PGE. By using a single cell conjugation assay, K562 tumor cells were found to bind equally well to treated or untreated monocytes. In contrast, the lytic activity of treated monocytes against K562 target cells was abolished. The presence of protein synthesis inhibitor, cycloheximide, was found to inhibit PGE production by monocytes cultured alone or with K562 tumor cells. Supernatants from K562 tumor cell cultures were also capable of inducing monocytes to produce PGE, and their effect on PGE production from monocytes was suppressed by cycloheximide. In addition, pretreatment of either K562 tumor cells or monocytes with an irreversible protein synthesis inhibitor, emetine, also suppressed the production of PGE upon co-culture with the untreated counterpart. The production of PGE by monocytes in response to exposure to tumor cells may represent a mechanism whereby tumor cells subvert host immune defense against them.
Augmentation of NK cell activity by soluble and particulate fractions of Toxoplasma gondii.
Authors: Hauser W E , Sharma S D , Remington J S 
Published: December 2022

Abstract
The ability of sonicates of Toxoplasma gondii and of subcellular fractions of the organism to enhance natural killer (NK) cell activity in mice was examined. Treatment of BALB/c mice with the sonicate preparations enhanced peritoneal and splenic NK activity to the level obtained with intact tachyzoites. Similar augmentation of NK activity in A/J, C57BL/6, and C3H/HeJ mice was also observed. Administration of Toxoplasma sonicate intraperitoneally, intravenously, or subcutaneously enhanced both peritoneal and splenic NK activity. Treatment of mice with a sonicate of L929 fibroblast failed to enhance their NK activity. Concentrations of sonicates ranging from 400 to 4 micrograms of protein enhanced both peritoneal and splenic NK activity. Both the soluble and particulate fractions of the sonicate obtained by differential centrifugation were capable of enhancing peritoneal NK activity, whereas splenic NK activity was enhanced only by the particulate fraction. Heat, protease, and sodium periodate treatment of the Toxoplasma sonicate completely abolished its capacity to augment NK activity. Gel filtration studies revealed that the NK augmenting activity of the Toxoplasma sonicate is distributed over a wide molecular weight range.