bluuebunny/crossref_metadata_2025_split huggingface dataset:
Localization of the phosphocholine-binding sites on C-reactive protein by immunoelectron microscopy.
Authors: Roux K H , Kilpatrick J M , Volanakis J E , Kearney J F 
Published: December 2022

Abstract
C-reactive protein (CRP) was reacted with monoclonal IgG antibody or Fab antibody fragments directed against the phosphocholine- (PC) binding site or a second unrelated site. The resulting immune complexes were viewed by a negative stain immunoelectron microscopy technique. Monoclonal anti-PC-binding site antibody bound to a single epitope on each of the five CRP subunits. The orientation of the PC-binding sites was determined to be slightly medial to one of the planar faces (A-face) of the molecule. The second monoclonal antibody, which was not PC-binding site related, bound to epitopes (one per CRP subunit) that were located slightly lateral to the other planar face (B-face) of the CRP molecule, i.e., opposite of the PC-binding site. Thus, the PC-binding site and the non-PC-binding site are oriented nearly perpendicular but on opposite sides with respect to the plane of the CRP molecule. The functional significance of this configuration is discussed.
Biosynthesis and postsynthetic processing of human C-reactive protein.
Authors: Tucci A , Goldberger G , Whitehead A S , Kay R M , Woods D E , Colten H R 
Published: December 2022

Abstract
Human C-reactive protein (CRP) is one of several plasma proteins that increase after tissue injury or inflammation. The magnitude of the increase in CRP (100 to 1000-fold over the resting state) makes this an excellent model for studies of eukaryotic gene control. Accordingly, the biosynthesis and postsynthetic processing of human CRP was examined under cellfree conditions and in Xenopus oocytes injected with liver mRNA. The primary translation product is larger than native serum CRP by an 18-amino acid amino terminal extension. The sequence of this signal peptide was derived from nucleotide sequencing of a 1.8-kilobase (Kb) CRP-specific cDNA clone. Northern blot analysis revealed a CRP mRNA of approximately 2.2 Kb, a size more than three times that required (615 bases) to code for the primary translation product. These data form the basis for study of molecular control of the acute phase response.
Identification of the apparently lymphocyte-specific human liver-derived inhibitory protein (LIP) as cytoplasmic liver L-arginase.
Authors: Brusdeilins M , Hapke C , Huberts H H , Schumacher K 
Published: December 2022

Abstract
This paper describes the identification of a human liver-derived inhibitory protein (LIP), which has recently been purified, as cytoplasmic liver arginase. Arginase activity was purified to homogeneity parallel to lymphocyte proliferation inhibitory activity. The reaction products were identified by thin-layer chromatography to be ornithine and urea from arginine. The enzyme activity could be increased by the addition of manganese ions, and the inhibitory effect on cell proliferation could be reversed by additional arginine. An antiserum against LIP cross-reacted with cytoplasmic calf liver arginase.
In vitro induction of cytotoxic polymorphonuclear leukocytes by supernatant from a concanavalin A-stimulated spleen cell culture.
Authors: Inoue T , Sendo F 
Published: December 2022

Abstract
Rat polymorphonuclear leukocytes (PMN) pretreated with supernatant of a spleen cell culture stimulated with concanavalin A (Con A sup) inhibited 3H-thymidine uptake of various syngeneic, allogeneic, and xenogeneic tumor cells. Con A sup-treated PMN were cytostatic not only to tumor cells but also to embryonal fibroblasts and normal Con A blasts. Stimulated PMN also killed some tumor cells, as shown by 3H-uridine release assay. Cytostasis by Con A sup-treated PMN began at a very early phase of incubation, but in the cytolysis assay, incubation for more than 12 hr was required to obtain significant killing. The time required for activation of cytostatic PMN by Con A sup was short (5 min was enough) if high titers of Con A sup were used for activation. PMN-stimulating activity of Con A sup was not abrogated by treatment at 60 degrees C for 30 min or by change of pH from 1 to 11. The mechanisms of cytotoxicity by Con A sup-treated PMN are discussed.
Intracamerally induced concomitant immunity: mice harboring progressively growing intraocular tumors are immune to spontaneous metastases and secondary tumor challenge.
Authors: Niederkorn J Y , Streilein J W 
Published: December 2022

Abstract
Intracameral inoculation of allogeneic P815 mastocytoma cells (DBA/2) into BALB/c mice resulted in progressively growing intraocular tumors. Intraocular tumor cells disseminated rapidly to the spleen and cervical lymph nodes, yet extraocular nests of tumor cells never developed into fulminant tumors. Further experiments showed that tumor cells were continuously seeded from the primary intraocular tumor and were rapidly cleared from extraocular sites. Hosts harboring intraocular P815 mastocytomas rejected tumorigenic doses of P815 cells inoculated subcutaneously or even into the contralateral anterior chamber. This systemic tumor immunity was found to be radiosensitive and T cell dependent. Spleen cells from animals with progressively growing intraocular tumors protected recipient mice challenged with intracamerally inoculated tumor cells and thus suggests that a cell-mediated mechanism is the underlying basis for this form of tumor immunity. The data indicate that mice harboring progressively growing intraocular tumors develop a potent state of "concomitant immunity," that prevents the development of metastases, yet is ineffective in controlling the primary tumor.
Comparison of approaches for augmenting the serologic response to the individually specific methylcholanthrene-induced sarcoma-Meth A: pretreatment with cyclophosphamide is most effective.
Authors: Livingston P O , DeLeo A B , Jones M , Oettgen H F 
Published: December 2022

Abstract
We have previously reported the production of antisera against a highly restricted antigen expressed on the BALB/c sarcoma Meth A. Because induction of the antibody required many vaccinations with irradiated and unirradiated Meth A cells over a prolonged period, we have investigated methods of improving the efficiency of producing Meth A antibody in BALB/c mice. Three general approaches were used: immunizing with irradiated Meth A cells mixed with adjuvants, immunizing with irradiated Meth A cells modified by treatment with chemicals, or administration of tumor cell vaccines in conjunction with low dose cyclophosphamide. These vaccine preparations were injected subcutaneously into groups of BALB/c mice five to six times at 2-wk intervals. Sera from all mice were screened for reactivity to Meth A by complement-dependent cytotoxicity, protein A, and mixed hemadsorption assays. Twenty-three vaccine preparations containing adjuvants or modified cells were tested in individual groups of mice. Mice in some groups receiving adjuvants and in all groups receiving modified cells produced antibody, but only after four to six vaccinations. In contrast, nine of the 14 mice immunized with irradiated Meth A cells (unmodified and without adjuvant) in conjunction with 10 or 100 mg/kg body weight of cyclophosphamide, and all nine of the mice receiving 25 mg/kg cyclophosphamide made Meth A antibodies after only one or two vaccinations. The titer of antibodies produced after one treatment with cyclophosphamide and irradiated Meth A cells was at least as high as that achieved after five or six vaccinations in our other trials. The specificity of these antibodies for the Meth A antigen was established by absorption analysis. We conclude that treatment with cyclophosphamide before vaccination is highly effective in augmenting the humoral immune response to the Meth A antigen.
IgA responses in xid mice: oral antigen primes Peyer's patch cells for in vitro immune responses and secretory antibody production.
Authors: Kiyono H , Mosteller L M , Eldridge J H , Michalek S M , McGhee J R 
Published: December 2022

Abstract
Because the gut-associated lymphoreticular tissue (GALT), e.g., Peyer's patches (PP), of X-linked immunodeficient (xid) mice possesses a subpopulation of mature B cells, we have characterized the ability of xid mice to respond to the thymic-dependent antigen sheep erythrocytes (SRBC) given by the oral route. Gastric intubation of SRBC to xid (CBA/N X DBA/2) F1 male or CBA/N mice, followed by the in vitro culture of dissociated PP cells with SRBC, resulted in IgM, IgG1, IgG2, and high IgA anti-SRBC plaque-forming cell (PFC) responses. The addition of unprimed PP but not splenic T cells to splenic xid B cell cultures resulted in IgM anti-SRBC PFC responses, suggesting the importance of GALT T cells for support of the immune responses to SRBC by splenic B cells from xid mice. Furthermore, purified PP T cells from SRBC orally primed xid mice supported in vitro IgA anti-SRBC PFC responses in B cell cultures from either the PP or the spleens of nonprimed xid mice. Higher IgA responses, however, occurred in PP, when compared with splenic B cell cultures. Additional evidence that the GALT of xid mice contains functional IgA precursor cells was provided by the finding that cloned H-2k PP T helper cells (PP Th A) supported IgA responses in PP B cell cultures derived from (CBA/N X C3H/HeN) F1 male (xid) mice. On the other hand, splenic B cells from these xid mice, in the presence of PP Th A cells, did not support in vitro responses. These results suggest that unique subpopulations of T cells occur in the GALT of xid and normal mice; one T cell subpopulation may induce immature B cells to become precursor IgA cells in the PP. A separate GALT T cell subpopulation, e.g., isotype-specific helper T cells, effectively collaborates with mature IgA B cells for the induction of IgA responses to orally administered antigen. When xid mice were gastric intubated with SRBC, followed by i.p. injection of SRBC, good splenic IgA anti-SRBC PFC responses were seen. Salivary and serum IgA antibodies were also detected in these xid mice. Nevertheless, the magnitude of the anti-SRBC response in xid mice was lower than that seen in similarly treated normal mice. These studies indicate that the GALT of both xid and normal mice possess unique populations of T cells that support in vitro responses in xid B cell cultures from either the spleen or the PP, which direct the mature B cell populations present toward IgA isotype-specific responses.(ABSTRACT TRUNCATED AT 400 WORDS)
Polarization of NK cell cytoskeleton upon conjugation with sensitive target cells.
Authors: Carpén O , Virtanen I , Lehto V P , Saksela E 
Published: December 2022

Abstract
We studied the cytoskeletal changes in natural killer (NK) cells during conjugate formation, i.e., when NK cells make contact with sensitive vs resistant target cells. F-actin and vinculin were seen to polarize at the contact sites upon conjugation with sensitive K562 cells, whereas in conjugates with resistant Raji target cells such an orientation was an infrequent finding. Myosin and two other cytoskeletal proteins, spectrin and vimentin, on the other hand, showed a random distribution in conjugating NK cells regardless of the target cell type. Hence the cytoskeletal redistribution associated with conjugation seems to be different from the receptor capping phenomenon, which is accompanied by clustering of actin, myosin, vimentin, and spectrin. On the basis of these results it seems probable that the lytic conjugate formation in NK-mediated cytotoxicity is associated with the formation of a specific type of junction that involves actin and vinculin. This cytoskeletal reorganization precedes and could be a prerequisite for the polarization of the cellular secretory apparatus and may be functionally responsible for the required cytokinetic movements.
Peroxidase-positive mononuclear leukocytes as possible precursors of human dendritic reticulum cells.
Authors: Parwaresch M R , Radzun H J , Feller A C , Peters K P , Hansmann M L 
Published: December 2022

Abstract
In this report, we provide evidence that suggests the dendritic reticulum cells (DRC) occurring in germinal centers of lymphatic follicles originate from a distinct endogenous peroxidase-positive mononuclear blood cell subset. The new monoclonal antibody Ki-M4 showed a highly restricted reactivity, tested by immune histochemistry, being confined to DRC, lining cells of lymph node sinuses, and to 0.001% of nonadherent mononuclear blood cells separated at a density of 1.077 g/ml; the latter exhibited endogenous peroxidase activity in cytoplasmic granules. Such granules being specific for myelomonocytic cells implies that DRC may derive from a committed nonadherent subpopulation of this cell line, which in turn originates from bone marrow. The Ki-M4-reactive antigen was found to be destroyed by the majority of fixatives and to resist 4% paraformaldehyde for 10 min and cold acetone for 30 sec. In cell suspensions from human tonsils, Ki-M4 showed strong reactivity with the outer surface of DRC plasma membrane. This observation demonstrates the possibility of using Ki-M4 to separate DRC from cell suspensions in functional tests.
Cyclophosphamide-sensitive contrasuppression in TNP-anterior chamber associated immune deviation (TNP-ACAID).
Authors: Waldrep J C , Kaplan H J 
Published: December 2022

Abstract
Injection of trinitrophenyl (TNP)-modified splenocytes (TNP-Sp) into the anterior chamber of the eye results in systemic tolerance to TNP, a phenomenon termed anterior chamber associated immune deviation (TNP-ACAID). Two distinct suppressor pathways develop after the induction of TNP-ACAID. The primary suppressor pathway (I) is antigen-specific, is mediated by a cyclophosphamide (Cy)-sensitive suppressor T cell (Ts-I), and requires a Cy-sensitive auxillary cell. The secondary suppressor pathway (II) is antigen nonspecific, is mediated by a Cy-resistant suppressor T cell (Ts-II), and requires a TNP-pulsed accessory macrophage. Suppression via pathway II is demonstrable only when Ts-I cells are functionally inactivated by Cy. Furthermore, the addition of T cells from Sp containing active Ts-I inhibits Ts-II. This suppression of a suppressor cell (i.e., contrasuppression) is mediated by either Ts-I or a third T cell population, which is also Cy sensitive.
Studies of congenic MRL-Ipr/Ipr.xid mice.
Authors: Steinberg E B , Santoro T J , Chused T M , Smathers P A , Steinberg A D 
Published: December 2022

Abstract
Highly inbred MRL-Ipr/Ipr.xid congenic mice were bred and compared with their + littermates. The xid-bearing congenics developed lymphadenopathy consisting of dull Ly-1+ T cells and impairment of cellular proliferation and IL 2 production in response to the T cell mitogen Con A. Thus, the lpr gene was fully expressed. The xid gene, however, was also expressed as indicated by the failure to respond to immunization with TNP-Ficoll and flow cytometric analysis of splenic B cells. The xid gene was associated with a marked reduction in IgM anti-ssDNA and anti-nDNA of both classes, and serum Ig-bound gp 70. Kidney disease was markedly retarded as was death from the autoimmune process. These studies suggest that the T cell lymphoproliferation and dysfunction characteristic of MRL-Ipr/Ipr mice is not sufficient to induce accelerated autoimmunity; xid is able to markedly slow the process. The xid gene interferes with the development of a B cell subset necessary for maximum autoantibody production, anti-gp 70 production, and the resultant immune complex renal and cardiac disease. The present finding of protection against accelerated autoimmunity in MRL-Ipr/Ipr mice by xid, coupled with previous demonstrations of protection against autoimmunity in other autoimmune mouse strains, suggests that a common approach to the therapy of systemic lupus may be possible.
Sensitization to epithelial antigens in chronic mucosal inflammatory disease. I. Purification, characterization, and immune reactivity of murine epithelial cell-associated components (ECAC).
Authors: Aronson R A , Cook S L , Roche J K 
Published: December 2022

Abstract
To explore the autoantigenic potential of mucosal epithelium that is the site of several chronic, progressive, inflammatory and yet idiopathic diseases, epithelial cell-associated components (designated ECAC) have been isolated in aqueous-soluble form from everted, inflated loops of murine small intestine, initially characterized biochemically and immunologically, and then purified to homogeneity and studied for a disease association through quantitating, by microcytotoxicity assay, their reactivity with patient mononuclear cells and sera. Hydroxyapatite chromatography successfully separated ECAC into several series of major and minor components, with each series (designated 1, 2A, 2B, and 2C) having a unique chemical profile in terms of total carbohydrate, protein, and specific sugars (sialic acid, fucose, galactose). Furthermore, components within each series were shown not to behave as simple blood group substances antigenically, to be free of contaminating intestinal proteases (less than 0.25 micrograms chymotrypsin or equivalent per milliliter) and to possess shared as well as unique antigenic determinants (1 through 4), all of which appeared to be organ-specific for intestine. Gel filtration on Sephacryl S-200 gave a four-peak elution profile for ECAC consistent with a m.w. for components of 3000 to 232,000. Preparative polyacrylamide gel electrophoresis did isolate individual constituents of ECAC, four of which (P1, P2, P4, and P5) were homogeneous and that could, by a hemagglutination inhibition technique, be shown to possess unique organ-specific antigenic determinants. ECAC-specific reactivity of peripheral blood mononuclear cells and sera from patients in the active phase of a chronic inflammatory disorder involving mucosal epithelium indicated autosensitization had occurred, with involvement of several purified epithelium-derived macromolecules. This reactivity appeared to be antibody dependent, occurred at relatively low effector to target ratios, and was not simultaneously directed to control antigens, isolated from kidney in a manner analogous to that used for ECAC. ECAC, isolated by these techniques, may be sufficiently purified to allow an evaluation of their role in the initiation and/or progression of chronic autoaggressive processes occurring in mucosa.
Identification and quantitation of T lymphocyte subsets found in the spinal cord of the Lewis rat during acute experimental allergic encephalomyelitis.
Authors: Hickey W F , Gonatas N K , Kimura H , Wilson D B 
Published: December 2022

Abstract
Monoclonal antibodies specific for different rat T cell subsets and Ia-positive cells were used in a quantitative morphologic study of the cellular infiltrates in the spinal cords of Lewis rats during acute, actively induced experimental allergic encephalomyelitis (EAE). The predominant cell types in the inflammatory spinal cord lesions are W3/25-positive and Ia-positive cells. The relative percentages represented by each cell type remain quite constant regardless of the degree of clinical illness exhibited by the rat. These data demonstrate a quantitative profile of the infiltrating cells in acute, active EAE, and suggest that the principal inflammatory cells in these lesions are T helper cells and Ia-bearing cells (macrophages, B cells, or activated T helper cells).
Purification and characterization of TNP-specific immunoregulatory molecules produced by T cells sensitized by picrylchloride (PC1F).
Authors: Ptak W , Gershon R K , Rosenstein R W , Murray J H , Cone R E 
Published: December 2022

Abstract
T cell-derived TNP-specific factors associated with immunoregulatory activity were obtained by culture of T cells obtained from mice sensitized by skin-painting with picrylchloride. Culture medium was absorbed to TNP-Sepharose and TNP binding proteins were prepared by elution with TNP. The hapten affinity-purified proteins were characterized by size and charge and were found to be acidic 70,000 m.w. polypeptides that occur as monomers or oligomers. Oligomeric proteins interact with factors produced by mice injected with trinitrobenzenesulfonic acid to form factors that suppress specifically the ability of TNP-sensitized T cells to transfer contact sensitivity to TNP. Monomeric (no more than 70,000 m.w.) molecules do not form suppressor factors but can transfer contact sensitivity to TNP. Moreover, reduction and alkylation of oligomeric molecules inactivates their suppressor activity but causes them to be able to transfer contact sensitivity. The results suggest that T cell-derived antigen-specific molecules may have different effector functions dependent on their oligomeric state.
Fine specificity of cloned insulin-specific T cell hybridomas: evidence supporting a role for tertiary conformation.
Authors: Glimcher L H , Schroer J A , Chan C , Shevach E M 
Published: December 2022

Abstract
Two groups of cloned insulin-specific T cell hybridomas were derived from the fusion of (BALB/c X A/J)F1 T cells with the BW5147 tumor line. Group I responded only to the immunogen pork insulin and failed to respond to rat insulin, which differs only at amino acids A4 and B3. The second group of T cell hybridomas exhibited a broader pattern of reactivity to heterologous insulins because they could be stimulated with the B chain-identical pork, beef, sheep, and human insulins, as well as by isolated oxidized B chain. These hybridomas, however, displayed a much greater reactivity to pork insulin than to beef insulin or to the oxidized B chain. Comparison of the reactivity profiles of these two groups of hybridomas with the three-dimensional structure of the insulin molecule strongly suggested that group I cells were recognizing an immunogenic moiety composed of residues A4 and/or B3 in association with A chain loop determinants and that group II hybrids recognized a moiety composed of the amino acid sequence of the B chain and the A chain loop. Both groups of hybrids were restricted to the high-responder I-Ad allele but could be distinguished by their pattern of alloreactivity. We were unable to show any effect of a panel of monoclonal anti-insulin antibodies on the induction of interleukin 2 secretion by these hybridomas or to demonstrate the presence of idiotypic determinants on these T hybrids by using a panel of anti-idiotypic reagents raised against the monoclonal anti-insulin antibodies.