bluuebunny/crossref_metadata_2025_split huggingface dataset:
Molecular basis for the temperature-dependent insolubility of cryoglobulins. X. The amino acid sequence of the heavy chain variable region of McE.
Authors: Gerber-Jenson B , Kazin A , Kehoe J M , Scheffel C , Erickson B W , Litman G W 
Published: December 2022

Abstract
The amino acid sequence of the VH region of McE, a monoclonal IgM cryoimmunoglobulin, has been determined employing automated sequencing methodology. Digestion of the intact Fab mu component, derived by trypsin cleavage of the parent protein at elevated temperature with CNBr, followed by complete reduction and alkylation, yielded the intact light chain as well as the 2 CNBr fragments that constituted the VH. N-terminal sequencing of the larger unblocked CNBr fragment, along with a component fragment derived by cleavage by BNPS-Skatole, established the structure of the VH from position 88 through the V leads to C switch region. Citraconylation of the smaller, blocked fragment effected sufficient solubilization for enzymatic deblocking and direct sequencing of the N-terminal 20 residues of the VH. Complete trypsin digestion of the N-terminal CNBr fragment yielded 9 peptides that could be isolated by preparative cation exchange chromatography and gel filtration. The complete sequence of these peptides along with 4 chymotryptic peptides completed the primary structure of the VH region. The primary structure of McE appears to resemble that of He, previously identified as belonging to the VH II subgroup. The presence of characteristic CDR and FR regions as well as the identification of a probable site of glycosylation suggest that the cryoimmunoglobulin closely resembles noncryoglobulins in terms of overall structural composition. The cryoglobulin property may arise through alterations in individual residues or unfavorable arrangements of CDR and FR segments.
Human thy-1: unusual localization and possible functional significance in lymphoid tissues.
Authors: McKenzie J L , Fabre J W 
Published: December 2022

Abstract
BALB/c mice were immunized with purified human brain Thy-1 and used in cell fusion experiments to derive an anti-human Thy-1 monoclonal antibody. Specificity was proven by a) showing that the antigen recognized had precisely the tissue distribution expected of human Thy-1 from previous studies, and b) demonstrating that the molecule purified from human brain by monoclonal antibody affinity columns 1) had the same mobility on SDS PAGE as pure rat Thy-1 and 2) could inhibit an assay previously shown to be directed at the human-rat cross-reactive component of Thy-1. Studies with the fluorescence-activated cell sorter confirmed that Thy-1 is absent from human blood lymphocytes and cell suspensions from human lymphoid organs, except that very weak fluorescence could be detected on 7% of thymus cells in suspension. However, fluorescence studies on frozen sections showed bright staining restricted mainly to the periphery of the thymus lobule, the marginal zone and some periarteriolar lymphocytes in the spleen, and the post-capillary venules of lymph node. In some lymph nodes, a halo of Thy-1 positive cells was seen around lymphatic nodules or germinal centers, but this was not a constant finding. This distribution is different from the known distribution of Thy-1 in the lymphoid tissues of the mouse and rat. Our studies suggest that human Thy-1 might be involved in lymphocyte recirculation, and that it is a marker for early T lymphocytes in man. The studies also show that the few Thy-1 positive cells in human lymphoid organs are selectively lost in the preparation of single-cell suspensions.
Age-associated increase in expression of the T cell surface markers Thy-1, Lyt-1, and Lyt-2 in congenitally athymic (nu/nu) mice: analysis by flow microfluorometry.
Authors: MacDonald H R , Lees R K , Sordat B , Zaech P , Maryanski J L , Bron C 
Published: December 2022

Abstract
The expression of T cell-associated surface markers by lymphoid cells from congenitally athymic (nude) mice has been quantitatively investigated using flow microfluorometry. Spleen and lymph nodes from old (greater than 6 mo) nude mice on either a C57BL/6 or BALB/c genetic background were found to contain significant numbers (5 to 13% in spleen and 15 to 24% in lymph nodes) of cells expressing Thy-1 antigen. The proportion of Thy-1 positive cells in nude spleen was dramatically increased (to 22 to 67%) after passage of the cells over nylon wool columns. In contrast to older animals, young (1- to 2-mo-old) nude mice had undetectable levels (less than 1%) of Thy-1 bearing cells in spleen and reduced levels (6%) in lymph nodes. After passage of their spleen cells over nylon wool, some Thy-1 positive cells (10%) were detectable in 2-mo-old nude mice but none were detectable at 1 mo. In addition to Thy-1, we were able to detect the T cell alloantigens Lyt-1 and Lyt-2 on nylon wool-passed spleen cells from older C57BL/6 or BALB/c nu/nu mice. In general, the proportion of Lyt-1 bearing cells in nude lymphoid populations was similar to the proportion of Thy-1 positive cells. A smaller fraction of nude cells (corresponding to 35 to 59% of the total Thy-1 positive cells) were found to express Lyt-2. Analysis of the forward light scatter distributions of nude lymphoid cells bearing either Thy-1, Lyt-1, or Lyt-2 antigens further demonstrated that an overlapping population of relatively large-size cells expressed these surface markers. These data strongly imply that at least 2 subsets of T cells (i.e., Lyt-1+2- and Lyt-1+2+) develop in older nude mice in the apparent absence of thymic influence.
Accessory cells in the in vitro generation of type C viruses specific T killer lymphocytes. I. Role of macrophages in primary anti-FMR reaction.
Authors: Gomard E , Wybier-Franqui J , Levy J P 
Published: December 2022

Abstract
The role of macrophages has been studied in in vitro cytolytic T lymphocytes- (CTL) mediated responses directed against the FMR cell-surface antigens induced by C type viruses. Macrophages, defined as Thy 1.2-negative, Ia-positive, adherent, phagocytic, radioresistant cells present in the spleen and the peritoneal cavity, are required to obtain primary in vitro anti-FMR responses. In most of our experiments they were not necessary in secondary reactions. In primary responses, macrophages and responder T cells must be compatible at least at the I region of the major histocompatibility complex. Anti-Ia antibodies inhibit the response. A rat soluble factor (Interleukin 2) can replace macrophages in primary anti-FMR CTL-mediated reactions. These results suggest that macrophages function during primary anti-FMR response by interacting with a helper T cell rather than with CTL precursors. In agreement with this hypothesis, it appears that the H-2 restriction of F1 hybrid anti-FMR CTL generated in vitro in primary reaction is not related to the H-2 specificities of the parental macrophages used and depends only on the H-2 antigens of the stimulating tumor cells.
Tuftsin: a naturally occurring immunopotentiating factor. I. In vitro enhancement of murine natural cell-mediated cytotoxicity.
Authors: Phillips J H , Babcock G F , Nishioka K 
Published: December 2022

Abstract
Tuftsin is a physiologic tetrapeptide, which has recently been shown to possess immunoadjuvant properties including the stimulation of macrophage and granulocyte phagocytosis, migration, bactericidal, and tumoricidal activities. Tuftsin has also been reported to possess in vivo immunologically mediated anti-tumor potential. To determine the potential role of tuftsin as an antineoplastic immunoadjuvant, the in vitro effects of tuftsin on murine natural cell-mediated cytotoxicity were studied. We observed that in vitro treatment of mouse splenic effector cells with synthetic tuftsin induced a pronounced enhancement of natural killer cell (NKC) cytotoxicity against the T cell lymphoma Yac-1. The magnitude of NKC enhancement was directly dependent upon the concentration of tuftsin employed, with maximum NKC stimulation observed at tuftsin concentrations of 50 to 100 microgram/ml. The tuftsin induced enhancement of NKC activity was not strain specific, since equivalent stimulation was seen in CBA/J, C56BL/10, and DBA/2 mice. Elimination of macrophages, monocytes, T cells, and immunoglobulin-bearing cells had no effect on the dose-dependent tuftsin stimulation of natural cell-mediated cytotoxicity; thus the characteristics of the effector cells activated by tuftsin were consistent with those reported for NKC. We also observed that treatment of splenic effector cells with tuftsin prolonged the cytotoxic capabilities of these cells beyond 18 hr.
Induction of IgG memory responses with polyvinylpyrrolidone (PVP) is antigen dose dependent.
Authors: Lite H S , Braley-Mullen H 
Published: December 2022

Abstract
Irradiated recipients of spleen cells from mice primed with a very low dose (0.0025 microgram) of the thymus-independent (TI) antigen polyvinylpyrrolidone (PVP) produced PVP-specific IgG memory responses after secondary challenge with a T-dependent (TD) form of PVP, PVP-HRBC. The IgG memory responses induced by low doses of PVP were similar in magnitude to those induced by the TD antigen PVP-HRBC. The induction of IgG memory by the TI form of antigen was markedly dependent on the dose of PVP used to prime donor mice. Spleen cells from mice primed with an amount of PVP (0.25 microgram) that induces an optimal primary IgM response did not produce significant IgG antibody after challenge with PVP-HRBC. The inability of higher doses of PVP to induce IgG memory may be due, at least in part, to the fact that such doses of PVP were found to induce tolerance in PVP-specific B cells and could suppress the induction of memory induced by PVP-HRBC. Low doses of PVP did not interfere with the induction of memory by PVP-HRBC. Expression of IgG memory responses in recipients of PVP-HRBC or low-dose PVP-primed cells was found to be T cell dependent. Moreover, only primed T cells could reconstitute the response of recipients of primed B cells, suggesting that the ability of PVP to induce IgG memory may be related to its ability to prime T helper cells. Expression of the IgG memory response in recipient mice also required the use of a TD antigen for secondary challenge, i.e., mice challenged with PVP did not develop IgG. The inability of PVP to elicit IgG antibody was due in part to the fact that 0.25 microgram PVP was tolerogenic, i.e., it could interfere with the expression of memory in mice simultaneously challenged with both PVP and PVP-HRBC.
Identification of H-2-controlled structural variants of the murine Slp protein and demonstration of cis-regulation of its expression.
Authors: Parker K L , Carroll M C , Shreffler D C , Capra J D 
Published: December 2022

Abstract
H-2 haplotype-related structural variation in Slp beta-chains was detected by the limited proteolysis peptide mapping technique. Two distinct peptide patterns were distinguished: Slp.1 was found in strains carrying the S regions of the H-2d and H-2s haplotypes, and Slp.2 was found in strains bearing the S region of H-2w7. These different patterns were expressed codominantly in male (Sd X Sw7)F1 hybrids, whereas only the Slp.2 pattern was expressed in female heterozygotes. The 2 beta-chains are most likely the products of alleles of the Slp structural gene, which must then be located in the murine major histocompatibility complex, very probably in the S region.
Alterations of interferon production in a mouse model of thermal injury.
Authors: Suzuki F , Pollard R B 
Published: December 2022

Abstract
The effect of thermal injury on the response of interferon (IFN) production in vivo and in vitro after stimulation with eight representative inducers was investigated in a mouse model. The response of mice to immune IFN (IFN-gamma) inducers, staphylococcal enterotoxin A, concanavalin A, and a specific antigen for BCG-sensitized lymphocytes (purified protein derivative) was impaired after a 30% total body surface area third-degree burn. Suppression of IFN-gamma production was observed at day 2 and persisted until day 7 after burn. Decreased IFN-gamma production correlated closely with the percentage of total body surface area burned. When virus type IFN (IFN-alpha/beta) inducers, Newcastle disease virus, polyriboinosinic-polyribocytidylic acid, 10-carboxymethyl-9-acridanone, and E. coli endotoxin, were administered to mice, no change in IFN response was observed after thermal injury. Similar results were obtained when spleen cells obtained from thermally injured mice were stimulated with IFN-gamma inducers in vitro. These studies suggest that although the capacity for IFN-alpha/beta production remains intact in thermally injured mice, IFN-gamma production may be selectively decreased in burned animals and in their spleen cells.
Mechanism for the suppression of gamma-interferon responsiveness in mice after thermal injury.
Authors: Suzuki F , Pollard R B 
Published: December 2022

Abstract
As reported previously, gamma-interferon production was decreased after the administration of inducers to thermally injured mice as compared with noninjured controls. Similarly, spleen cells from injured mice had decreased ability to produce interferon in vitro after stimulation with inducers. The present study demonstrated that the decrease in interferon production was associated with the presence of suppressor cells in the spleen of burned mice that were capable of inhibiting interferon production by normal splenic lymphocytes in vitro. Passive transfer of spleen cells containing suppressor cell activity derived from injured mice induced suppression in normal mice, and the time of the appearance of suppressor cell activity in injured mouse spleens closely approximated the time of the appearance of the suppression of interferon production observed in mice after thermal injury. The suppressor cells were characterized as a population of macrophages by the following: they adhered to plastic surface and could be removed from spleen cells by carbonyl-iron treatment; treatment of plastic-adherent cells with anti-Thy-1.2 and anti-mouse immunoglobulin antisera followed by complement failed to abrogate the suppression produced by these cells.
Cell surface alpha 1-protease inhibitor on human peripheral mononuclear cells in culture.
Authors: Boldt D H , Chan S K , Keaton K 
Published: December 2022

Abstract
We have studied expression of alpha 1-protease inhibitor (alpha 1-PI) by human mononuclear cells. alpha 1-PI was detected on 50% of freshly isolated peripheral mononuclear cells. Unless a proliferative stimulus was provided, alpha 1-PI subsequently disappeared from the cell surfaces. Plant mitogens, periodate, neuraminidase-galactose oxidase, or allogeneic cells all were effective stimuli of alpha 1-PI expression. Concanavalin A stimulated de novo synthesis of alpha 1-PI in cell cultures containing both lymphocytes and mononuclear phagocytes, and alpha 1-PI simultaneously appeared on surfaces of activated lymphocytes. Inhibition of protein synthesis by cycloheximide or monocyte depletion abolished de novo alpha 1-PI synthesis, but only monocyte depletion inhibited alpha 1-PI expression. Lymphocytes, but not monocytes, displayed saturable binding of radioiodinated alpha 1-PI. The data are consistent with the interpretation that human mononuclear phagocytes synthesize and secrete alpha 1-PI. When protein synthesis is inhibited, mitogenic stimuli may provoke release of previously synthesized alpha 1-PI from mononuclear phagocytes. Secreted alpha 1-PI then may bind to specific lymphocyte cell surface receptors. This pattern of alpha 1-PI synthesis, secretion, binding, and expression on lymphoid cell surfaces appears to be a common characteristic of many immunologic reactions in vitro.
Analysis of cloned T cell function. I. Dissection of cloned T cell proliferative responses using cyclosporin A.
Authors: Orosz C G , Fidelus R K , Roopenian D C , Widmer M B , Ferguson R M , Bach F H 
Published: December 2022

Abstract
CsA interferes in a specific manner with the expansion of T cell clones in that it inhibits the antigen-driven component of the proliferative responses made by cloned helper T cells, cloned conventional cytolytic T cells, and cloned helper-independent cytolytic T cells. Cloned helper T cells and helper-independent cytolytic T cells, which share the ability to proliferate when cultured with specific alloantigen, fail to proliferate when cultured with specific alloantigen, fail to proliferate in response to this stimulus in the presence of CsA (10 to 100 ng/ml). In contrast, the proliferation observed when these cells are cultured with exogenous growth factors (but not alloantigen) is little influenced by as much as 1000 ng/ml CsA. When cloned helper T cells or helper-independent cytotoxic T cells are cultured with alloantigen plus exogenous growth factor, additive or synergistic proliferation occurs. However, CsA (10 to 1000 ng/ml) blocks only the component of proliferation induced by alloantigen, and leaves the lymphokine-driven component intact. CsA has similar effects on the proliferation of cloned conventional cytolytic T cells. Thus, CsA separates cloned T cell proliferation into two components: one driven by contact with alloantigens, the other driven by contact with mitogenic lymphokines.
In vivo allogeneic effects: shift in the isotype profile of primary TI-2 responses in mice undergoing graft-vs-host reaction.
Authors: Golding H , Rittenberg M B 
Published: December 2022

Abstract
We showed previously that primary responses to T-dependent (TD) and T-independent type 2 (TI-2) antigens were differentially affected by allogeneic effects induced in vivo during a graft-vs-host reaction (GVH). TD responses were greater than or equal to 80% suppressed, whereas the TI-2 responses were greatly enhanced, particularly the IgG component, which normally is very low. We have analyzed the IgG subclass distribution in primary responses of normal and GVH F1 mice in order to determine whether the strong T cell signals that occur during GVH reactions also induce shifts in the isotype profile. The effect of GVH on responses to TI-2 antigens was of particular interest because they are usually dominated by IgM and IgG3 classes in normal mice. We found a threefold to 10-fold increase in the PFC numbers of all four IgG subclasses in the response to TI-2 antigens, with an apparent shift from the usual IgG3 dominance to IgG1 in GVH mice. This IgG1 dominance was not found in serum antibodies where IgG3, IgG1, and IgG2b were equally expressed, although total IgG was increased greater than 20-fold. No isotype shift was found in either the TNP-KLH response, which was greater than or equal to 75% suppressed (IgG1 dominance was retained), or in the TI-1 response to TNP-Ba. The latter response was reduced (25 to 50%) in GVH mice and continued to be dominated by IgG2b/2a and IgG3. Unlike the unique isotype patterns found in primary responses, TNP-KLH primed mice challenged with TD, TI-1, or TI-2 antigens gave memory responses with identical isotype profiles that were dominated by IgG1 PFC. The role of T cells in B cell differentiation and isotype expression is discussed.
Alteration of in vitro immunoglobulin secretion by amosite asbestos.
Authors: Lawrence E C , McClung H W , Wilson R K , Key M M , Dodson R M , Hurst G A 
Published: December 2022

Abstract
We investigated the in vitro effects of amosite asbestos on immunoglobulin (Ig) secretion by human peripheral blood mononuclear leukocytes (MNL). Concentrations of 100 to 300 micrograms/ml of amosite asbestos reduced the number of Ig-secreting cells recovered from 6-day cultures of unstimulated MNL or MNL stimulated with Epstein Barr virus. By contrast, the Ig secretory response to pokeweed mitogen was enhanced by 10 to 100 micrograms/ml concentrations of amosite asbestos; however, amosite asbestos no longer enhanced the response to pokeweed mitogen when MNL were first partially depleted of monocytes (to less than 2%) esterase-positive cells remaining). These results indicate that amosite asbestos has multiple effects on the cells involved in Ig secretion: 1) amosite asbestos inhibits unstimulated B cell function; 2) amosite asbestos inhibits the function of B cells stimulated with the direct B cell activator Epstein Barr virus; and 3) amosite asbestos may alter regulator monocyte function allowing enhanced Ig secretion in the presence of monocyte-dependent B cell triggers such as pokeweed mitogen.
Selective induction of autoantibody secretion in human bone marrow by Epstein Barr virus.
Authors: Fong S , Vaughan J H , Tsoukas C D , Carson D A 
Published: December 2022

Abstract
The bone marrow is an important site for B lymphocyte differentiation and antibody synthesis in animal and man. However, few experiments have examined directly its immunologic functions in humans. In the present experiments, we have induced bone marrow B lymphocytes from human donors with degenerative arthritis of varying ages to secrete two autoantibodies, IgM and anti-IgG (rheumatoid factor) and IgM anti-human thyroglobulin (Tg), by stimulation with the polyclonal B cell activator Epstein Barr virus (EBV). The EBV-stimulated bone marrow cells secreted significantly more IgM anti-IgG (p less than 0.01) and IgG anti-Tg (p less than 0.01) than matched, identically treated peripheral blood cells. Bone marrow cultures from donors over the age of 60 yr, particularly females, produced more rheumatoid factor than cultures from younger donors (p less than 0.01). The EBV-inducible autoantibodies were immunospecific as demonstrated by adsorption studies. A potential pathogenic role in the inflammatory process was suggested by the finding that the EBV-inducible IgM anti-IgG autoantibodies were capable of activating the classical complement pathway as assessed by the cleavage of C4. These results indicate that the human bone marrow is a selective reservoir for EBV-inducible autoantibody precursor B lymphocytes, and that the size of the reservoir increases with age.
Rapid induction of seven proteins in human lymphocytes by interferon; correlation to natural killer cell activity.
Authors: Gustafsson A , Sundström S , Ny T , Lundgren E 
Published: December 2022

Abstract
The early effects of interferon (IFN) on the synthesis of protein in human nylon wool-nonadherent lymphocytes have been stimulated by use of two-dimensional electrophoresis. IFN-alpha or -beta as well as Escherichia coli-produced IFN-alpha 2 induced the rapid formation of seven proteins (Mr 80, 75, 62, 53, 38, 36, and 33 kD). At least five proteins were expressed within 2 hr of incubation with IFN. The synthesis of the seven proteins seemed to require rapid transcription of new RNA, because actinomycin D markedly inhibited their formation only when added less than 30 min after IFN. A good correlation was found between the ability of actinomycin D to inhibit both the formation of new proteins and the augmentation of natural killer (NK) cell activity. Screening of a panel of 10 hematopoietic and two anchorage-dependent cell lines revealed that p62 and p38 were induced in most cell lines, whereas p80 and p33 were preferentially induced in lymphoid cell lines. Three proteins could not be induced by IFN in any of the 12 cell lines, and thus could represent molecules mediating differentiated functions, possibly involved in NK cell function.