bluuebunny/crossref_metadata_2025_split huggingface dataset:
T cell induction of macrophage IL-1 during antigen presentation. Characterization of a lymphokine mediator and comparison of TH1 and TH2 subsets.
Authors: Weaver C T , Duncan L M , Unanue E R 
Published: December 2022

Abstract
We described in a previous study two pathways by which Th cells induced macrophage membrane IL-1(mIL-1) during Ag presentation. One pathway was lymphokine-independent and mediated by cell-cell contact. The second was lymphokine-dependent. We have now characterized this lymphokine and show that it belongs to the TNF family of proteins. All TH1 and most TH2 clones produced the lymphokine, although TH1 levels were markedly greater. Both types of clones also induced macrophage mIL-1 by cell-cell contact (i.e., in the absence of lymphokine release). Examination of macrophages by in situ hybridization showed that both IL-1 alpha and IL-1 beta mRNA were coordinately induced during Ag presentation to either TH1 or TH2 clones.
Reactivity of anti-human milk fat globule antibodies with synthetic peptides.
Authors: Xing P X , Tjandra J J , Reynolds K , McLaughlin P J , Purcell D F , McKenzie I F 
Published: December 2022

Abstract
The nucleotide sequence of partial cDNA clones coding for the core protein of a human polymorphic epithelial mucin has recently been obtained, this mucin consists of a highly conserved 60 bp tandem repeat and the amino acids commonly found are PDTRPAPGSTAPPAHGVTSA. We synthesized three peptides, 1) P1.24 containing the 20 amino acids and four amino acids (PDTR) of the adjoining repeat; 2) P1.15 consisting of the first fifteen (PDTRPAPGSTAPPAH) and P1.09 the second nine amino acids (GVTSAPDTR) of peptide P1.24. The reactivities of the synthetic peptides with mAb known to react with breast cancer (BC1, BC2, BC3, HMFG-1, 3E1.2, and RCC-1) were studied. The synthetic peptide, P1.24, corresponding to the antigenic sequence predicted from the tandem repeat reacted with antibodies BC1, BC2, and BC3 (known to react with human milk mucin and mucin expressed in breast cancer) and the antibody HMFG-1 which was used to select the cDNA clones. In addition, the epitopes recognized by BC1, BC2, and BC3 appear to be in the same region of the molecule represented by their reactions with the nine amino acids in peptide P1.09 (GVTSAPDTR). By contrast, other antibodies such as 3E1.2 which reacts only weakly with components of human milk, and RCC-1 that detects a low Mr component (95 kDa) in breast cancer, had no specific reaction with the synthetic peptides, indicating that their epitopes are distinct from those of BC1, BC2, BC3, and HMFG-1. Inasmuch as the antibodies HMFG-1, BC1, BC2, and BC3 react with the fully processed milk mucin, it is likely that some of the peptide is exposed, even in the fully glycosylated molecule. Identification of the different epitopes could lead to the development of "second generation" mAb with enhanced specificity for breast carcinoma using the appropriate synthetic peptides as immunogens.
HIV-1 and its envelope glycoprotein down-regulate chemotactic ligand receptors and chemotactic function of peripheral blood monocytes.
Authors: Wahl S M , Allen J B , Gartner S , Orenstein J M , Popovic M , Chenoweth D E , Arthur L O , Farrar W L , Wahl L M 
Published: December 2022

Abstract
Peripheral blood monocytes from AIDS patients exhibit defective migratory responses to chemotactic stimuli in vitro and to inflammatory sites in vivo. In studies presented here, normal monocytes were infected with the HIV-1/HTLV-IIIBa-L isolate in vitro and evaluated for chemotactic responsiveness. Within 2 days after viral exposure, but before evidence of virus production in the monocytes, chemotactic activity was significantly impaired. Decreased chemotactic activity was associated with modulation of receptors for the chemotactic ligands, C5a and FMLP, on the monocyte cell surface. In addition to HIV-1, monocytes treated with purified HIV-1 envelope glycoprotein gp120 demonstrated a comparable modulation of chemotactic ligand receptors and migratory function. In addition, the HIV-1 or HIV-1 gp120-treated monocytes were induced to undergo differentiation as monitored by HLA-DR expression. Immunoprecipitation of the gp120 with a specific antibody reversed its effects on monocyte chemotaxis and HLA-DR expression. Taken together, these data indicate that the initial interaction of HIV-1 with the monocyte is not passive, but that the binding of HIV-1 and/or HIV-1 gp120 to the CD4R on monocytes transduces a signal leading to transient monocyte activation.
Effects of neonatal injections of anti-CD3 epsilon monoclonal antibodies on the T cell functions of adult mice.
Authors: Rueff-Juy D , Drapier A M , Cazenave P A 
Published: December 2022

Abstract
The effect of neonatal injections of anti-CD3 mAb on the subsequent immune responsiveness of adult mice has been investigated. The data indicate that neonatal treatment with three injections of 50 microliters of anti-CD3 epsilon ascitic fluid induce a profound depletion of T cells in the peripheral lymphoid organs but do not modify the absolute number of thymocytes. This treatment completely abolishes the T cell functions of mice at least 3 wk after the last injection of mAb. In the thymus, this suppression is associated with a decrease in the number of TcR/CD3 molecules in the dull CD3+ cells and with a drastic reduction the bright CD3+ population. However, the amount and the size of the TcR alpha,beta and CD3 epsilon mRNA transcripts are not modified, suggesting that the down-regulation of the TcR/CD3 complex induced by anti-CD3 mAb does not exert a feedback inhibition on the transcription of TcR genes. The suppression induced by neonatal injections of anti-CD3 epsilon mAb is reversible and the induction of immune responses requires the reappearance of a minimal number of bright CD3+ cells. However, this suppression can be maintained without side effects for several months provided that anti-CD3 mAb were administered at 7-day intervals from birth. This injection schedule should allow the study of the effect of anti-CD3 antibodies during the T cell ontogeny on the establishment of the B and T cell repertoires.
Class II restriction in mice to the malaria candidate vaccine ring infected erythrocyte surface antigen (RESA) as synthetic peptides or as expressed in recombinant vaccinia.
Authors: Lew A M , Langford C J , Pye D , Edwards S , Corcoran L , Anders R F 
Published: December 2022

Abstract
The immune response to three peptides corresponding to the repeat regions of the malaria candidate vaccine ring infected E surface Ag (RESA) were studied. Both antibody responses and lymphocyte stimulation in mice injected with these peptides without carrier were found to be restricted to certain MHC class II haplotypes. Mice bearing IAk were strong responders to all three peptides. Mice bearing IAd were strong responders only to the 3' repeat peptides, the octamer and tetramer. Mice bearing Is or Iq did not respond to any repeat peptides. Remarkably, the pattern of genetic restriction of the antibody response to the entire RESA as expressed in vaccinia indicated that there were no other epitopes besides the three repeats. Because only one class II haplotype (i.e., k) out of five tested responded strongly to this peptide and only two out of five (i.e., k and d) responded to the octamer or tetramer, it may be difficult to achieve a good immune response against RESA in most or all humans.
Increment in the Ta1+ cells in the peripheral blood and thyroid tissue of patients with Graves' disease.
Authors: Eguchi K , Ueki Y , Shimomura C , Otsubo T , Nakao H , Migita K , Kawakami A , Matsunaga M , Tezuka H , Ishikawa N 
Published: December 2022

Abstract
The present study utilized the anti-Ta1 mAb to characterize the cell surface phenotypes of peripheral blood and intrathyroidal lymphocytes in patients with Graves' disease. We found an increase in PBL bearing the Ta1 Ag in untreated patients. The euthyroid patients in remission, induced by antithyroidal drugs, radioisotope therapy, and subtotal thyroidectomy, had lower percentages of Ta1+ cells than did untreated patients. An increased percentage of Ta1+ cells in untreated patients was found in both CD4+ cells and CD8+ cells. The ratio of CD4+Ta1+ cells to CD8+Ta1+ cells in untreated patients was significantly higher than that of normal subjects. There was a positive correlation between the percentage of Ta1+ cells and the level of anti-TSH receptor antibody. In this prospective study, the proportion of Ta1+ cells was decreased in parallel with the reduction in anti-TSH receptor antibody and free T3 levels. In the chronically treated patients, the proportion of Ta1+ cells in the thyroid tissue was, yet similar to that in the peripheral blood, markedly increased in comparison to that of normal subjects. In contrast to Ta1+ cells, the thyroid tissue had a significantly higher percentage of HLA-DR+ T cells than did the paired peripheral blood. The proliferative responses of the Ta1+ cell-enriched population isolated from untreated patients toward thyroglobulin and microsomal Ag were markedly higher than those in a Ta1+ cell-depleted population, but both populations were able to respond equally to PHA. These results suggest that the Ta1+ cells may include Ag-triggered memory cells that are reactive with thyroid-specific Ag. Furthermore, monitoring such cells may provide an objective measure of abnormal immunologic activity.
Influence of IL-1 alpha and -1 beta on the survival of human bone marrow cells responding to hematopoietic colony-stimulating factors.
Authors: Hangoc G , Williams D E , Falkenburg J H , Broxmeyer H E 
Published: December 2022

Abstract
Purified recombinant human (rhu) IL-1 alpha and IL-1 beta were evaluated for their effects on the proliferation and survival of granulocyte-macrophage (CFU-GM) and erythroid (BFU-E) progenitor cells from normal human bone marrow (BM). Using nonadherent low density T lymphocyte depleted (NALT-) BM cells cultured in the presence or absence of IL-1, CSF-deprivation studies demonstrated that IL-1 alpha or IL-1 beta by itself did not enhance the proliferation of CFU-GM or BFU-E. They did, however, promote the survival of progenitors responding to the delayed addition of media conditioned by the 5637 cell line (5637 conditioned medium), rhu GM-CSF and erythropoietin. The survival promoting effects of IL-1 alpha on CFU-GM and BFU-E were neutralized by anti-IL-1 alpha mAb added to the cultures. The survival promoting effect of IL-1 alpha did not appear to be mediated by CSF, because neither CSF nor erythroid burst promoting activity were detectable in cultures in which NALT- cells were incubated with rhuIL-1 alpha. In addition, suboptimal concentrations of rhu macrophage CSF (CSF-1), G-CSF, GM-CSF, and IL-3, which were just below the levels that would stimulate colony formation, did not enhance progenitor cell survival. Survival of CFU-GM and BFU-E in low density (LD) bone marrow cells did not decrease as drastically as that in NALT- BM cells, and exogenously added IL-1 did not enhance progenitor cell survival of CFU-GM and BFU-E in LD BM cells. However, addition of anti-IL-1 beta decreased survival of CFU-GM and BFU-E in LD BM cells. These results implicate IL-1 in the prolonged survival of human CFU-GM and BFU-E.
Interspersion of the VHQ52 and VH7183 gene families in the NFS/N mouse.
Authors: Kleinfield R W , Weigert M G 
Published: December 2022

Abstract
Deletion mapping analysis has shown that members of the VH7183 and VHQ52 gene families are interspersed in the NFS/N mouse. To obtain direct evidence that members of these gene families are physically linked, an NFS/N liver library was constructed and genomic clones were analyzed for hybridization to both VHQ52 and VH7183 gene probes. Four clones were identified which contained both VHQ52 and VH7183 hybridizable restriction fragments. Two clones containing rearranged VHQ52 genes were also found to hybridize with the VH7183 gene probe. Sequence analysis of three of the VH7183-containing restriction fragments indicate that all are pseudogenes which contain interruptions at either the 5' and/or 3' ends of the VH coding region. Given the D-proximal location of at least a portion of the VHQ52 gene family relative to VH7183 in NFS/N mice, and the known correlation between D proximity and the frequency of VH gene utilization, 22 NFS/N-derived pre-B cell lines were analyzed for VHQ52 gene utilization. More than 40% of the identified H chain (VHDJH) rearrangements in this survey used members of this gene family. Furthermore, analysis of poly(A)+ RNA from NFS/N fetal liver and adult spleen also indicates preferential utilization of VHQ52 family in fetal liver. Kinetic studies show, however, that there are no changes in relative utilization throughout fetal ontogeny. The implications of these findings for the expression and randomization of the VH repertoire are discussed.
Late events in B cell activation. Expression of membrane alkaline phosphatase activity.
Authors: Burg D L , Feldbush T L 
Published: December 2022

Abstract
Alkaline phosphatase (APase) has been previously described as a membrane marker correlating with B cell proliferation after stimulation by selected B cell mitogens. We have found, however, that the appearance of B cell membrane APase correlates more closely with differentiation than with proliferation. This conclusion has been drawn from the following observations: 1) APase activity appears well after peak B cell thymidine uptake, 2) mitogens which stimulate only B cell proliferation (Salmonella typhimurium mitogen) fail to induce expression of the enzyme, and 3) when proliferation of mitogen-activated B cells is inhibited, APase activity is not suppressed and may even be augmented. In addition to membrane expression, APase is also spontaneously shed into the surrounding milieu, perhaps as a result of endogenous phospholipase activity. By using a group of well-characterized inhibitors, the APase activity was shown to belong to class I (similar to the bone/liver/kidney class). Because APase always appears in differentiating but not proliferating cells, we would propose that the enzyme appearance is a late marker of B cell activation, associated with cell progression to differentiation and consequent IgM synthesis.
Delineation of several DR-restricted tetanus toxin T cell epitopes.
Authors: Demotz S , Lanzavecchia A , Eisel U , Niemann H , Widmann C , Corradin G 
Published: December 2022

Abstract
We have characterized five human T cell clones specific for tetanus toxin. The combination of different techniques allowed us to precisely map two T cell epitopes within fragments 830-843 and 1273-1284 of tetanus toxin, as formally demonstrated by the use of corresponding synthetic peptides. The three other T cell clones were specific for regions 2-602, 604-742, and 865-1315 of tetanus toxin, respectively. The five T cell clones were shown to be restricted to HLA-DR Ag. Furthermore, the allele of HLA-DR utilized by the various epitopes has been determined. The use of HLA-DR-transfected L cells as APC directly demonstrated that two epitopes, one of which represented by fragment 1273-1284, were recognized in association with HLA-DRw52a. For the other three T cell epitopes, the data strongly suggested they were recognized in association with HLA-DR5. Finally, a sixth T cell clone was shown to be specific for tetanus toxoid, the vaccinal preparation of tetanus toxin, and not for other tetanus toxin fragments. This indicated that immunization with tetanus toxoid probably elicits a T cell response directed only in part against native tetanus toxin.
T help requirements for the generation of an in vivo IgE response: a late acting form of T cell help other than IL-4 is required for IgE but not for IgG1 production.
Authors: Finkelman F D , Holmes J , Urban J F , Paul W E , Katona I M 
Published: December 2022

Abstract
To further define requirements for T cell help in the stimulation of an in vivo IgE response, we studied a system in which the injection of mice with a goat antibody to mouse IgD (GaMD) stimulates large polyclonal IgG1 and IgE responses. In this system, both responses are blocked by anti-CD4 antibody, but only the IgE response is blocked by (anti-IL-4) antibody. Anti-CD4 antibody, if injected 5 days after GaMD, was found to inhibit the GaMD-induced IgE response to a much greater extent than the IgG1 response, even though both responses occur simultaneously and are inhibited to an equal extent by optimal or suboptimal doses of anti-CD4 antibody administered 2 days after GaMD. Even a suboptimal, 50-micrograms dose of anti-CD4 antibody, when injected 5 days after GaMD, inhibited the IgE response to a much greater extent than did an optimal 10-mg dose of anti-IL-4 antibody injected at the same time, even though 10 mg of anti-IL-4 antibody more completely inhibited GaMD-induced IgE production than did 50 micrograms of anti-CD4 antibody when injected 2 days after GaMD. These observations provide evidence that a late acting form of T cell help other than IL-4 is important for the generation of an IgE response but not an IgG1 response in GaMD-immunized mice.
Different patterns of arachidonate metabolism in autologous human blood monocytes and alveolar macrophages.
Authors: Balter M S , Toews G B , Peters-Golden M 
Published: December 2022

Abstract
As peripheral blood monocytes (PBM) differentiate into tissue macrophages, they undergo a variety of functional changes. One such difference which has been described is an enhanced metabolism of arachidonic acid (AA) via the 5-lipoxygenase (5-LO) pathway in alveolar macrophages (AM) as compared to PBM. In order to elucidate a possible mechanism for this difference, we compared the metabolism of endogenously released AA mobilized by agonists and of exogenously supplied fatty acid in adherent autologous PBM and AM obtained from six normal subjects. Exogenous AA was metabolized to larger amounts of both cyclooxygenase (CO) and 5-LO products by PBM as compared with AM. Although the two cell types released similar amounts of endogenous AA in response to ionophore A23187, marked differences in the pattern of its metabolism were observed. In PBM, a large proportion of released AA remained unmetabolized, and that which was metabolized was converted predominantly to CO products. In contrast, arachidonate released by AM was efficiently metabolized, predominantly via the 5-LO pathway. Similar results were obtained when cells were stimulated with the particulate zymosan, with PBM synthesizing mainly CO and AM, mainly 5-LO eicosanoids. In addition, culture of PBM for up to 5 days in an aerobic environment did not alter their response to A23187 stimulation. These results suggest that the lesser 5-LO metabolism by PBM than AM is not explained by lesser phospholipase or 5-LO activities, but rather a compartmentalization of the endogenous AA deacylated by phospholipase and the 5-LO enzyme in the PBM. The acquisition of the capacity to metabolize endogenous AA to large quantities of 5-LO products as mononuclear phagocytes differentiate in the lung may equip them with the ability to mount an inflammatory response in the alveolar space.
Decay accelerating factor regulates complement activation on glomerular epithelial cells.
Authors: Quigg R J , Nicholson-Weller A , Cybulsky A V , Badalamenti J , Salant D J 
Published: December 2022

Abstract
Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present on cultured rat GEC. These proteins regulate C activation in vitro and may play a role in controlling C activation on GEC in vivo.
Enhanced cell-mediated protection against fatal Escherichia coli septicemia induced by treatment with recombinant IL-2.
Authors: Goronzy J , Weyand C , Quan J , Fathman C G , O'Hanley P 
Published: December 2022

Abstract
Administration of rIL-2 to BALB/c mice induces a rapid, cell-mediated response that is sufficient to protect mice from a lethal i.p. dose of Escherichia coli. Mice were protected from septic death if IL-2 was administered i.p. within 1 h after the bacterial challenge. Optimal protection was provided by treating the lethally challenged mice with rIL-2 at 1 and 5 h or 1, 5, and 10 h after the bacterial challenge and was dose-dependent (greater than or equal to 5.0 x 10(5) U/kg). Furthermore, treatment of mice with anti-IL-2R antibody abolished the protective effect induced by rIL-2 administration. These data suggest that the rIL-2-induced protection against septic death in mice is mediated by a cell type expressing a functional IL-2R. One potentially important therapeutic application of rIL-2 may be to modulate the course of sepsis once the host has been exposed to potentially lethal microbial pathogens.
Human lymphocyte proliferative response to a sporozoite T cell epitope correlates with resistance to falciparum malaria.
Authors: Hoffman S L , Oster C N , Mason C , Beier J C , Sherwood J A , Ballou W R , Mugambi M , Chulay J D 
Published: December 2022

Abstract
To identify vaccine relevant T cell epitopes on the circumsporozoite (CS) protein of Plasmodium falciparum, the lymphocyte proliferative responses to 10 CS protein derived peptides were studied in 28 adult Kenyans, and correlated with resistance to malaria. Eight peptides, six of which were not overlapping, induced proliferation of lymphocytes from one to five volunteers, suggesting either genetic restriction of response to each of the T epitopes, or dominance of some T sites on the immunizing sporozoites. The 28 volunteers were radically cured of malaria and during the next 126 days 25 of the 28 were reinfected. Resistance to malaria was not correlated with antibodies to malaria Ag, but was significantly correlated with lymphocyte responses to CS protein residues 361-380 and 371-390. Among the 25 volunteers who became re-infected with malaria, lymphocytes from only two responded to a peptide including residues 361-380 of the P. falciparum CS protein, and only one to peptide 371-390. In contrast, lymphocytes from all three volunteers who did not become infected responded to peptide 361-380 (p = 0.003), and lymphocytes from two of the three responded to peptide 371-390 (p = 0.023). The significant correlation between proliferation to peptides 361-380 and 371-390 and resistance to malaria suggests that at least one epitope within these overlapping peptides is involved in a protective cellular immune response. The data support inclusion of these residues in future CS protein vaccines.