bluuebunny/crossref_metadata_2025_split huggingface dataset:
The accessory cell function of human alveolar macrophages in specific T cell proliferation.
Authors: Toews G B , Vial W C , Dunn M M , Guzzetta P , Nunez G , Stastny P , Lipscomb M F 
Published: December 2022

Abstract
The capacity of alveolar macrophages to support mitogen- and antigen-induced proliferation of autologous, monocyte-depleted T cells in normal, nonsmoking volunteers was studied. Purified T cells failed to proliferate in response to mitogen or antigen, whereas co-culture with peripheral blood monocytes restored responsiveness. Alveolar macrophages (AM) reconstituted the response of T cells to mitogen, indicating that AM can deliver a second proliferative signal. AM, however, were markedly inferior to monocytes in supporting antigen-induced proliferation. Thus, in 19 normal volunteers, the mean response of immune T cells to diphtheria toxoid in cultures reconstituted with normal AM was only 25% of the proliferative response to diphtheria in cultures with monocytes. Although four volunteers demonstrated antigen-presenting function equivalent to monocytes, in the remaining 15 antigen-presenting ability of AM was less than 15% that of monocytes. The difference in antigen-presenting function between AM and monocytes was not due to a difference in their display of HLA-D/DR determinants because 80% of AM were HLA-DR positive. The role of suppression in the diminished antigen-presenting function of AM was assessed in 12 volunteers utilizing mixing experiments. Eight volunteers demonstrated suppressor AM but four did not, suggesting that AM from at least some normal individuals have a faulty antigen-processing mechanism. Taken together, these studies demonstrate that AM may play three different roles in modulating T lymphocyte responses, i.e., they may present antigen, they may suppress normal responses, or they may remain immunologically inert. The factors that determine which function is expressed in vivo may determine the pulmonary response to inhaled antigen.
Prevention of granuloma development in the mouse by using T cell hybridoma products.
Authors: Ginsburg C H , Dambrauskas J T , Whitaker R B , Falchuk Z M , Greene M I 
Published: December 2022

Abstract
The ability of an azobenzenearsonate (ABA)-specific suppressor T cell factor, a soluble extract from first order suppressor T cells (Ts1), and suppressor molecules produced by a long-term T cell hybridoma to regulate ABA-specific granuloma formation was studied. ABA-derivatized syngeneic spleen cells (ABA-SC) administered subcutaneously induced persistent delayed-type hypersensitivity (DTH) responses, detected by footpad swelling and hapten-specific granuloma formation by 72 and 96 hr after challenge with ABA-bovine serum albumin coupled to polyacrylamide beads (ABA-BSA-PAB). Soluble factors from ABA-specific Ts1 prevented DTH and granulomatous development after subcutaneous administration of ABA-SC. Moreover, the in vivo administration of a factor that is derived from a Ts1 functioning hybrid cell line induced a second set of suppressor cells (Ts2) that upon transfer to syngeneic ABA-primed mice were able to inhibit granuloma formation in the footpad, as well as in the gastrointestinal tract after challenge with ABA-BSA-PAB. These experiments demonstrate the dependence of the granulomatous reaction on T cell-mediated events, as well as the potential therapeutic efficacy of an antigen-specific suppressor T cell factor and a hybridoma T cell product in limiting antigen-specific granuloma formation in vivo.
Cell surface antigens expressed by subsets of pre-B cells and B cells.
Authors: McKearn J P , Baum C , Davie J M 
Published: December 2022

Abstract
A large number of monoclonal antibodies, produced by immunizing rats with mouse pre-B cell lines, have been analyzed for their ability to define cell surface antigens expressed by B cells at early stages of differentiation. Whereas many antibodies recognized antigens on pre-B cell lines, only two clones detected cell surface antigens that were distinguished by their restricted distribution among a panel of continuous cell lines and cells from various tissues. Monoclonal antibody clone AA4.1 recognized a cell surface antigen found on all pre-B lymphomas and on one of three B lymphomas tested. This antigen was found on cells at highest frequency in the bone marrow. Adult spleen and fetal liver also have detectable numbers of AA4.1+ cells. Cells that did not express this antigen include plasmacytomas, two of three B lymphomas, T lymphomas, a stem cell line, adult liver, brain, thymus, and lymph node cells. Clone GF1.2 detected an antigen on some pre-B cell lines, one of three B lymphomas tested, and a small fraction of cells from adult bone marrow, spleen, lymph node, and fetal liver. Plasmacytomas, some pre-B lymphomas, two B lymphomas, T lymphomas, adult liver, brain, and thymus cells were negative. In adult bone marrow, AA4.1 bound to all cytoplasmic IgM+ pre-B cells, whereas GF1.2 detected one-half of these cells. Both antibodies recognized approximately 50% of surface IgM+ (sIgM+) bone marrow cells. A small population of bone marrow cells lacking any detectable Ig (surface or cytoplasmic) also reacted with these antibodies. Depletion of AA4.1 or GF1.2 antigen-bearing cells from bone marrow reduced the ability of bone marrow B cells to respond to LPS by 50 to 65%. Experiments with a cloned pre-B lymphoma demonstrate that AA4.1+ pre-B cells become sIgM+ GF1.2+ B cells after activation with LPS. These antibodies recognize cell surface determinants with restricted distribution among the B lymphocyte lineage because they detect antigens displayed by normal and transformed immature B lymphocytes.
In vitro stimulation of C3H/HeJ spleen cells and macrophages by a lipid A precursor molecule derived from Salmonella typhimurium.
Authors: Vogel S N , Madonna G S , Wahl L M , Rick P D 
Published: December 2022

Abstract
C3H/HeJ mice possess a genetic lesion that renders them significantly less responsive to the biologic effects of protein-free lipopolysaccharide (LPS) preparations, and more specifically, to the lipid A region of the LPS molecule. The in vivo manifestations of this mutation are also reflected in vitro in that cells derived from this mouse strain fail to respond to LPS when compared with cells derived from fully endotoxin-responsive mouse strains. The precise nature of this gene defect has not yet been established. In this study, we have examined in vitro the biologic activities of a structurally less complex "lipid A precursor" molecule, produced by a conditionally lethal, temperature-sensitive mutant of Salmonella typhimurium. In contrast to the intact LPS or wild-type lipid A extracted from the parental strain of Salmonella typhimurium, the lipid A precursor induced a highly significant, polymyxin B-inhibitable mitogenic response in splenic cultures derived from LPS-hyporesponsive C3H/HeJ and C57BL/10ScN (nu/nu) mice. In addition, the lipid A precursor was found to stimulate cultures of C3H/HeJ macrophages to produce significant levels of both interleukin 1 (IL 1, previously referred to as "lymphocyte activating factor" or "LAF") and prostaglandins of the E series (PGE). These findings suggest the possibility that the defect in endotoxin responsiveness exhibited by C3H/HeJ mice may be related to a defect in the processing of wild-type lipid A or LPS to a suitably stimulatory form that is structurally related to the lipid A precursor molecule.
Selective transport of serum-derived IgA into mucosal secretions.
Authors: Sheldrake R F , Husband A J , Watson D L , Cripps A W 
Published: December 2022

Abstract
The relative contribution of serum-derived and locally produced IgA has been estimated in sheep mammary secretion at various stages of lactation by comparing the transport of radiolabeled IgA and IgG2 from serum to secretions. During early and mid-lactation, but not during involution, serum IgA was selectively transported to mammary secretion on a large scale; in comparison, there was no transport of serum IgA into intestinal secretion. Estimates of local production indicated that the bulk of the IgA in mammary involution secretion and intestinal secretion was locally produced, whereas there was no evidence for local production of IgA in early or mid-lactation secretion. Our studies reveal an inverse relationship between the extent of local production of IgA by plasma cells underlying secretory epithelia and the selective transport of IgA from serum. This finding suggests that selective transport of serum IgA occurs at a number of mucosal sites, but is dependent on secretory component availability, because where local production is predominant, there are fewer secretory component molecules available for serum IgA transport. For this reason, bile transport of IgA does not represent a unique mechanism for the removal of IgA from serum.
Effect of erythrocyte membrane modulation by lysolecithin on complement-mediated lysis.
Authors: Silverman B A , Weller P F , Shin M L 
Published: December 2022

Abstract
Alterations of the physiochemical properties of membranes, such as acyl chain length of phospholipids, cholesterol content, and disturbance of the bilayer packing, affect the efficiency of membrane attack by C5b-9. In the present study, we explored the effect of lysolecithin (LL), a naturally occurring derivative of membrane phospholipids, on membrane damage by C5b-9. Sublytic doses of the L isomer of palmitoyl-lysolecithin were incorporated into the erythrocyte membranes of guinea pig (gpE) or sheep (shE) and the cells were then lysed with C5b6-C9. Marked enhancement of complement-mediated lysis was observed with LL-treated gpE after 2 hr of incubation, whereas the lytic enhancement was either nil or only marginal in shE. Studies on the kinetics of LL incorporation and metabolism in gpE membranes with 14C-LL showed that LL was rapidly incorporated and catabolized to generate free fatty acid (FA). Maximal accumulation of labeled FA in the membrane and loss of membrane-incorporated LL, resulting in approximately equimolar amounts of LL and FA, occurred at 2 hr, concomitant with enhancement of complement-mediated lysis. In shE such a breakdown of LL occurred only minimally. This quantitative difference in LL breakdown between gpE and shE was in accord with lysophospholipase activity that was two and one-half to seven times more active in gpE than shE membranes. When an ether-linked analog of LL (1-O-hexadecyl-sn-phosphorylcholine), which is resistant to lysophospholipase, was incorporated in gpE, the lytic enhancement was not observed. The results of our experiments indicate that the membrane modulating effect of LL on lysis by C5b-9 requires the enzymatic breakdown of LL.
Use of monoclonal antibodies against factor H to investigate the role of a membrane-associated protein antigenically related to H in C3b-receptor function.
Authors: Schulz T F , Scheiner O , Alsenz J , Lambris J D , Dierich M P 
Published: December 2022

Abstract
Three murine monoclonal IgG1 kappa-antibodies, MAH-1, MAH-2, and MAH-3, were raised against factor H purified from human plasma. In cross-inhibition studies MAH-3 did not compete with MAH-1 and MAH-2, and vice versa, for the binding to H, whereas MAH-1 and MAH-2 inhibited each other. MAH-1 and MAH-2 inhibited the binding of H to C3b attached to an ELISA plate as well as to C3b bound to sheep erythrocytes by means of the classical pathway convertase and of C3b to H attached to an ELISA plate. The determinant defined by MAH-1 and MAH-2 was no longer accessible on H bound to C3b. In contrast, MAH-3 interfere with the binding of H to C3b or vice versa only to a smaller extent but recognized a determinant still accessible on H bound to C3b and was able to agglutinate EAC14o23b-H in an indirect Coombs test. All three antibodies were shown to bind to tonsil cells and Raji cells in an indirect cell ELISA. The membrane-associated molecule detected by these antibodies had an apparent m.w. of 140,000 D in SDS-PAGE. All three antibodies partially inhibited the binding of EAC14o23b to tonsil lymphocytes and, in the presence of 0.1 mM DFP, to Raji cells; binding of EAC14o23bi and EAC14o23d to tonsil cells was not affected. We conclude that MAH-3 recognizes a determinant distinct from the ones recognized by MAH-1 and MAH-2, the latter possibly defining identical epitopes that are located close to the binding site for C3b. The fact that these two distinct epitopes could be detected on a 140,000-D membrane-associated protein from lymphoid cells strongly suggests that this molecule is at least antigenically related to serum H and shares with H a region carrying the binding site for C3b. The rosette inhibition studies imply that this structure is important for the binding of C3b-coated particles to lymphoid cells.
An antigen-activated DFP-inhibitable enzyme controls basophil desensitization.
Authors: Kazimierczak W , Meier H L , MacGlashan D W , Lichtenstein L M 
Published: December 2022

Abstract
Diisopropyl fluorophosphate (DFP), an inhibitor of serine esterases, enhances IgE-mediated histamine release from human basophils and blocks the desensitization process (i.e., the antigen-induced hyporesponsiveness) in these cells. Both activities occur at relatively low concentrations of DFP (0.1 to 0.5 mM) and are dependent on an antigen-activated intracellular event: if DFP is removed before antigen addition, it has neither effect. Neither hydrolyzed DFP nor the non-phosphorylating diisopropyl methyl phosphate enhanced histamine release or blocked desensitization. In addition to providing a demonstrable biochemical correlate of desensitization, our data suggest that the desensitization process controls the release of mediators of allergic reactions.
Prophylactic immunization against experimental leishmaniasis. III. Protection against fatal Leishmania tropica infection induced by irradiated promastigotes involves Lyt-1+2- T cells that do not mediate cutaneous DTH.
Authors: Liew F Y , Howard J G , Hale C 
Published: December 2022

Abstract
Protective immunity against fatal L. tropica infection in genetically vulnerable BALB/c mice can be induced by prophylactic immunization with irradiated promastigotes even when heat-killed. Such immunity is adoptively transferable transiently into intact or durably into sub-lethally irradiated (200 or 550 rad) syngeneic recipients by splenic T but not B cells. The effector T cells are of the Lyt-1+2- phenotype, devoid of demonstrable cytotoxic activity. The immune splenic T cell population expresses specific helper activity for antibody synthesis. A causal role for helper T cells in this capacity, however, seems unlikely, because it was shown in the accompanying paper that antibody does not determine the protective immunity against L. tropica. The immunized donors show no detectable cutaneous DTH or its early memory recall in response to live or killed promastigotes or a soluble L. tropica antigen preparation. Spleen, lymph node, and peritoneal exudate cells from protectively immunized donors similarly fail to transfer DTH locally or systemically. These cells also lack demonstrable suppressive activity against the expression or induction of DTH to L. tropica. Thus, protection against L. tropica induced by prophylactic i.v. immunization with irradiated promastigotes appears to be conferred by Lyt-1+2- T cells that are distinguishable from T cells mediating either both DTH and T help, or cytotoxicity.
Complete sequence of a cloned cDNA encoding rabbit secreted mu-chain of VHa2 allotype: comparisons with VHa1 and membrane mu sequences.
Authors: Bernstein K E , Alexander C B , Reddy E P , Mage R G 
Published: December 2022

Abstract
The complete sequence of a cDNA clone (pmu3) encoding a secreted IgM heavy chain from a rabbit of VHa2 allotype has been determined. Comparison of the nucleic acid and amino acid sequences with a comparable mouse mu-chain shows unusually high homologies of the sequences of the fourth domains and secretory portions of the molecules (80 to 90% vs 56 to 73% for the other domains). This high degree of homology is also seen with the sequences of the fourth domain and secreted terminus of human mu-chain. The DNA sequence of a second cDNA clone encoding the membrane form of rabbit IgM is approximately 90% homologous with the mouse and human coding sequences for the membrane terminus, and there is 98 and 97% amino acid sequence homology. We found an unusually long (156 base pair) 5' untranslated region in clone pmu3 and discovered that 105 bases at the 5' end were complementary to the terminal portion of the CH4 domain of our mu sequence. Southern blotting analyses and the finding of a 13 base pair segment in rabbit genomic V region DNA that is homologous to the complementary strand of a segment of the CH4 of rabbit mu strongly suggests that this extended sequence resulted from a reverse transcriptase "hooking error". We have also obtained and sequenced another cDNA clone from a VHa1 cDNA library. Comparison of the V region of clone pmu3 from VHa2 with the 117 available positions of a1 DNA sequence shows 25 differences, nine of which are in allotype-associated codons. There is also a two-codon deletion in the VHa1 compared to VHa2 in the third framework region that may contribute to allotypic differences. Development of VHa allotype-specific probes, now in progress, is complicated by the fact that most of the allotype-associated amino acids of a1, a2, and a3 can be derived from each other by single base changes.
Effect of mouse interferon on the expression of a porcine major histocompatibility gene introduced into mouse L cells.
Authors: Satz M L , Singer D S 
Published: December 2022

Abstract
Mouse L cells transformed with a swine genomic clone, which encodes a major histocompatibility (MHC) antigen (SLAd), stably express SLAd on their surface. Mouse interferon (IFN) markedly enhances the expression of the heterologous SLAd as well as endogenous H-2k antigens in two independent transformants, as measured by flow microfluorometry. The expression of an unrelated surface antigen, gp70, is not affected. The increased expression of SLAd antigens is the result of an increased pool of SLA mRNA in IFN-treated cells. In vitro nuclear transcription experiments suggest that this increased accumulation of SLA mRNA results largely from an enhanced transcription of the heterologous SLA gene. The effect of IFN is not restricted to the MHC coding sequences; the transcription of two DNA sequence elements flanking the SLA gene, which are constitutively expressed in one L cell transformant, is also enhanced by IFN. In contrast, in another transformant these same flanking sequences are not transcribed and do not respond to IFN. The results suggest that IFN enhances the transcription of MHC coding and the flanking sequences that are expressed in its absence, but it does not appear to induce do novo transcription of the silent flanking genes examined.
Analysis of surface mu-chain expression in human lymphoblastoid cell lines that do not produce light chains.
Authors: Hendershot L , Levitt D 
Published: December 2022

Abstract
It has been suggested that light chains (LC) are necessary for the surface expression of mu heavy chains. Fluorescent antibody screening of 42 human lymphoblastoid cell lines transformed in our laboratory, however, disclosed four lines that expressed surface mu-chains without LC. The biosynthesis, glycosylation, and turnover of mu-chains in these cell lines was compared to mu-chain production in cell lines synthesizing both heavy chains and LC. LC production could not be detected in the mu +LC- cell lines by either surface or biosynthetic labeling. The mu-chains expressed on the surface of the LC- cells appeared as disulfide-linked dimers and migrated slightly faster on SDS-polyacrylamide gels (70 Kd) than did mu-chains from IgM monomers (H2 L2) (78 Kd) after reduction. Biosynthetic labeling in the presence of tunicamycin demonstrated that the smaller size of free mu heavy chains was due to incomplete glycosylation of these molecules and not to amino acid deletions. The mu-chains produced by mu + LC- cells lines were degraded faster than mu-chains from LC+ cell lines, but their rate of transit to the cell surface was identical in both cell types. Thus, although LC are necessary for the formation of an intact antigen-binding site, they are not involved in the synthesis or expression of membrane mu-chains.
Cytotoxic T lymphocyte recognition of HLA-A/B antigens introduced into EL4 cells by cell-liposome fusion.
Authors: Engelhard V H , Powers G A , Moore L C , Holterman M J , Correa-Freire M C 
Published: December 2022

Abstract
HLA-A2 and -B7 antigens were introduced into EL4 (H-2b) cells by cell-liposome fusion and were used as targets or stimulators for cytotoxic T lymphocytes (CTL) generated in C57B1/6 (H-2b) mice. It was found that such EL4-HLA cells were not recognized by CTL that had been raised against either a human cell line bearing these HLA antigens or the purified HLA-A2 and -B7 antigens reconstituted into liposomes. In addition, EL4-HLA cells were not capable of inducing CTL that could recognize a human cell line bearing HLA-A2 and -B7 antigens. Instead, EL4-HLA cells induced CTL that specifically lysed EL4-HLA cells and not human cells expressing HLA-A2 and -B7. CTL recognition required the presence of HLA antigens on the EL4 cell surface and was inhibited by antibodies against either H-2b or HLA-A/B. Monoclonal antibody binding studies showed that the expected polymorphic determinants of the HLA-A2 and -B7 antigens were still present on EL4-HLA cells. However, the specificity of CTL or their precursors that are capable of recognizing HLA-A2 or -B7 was altered after these antigens became associated with the EL4 surface. Possible explanations for these results are discussed.
Immune reactivity and immunosuppressive intervention (TLI) in experimental nephritis. I. Immunopathologic correlates in the accelerated autologous form of nephrotoxic serum nephritis.
Authors: Lowry R P , Forbes R D , Blackburn J H 
Published: December 2022

Abstract
The progression of histologic changes observed in the accelerated autologous form of nephrotoxic serum nephritis (AA-NTSN) in the inbred LEW rat, ranging from minimal endocapillary proliferation to marked endo- and extra-capillary proliferation together with fibrin deposition and necrosis of glomerular tufts, was closely correlated (day 8) with parallel measures of albuminuria (1.6 leads to 280 mg/24 hr). In the induction phase of AA-NTSN (day 0) a direct linear correlation (r = 0.72, p less than 0.05) was obtained between anti-SGG antibody levels and 24-hr urine albumin excretion. Subsequent observations (day 7) yield an inverse correlation between anti-SGG antibody and albuminuria (r = -0.54, p less than 0.01), and this change was shown to be related to the loss of specific antibody in the urine (r = 0.59, p less than 0.025). Although splenic T cells of rats with AA-NTSN manifest a specific proliferative response to the inducing antigen SGG, and although the magnitude of this proliferative response (day 7) correlates directly with parallel measures of urine albumin excretion (r = 0.71, p less than 0.02), delayed-type hypersensitivity (DTH) to SGG measured by radiometric ear assay was inversely correlated with albuminuria in this model of experimental nephritis (r = 0.80, p less than 0.01). Additional data are presented that strongly suggest that persistent albuminuria at 1 mo after induction of AA-NTSN is independent of ongoing immunopathologic processes. Thus, glomerular injury in AA-NTSN, previously linked to prominent glomerular macrophage accumulation, is shown to be primarily dependent on a brisk antibody response to the planted heterologous (sheep) immunoglobulin, whereas cellular immunity, readily demonstrated in the splenic T cell compartment, is likely to be of lesser import in the pathogenesis of this lesion in the intact animal.