bluuebunny/crossref_metadata_2025_split huggingface dataset:
Maleyl-BSA and fucoidan induce expression of a set of early proteins in murine mononuclear phagocytes.
Authors: Johnston P A , Jansen M M , Somers S D , Adams D O , Hamilton T A 
Published: December 2022

Abstract
We examined the effect of maleyl-BSA on specific protein expression in murine peritoneal macrophages by radiolabeling treated macrophages with [35S]methionine followed by SDS-polyacrylamide gel electrophoresis. Such treatment induces the expression of a set of at least seven proteins (38, 42, 57, 65, 75, 80, and 85 kD). A similar set of proteins is also induced by treatment of macrophages with the algal polysaccharide fucoidan. The proteins resemble those induced in response to treatment of this same cell population with bacterial lipopolysaccharide (LPS), as judged by co-migration in both one- and two-dimensional electrophoresis. Two proteins induced by either LPS or maleyl-BSA (e.g., p57 and p85) show similar primary structure, as assessed by partial proteolytic peptide mapping confirming their identity. The induction of these proteins by maleyl-BSA is a transient phenomenon, being expressed as early as 1 hr after treatment and declining after 8 hr even in the continuous presence of the stimulus. The dose of maleyl-BSA required to induce the response varies to some extent with the protein in question, but agrees with the Kd for ligand-receptor binding. Chloroquine, which blocks the degradation of ligand, does not inhibit the induction of early protein synthesis. Whereas the induction of these proteins is blocked by inhibition of RNA synthesis with actinomycin D, the reversible inhibition of protein synthesis with cycloheximide during the induction phase does not prevent their expression. LPS, maleyl-BSA, and fucoidan previously have been shown to stimulate protease secretion and tumoricidal function in appropriately primed macrophages. The present findings now demonstrate that all three agents can also mediate the expression of early genes which may participate in the acquisition of functional competence.
Structural and antigenic characterization of a species- and promastigote-specific Leishmania mexicana amazonensis membrane protein.
Authors: Kahl L P , McMahon-Pratt D 
Published: December 2022

Abstract
A Leishmania mexicana amazonensis promastigote membrane glycoprotein (Mr 46,000) expressing the species-specific and promastigote-specific epitope of monoclonal antibody IX 2H7-E10(M-2) has been purified to homogeneity, and studies have been made to determine the minimum peptide fragment that retained antigenic activity. Peptide mapping experiments performed with the metabolically labeled or surface radioiodinated protein illustrated its highly folded nature and marked resistance to proteolytic digestion. The M-2 epitope was readily destroyed by limited proteolysis and/or reduction and alkylation, indicating disulfide bond involvement in its formation by at least the secondary protein structure. The stability of approximately half of the molecular mass of the protein (46kDa/M-2) was also dependent on disulfide bonding. Enzymic digests under various conditions generated a glycopolypeptide (Mr 22,000 to 27,000), extremely resistant to further enzymic digestion, that was the dominant immunogenic portion of the purified protein recognized by a specific rabbit heteroserum. No smaller or larger fragments were antigenic. Data obtained by using the radioiodinated hydrophobic probe 3-(trifluoromethyl)-3-([m-125]iodophenyl)-diazirine ([125I]TID) indicate that 46kDa/M-2 is an integral membrane protein with a component polypeptide (Mr 23,000 to 27,000), highly resistant to further enzymic cleavage and containing sequences within the external promastigote membrane. Data indicate that the [125I]TID-labeled fragment is identical to the immunodominant fragment. We suggest that hydrophobic interactions maintain the integrity of this fragment as amino acids within it fold through the parasite membrane.
Limited diversity and selection of rearranged gamma genes in polyclonal T cells.
Authors: Uppenkamp M , Pittaluga S , Lipford E H , Cossman J 
Published: December 2022

Abstract
The role of a T gamma gene product in the immune response is not known. To investigate the participation of the T gamma gene in functional T cells, we estimated its variable (V gamma) gene diversity among mature polyclonal T cells and assayed for in vivo selection of rearranged V gamma genes during the immune response. In this study, we present evidence that functionally mature, normal human T cells have rearranged their T gamma genes but display a limited range of gene rearrangement choices. In contrast to clonal T cell neoplasms, an invariant array of seven T gamma gene rearrangements was found to be proportionately distributed within normal polyclonal T cell populations, as well as in benign polyclonal T cell proliferations incited by a wide variety of pathological conditions. Findings presented here indicate that the likelihood of rearrangement of each human V gamma gene may be fixed. Lack of selection of V gamma genes during the mature T cell immune response implies a limited role of any single V gamma gene at this stage of T cell development.
Genomic DNA encoding rabbit T cell receptor beta-chains: isotypes and allotypes of C beta.
Authors: Komatsu M , Lamoyi E , Mage R G 
Published: December 2022

Abstract
We have discovered sequence differences in DNA encoding the first exon of rabbit T cell receptor beta-chains from unrelated rabbits that probably reflect allelic C beta 1 allotypes. Rabbit I was from a colony bred to maintain the K1-expression mutation Basilea, and rabbit II was from a colony bred to maintain the K1b9 allotype. Genomic DNA from rabbits I and II also exhibit restriction fragment length polymorphism of C beta on Southern blots. In addition, several different restriction enzyme digests of DNA from rabbit I give three bands, whereas DNA from rabbit II gives two when probed with C beta. An approximately 14-kb cloned genomic DNA fragment from rabbit I has two copies of C beta exon 1 and a 6-kb fragment has a third copy, suggesting that rabbit I has three different C beta genes. The DNA sequence of a germ-line genomic DNA fragment encoding the first exon of the beta-chain constant region from rabbit I also has an open reading frame encoding 140 amino acids immediately 5' of the C beta sequence. A corresponding sequence had previously been found in a cDNA clone from the second rabbit (rabbit II).
Natural cytotoxic cells and tumor necrosis factor activate similar lytic mechanisms.
Authors: Patek P Q , Lin Y , Collins J L 
Published: December 2022

Abstract
The lytic activity of natural cytotoxic (NC) cells has several characteristics which clearly distinguish it from other cell-mediated lytic activities and from most soluble cytolytic factors. An exception is the lytic activity mediated by tumor necrosis factor (TNF). In this paper, we report a detailed comparison of NC and TNF lysis of target cells which are used as prototype NC targets or TNF targets, and show that the two cytolytic activities have very similar, if not identical, lytic mechanisms. We present data showing that target cells which are NC-sensitive are also TNF-sensitive and that target cells which are NC-resistant are also TNF-resistant. Moreover, cells selected either in vivo or in vitro for NC resistance are selected for TNF resistance, and cells selected for TNF resistance are selected for NC resistance. The analysis of the kinetics of 51Cr release mediated by NC cells or by TNF show that both activities affect similar kinetics, in that there is no cell lysis for several hours after targets and effectors first interact. However, NC and TNF lytic activities can be distinguished. By using the cell lines 10ME or B/C-N as targets, it can be shown that whereas NC-mediated lysis is dependent on protein synthesis, TNF-mediated lysis is not. We also show that targets which are resistant to NC-mediated lysis because they express a protein synthesis-dependent resistance mechanism also require protein synthesis to resist TNF-mediated lysis, suggesting that the same resistance mechanism protects cells against both NC cells and TNF. Together, these data strongly support the hypothesis that NC cells and TNF activate the same lytic mechanism within target cells and that TNF may mediate the lytic activity of NC effector cells.
Interaction in vivo between hapten-specific suppressor T cells and an in vitro cultured helper T cell line.
Authors: Owens T , Miller J F 
Published: December 2022

Abstract
The interaction in vivo between hapten-specific suppressor T cells (Ts) and a hapten-specific T helper (Th) cell line was examined. Antigen-specific Ts were induced in CBA mice by i.v. priming with 3 X 10(7) syngeneic spleen cells (SC) that were chemically coupled with the hapten azobenzenearsonate (ABA). Transfer of splenic T cells from these mice by i.v. injection suppressed the induction in syngeneic assay hosts of ABA-reactive helper and cytotoxic T cell (Tc) responses. Although the Th responses and their suppression were ABA specific, in that they were not induced or activated by trinitrophenyl (TNP)-coupled SC, both Tc responses and their suppression were occasionally nonspecific. Induction of Th was assayed by measuring the release from primed lymph node cells of IL 2 and IL 3 in response to haptenated SC in vitro. Both cytotoxic and Th responses could be made dependent on the provision of exogenous Th by reducing the antigen dose. This stratagem allowed the assay in vivo of a long-term cultured ABA-specific Th cell line (E9). Injection of 10(5) E9 cells/mouse (with antigen, in the rear footpad) helped the induction of both Tc and Th in response to a reduced dose of antigen. These responses, which were dependent on the E9 cell line, were also suppressed by i.v. transferred Ts. When normal doses of antigen were used, the injection of 10(5) E9 Th overcame suppression. These results show that Ts act by inhibiting the activation of Th, thereby suppressing Th-dependent responses generally. The fact that the E9 Th cell line could be suppressed also shows that long-term culture of T cells does not affect their capacity to be regulated in vivo.
HLA DR, DQ, and DP antigen expression in rheumatoid synovial cells: a biochemical and quantitative study.
Authors: Teyton L , Lotteau V , Turmel P , Arenzana-Seisdedos F , Virelizier J L , Pujol J P , Loyau G , Piatier-Tonneau D , Auffray C , Charron D J 
Published: December 2022

Abstract
Because an increased expression of HLA class II antigens appears to be a central feature in local lesions of rheumatoid arthritis (RA), we have developed specific tools to quantify Ia expression in RA at both the protein and mRNA levels. An original dot immunobinding assay and a quick blot hybridization with chain-specific HLA class II probes allowed quantification of HLA DR antigens and chain transcripts on small-size samples of adherent synovial lining cells (ASLC) from normal individuals or RA patients. These methods associated with Western blot techniques detecting class II and beta-chain expression showed that ASLC from RA patients freshly put in short-term culture expressed greater amounts of class II transcripts and proteins than ASLC from controls. Class II proteins and mRNA rapidly disappeared in culture. Recombinant interferon-gamma (rIFN-gamma) induced their re-expression. A study of the kinetics and levels of the HLA-D products showed similar patterns of activation in RA patients and controls. A qualitative analysis of HLA class II antigens synthesized in ASLC after rIFN-gamma induction was performed by two-dimensional gel electrophoresis. It revealed a normal pattern for alpha- and beta-chains in ASLC from normal and RA patients, thus eliminating the possibility that abnormal protein structure of Ia antigen expressed on ASLC is responsible for the activation of T cell immune responses in RA. Nevertheless, the invariant chain exhibited a particular pattern in ASLC with additional basic spots, and this might interfere with transport and glycosylation of HLA class II antigens in such cells.
Monoclonal antibodies reactive with swine lymphocytes. II. Detection of an antigen on resting T cells down-regulated after activation.
Authors: Saalmüller A , Jonjic S , Bühring H J , Reddehase M J , Koszinowski U H 
Published: December 2022

Abstract
The expression of an antigen on porcine T lymphocytes detected by murine monoclonal antibody (mAb) 8/1 was investigated by functional studies and dual-parameter immunofluorescence. mAb 8/1 reacts with greater than 95% of thymocytes and in peripheral blood with all T lymphocytes and with cells of the monocyte/macrophage lineage, but not with B cells, erythrocytes, and platelets. Pretreatment of peripheral blood lymphocytes with mAb 8/1 plus complement abrogated the proliferative response in vitro to mitogen, soluble antigen, and MHC determinants. Dual-parameter immunofluorescence revealed that resting porcine T8+ as well as T4+ lymphocytes express the 8/1 antigen, whereas after in vitro activation, cell surface expression of the antigen was low or absent in both T cell subsets. Thus, the 8/1 antigen represents a marker that discriminates between resting and activated T lymphocytes. Distribution and functional criteria indicate that 8/1 represents a novel marker not described before for any other mammalian species.
Arachidonate metabolites, platelet-activating factor, and the mobilization of protein kinase C in human polymorphonuclear neutrophils.
Authors: O'Flaherty J T , Nishihira J 
Published: December 2022

Abstract
In contrast to our previous report (Biochem. Biophys. Res. Comm. 134:587, 1986), we now find that protein kinase C (PKC) is mobilized in human polymorphonuclear neutrophils (PMN) stimulated with platelet-activating factor (PAF) or leukotriene (LT)B4. Thus nanomolar concentrations of each compound caused PMN to lose cytosolic, PKC-specific protein phosphorylating activity, as well as receptors for phorbol myristate acetate (PMA). Smaller gains in membrane-associated PMA receptors accompanied these changes. Diacylglycerol and PMA had very similar effects on PKC. However, unlike these direct PKC activators, PAF and LTB4 induced only moderate decreases in cytosolic PKC; acted only on PMN pretreated with cytochalasin B; did not mobilize PKC in disrupted PMN or activate PKC in a cell-free system; and with respect to PAF, induced responses that partially reversed within 30 min. Furthermore, PAF, LTB4, and several of their structural analogues mobilized PKC at concentrations correlating closely with their respective affinities for cellular LTB4 or PAF receptors. Thus PAF and LTB4 acted by indirect and apparently receptor-mediated mechanisms. Four observations indicated that the cytochalasin B-dependent degranulating actions of PAF and LTB4 involved PKC. First, PKC mobilization and degranulation occurred at the same stimulus concentrations. Second, 5-hydroxyicosatetraenoate dramatically enhanced both PKC mobilization and degranulation when elicited by PAF; it had relatively little influence on LTB4-induced responses. Third, PAF-induced mobilization (t1/2 less than 7 sec) preceded degranulation (t1/2 approximately 20 sec). Finally, a PKC blocker, polymyxin B, was similarly effective in inhibiting degranulation responses to PAF, LTB4, and PMA. Because stimulated PMN may produce and use PAF, LTB4, and 5-hydroxyicosatetraenoate as secondary intracellular mediators, our results implicate PKC as a central and potentially critical regulator of function.
Cell-mediated amplification and down regulation of cytotoxic immune response against autologous human cancer.
Authors: Mukherji B , Guha A , Loomis R , Ergin M T 
Published: December 2022

Abstract
The cytotoxic host immune response toward autologous human cancer may be regulated by the immunoregulatory network. Here we show that helper T cells, cloned from peripheral blood lymphocytes that were sensitized in vitro against an autologous human malignant paraganglioma, proliferated against and made interleukin 2 when cocultured with the tumor-associated antigen in the presence of autologous accessory cells. Furthermore, the helper cell clones amplified cytotoxic immune response by peripheral blood lymphocytes against the paraganglioma cells in coculture with the blood lymphocytes and the paraganglioma cells. An autologous T cell line bearing suppressor phenotype, established from a lymph node that had been infiltrated with the paraganglioma tumor cells, in contrast to the helper cells, selectively suppressed the cytotoxic immune response by the blood lymphocytes against the paraganglioma cells in identical coculture. These results, therefore, demonstrate the existence of cell-mediated immunologic regulations of the cytotoxic immune response (concurrent amplification and suppression in the same host) against an autologous human tumor.
Aberrant T cells in beige mutant mice.
Authors: Biron C A , Pedersen K F , Welsh R M 
Published: December 2022

Abstract
Cytotoxic T lymphocyte (CTL) morphology and function was examined in beige (bg/bg) mutant mice during infection with lymphocytic choriomeningitis virus (LCMV). Virus-specific, class I-restricted CTL activity mediated by total spleen leukocytes isolated from bg/+ or +/+ mice on days 7 or 9 postinfection with LCMV was moderately higher than that mediated by spleen cells isolated from bg/bg mice. The CTL generated in bg/bg mice had aberrant morphology. Lyt-2+ cells isolated from bg/+ or +/+ mice had typical large granular lymphocyte (LGL) morphology and contained numerous small azurophilic granules, whereas Lyt-2+ cells isolated from bg/bg mice contained only one or two large atypical granules in their cytoplasm. Aberrant LGL morphology correlated with reduced lytic capacity. The bg/bg CTL were inefficient killer cells mediating, on a per cell basis, only one fourth of the lysis mediated by bg/+ CTL. The bg/bg mice appeared to mount a compensatory response to regulate virus replication, because frequencies of Lyt-2+ cells and cells that specifically bound to virus-infected target cells were elevated as compared with their frequencies in bg/+ mice. The higher proportion of the CTL phenotype cells appeared to be a consequence of expanded proliferation of Lyt-2+ cells. These results demonstrate that, in comparison with bg/+ and +/+ mice, bg/bg mice have CTL with reduced lytic capacities, but may compensate during virus infection by expanding the number of these cells. Furthermore, these data suggest that the depressed lytic activity may be a consequence of aberrant granule formation.
Modulation of the induction and circumvention of immunological tolerance to human gamma-globulin by interleukin 1.
Authors: Weigle W O , Scheuer W V , Hobbs M V , Morgan E L , Parks D E 
Published: December 2022

Abstract
As with agents capable of causing the release of IL 1, IL 1 itself is capable of modulating certain tolerance-inducing events. Under the condition used in the present study, it previously has been firmly established that injection of A/J mice with DHGG induces a state of antigen-specific tolerance in both T helper (Th) and B cells. The tolerance in the B cell is of long duration, whereas that in the B cell is of shorter duration. Recombinant IL 1 (rIL 1) given shortly after the tolerogen DHGG results in the inhibition of the induction of tolerance resulting in antibody production. The induction of tolerance is inhibited at both its antigen-specific Th cell and B cell levels, although the latter may be caused by the former. The inhibition of the induction of tolerance by rIL 1 is not correlated to the generation of antigen-specific T suppressor cells. IL 1 mimics lipopolysaccharide and 8-bromoguanosine, which generate IL 1 production, in its ability to interfere with the in vivo induction of tolerance. However, in contrast to these latter mitogens which cause both terminal differentiation of B cells and IL 1 production, IL 1 itself does not cause in vivo circumvention of long-term tolerant Th cells in the presence of competent B cells and antigen. These latter findings suggest that a signal(s) in addition to those delivered by IL 1 is required for activation of the B cell compartment recovering from tolerance to antibody production. AHGG (immunogen) is a potent generator of IL 1 release, whereas DHGG has no effect on IL 1 release from macrophages and AHGG inhibits the induction of tolerance by DHGG. These latter results suggest that the lack of an IL 1 signal may be responsible for the deliverance of a tolerogenic rather than an immunogenic signal to the Th cell.
Anti-RNA polymerase I antibodies: potential role in the induction and progression of murine lupus nephritis.
Authors: Stetler D A , Cavallo T 
Published: December 2022

Abstract
Antibodies against RNA polymerase I were detected in plasma and kidney eluates of NZB/W mice. Plasma concentrations of the antibodies were the highest in mice with incipient nephritis and the lowest in mice with progressive nephritis. Mice with attenuated nephritis due to immunosuppressive therapy had intermediate plasma concentrations of the antibodies. The specific concentrations (ng/microgram IgG) of anti-RNA polymerase I antibodies in kidney eluates were significantly (10- to 70-fold) greater than the corresponding plasma concentrations. These results indicated that the decreased plasma concentration of the antibodies in mice with more advanced disease was at least partially due to selective concentration of anti-RNA polymerase I antibodies in the kidneys. The degree of this selective concentration was directly proportional (R2 = 0.9962) to the severity of renal disease, as reflected by the concentration (microgram/g tissue) of IgG eluted from the kidneys. The concentration (microgram/g tissue) of anti-RNA polymerase I eluted from the kidneys also was increased in mice with more severe renal disease. Further, the extent of this increase was greater than that of total IgG, again suggesting that anti-RNA polymerase I antibodies had been selectively concentrated in the kidneys. These findings are strongly suggestive of an important role for the RNA polymerase I/anti-RNA polymerase I antibody system in the pathogenesis of murine lupus nephritis.
Superinduction of T lymphocyte-endothelial cell (EC) binding by treatment of EC with interleukin 1 and protein synthesis inhibitors.
Authors: Cavender D , Haskard D , Foster N , Ziff M 
Published: December 2022

Abstract
We have previously reported that marked enhancement of the in vitro binding of lymphocytes to endothelial cell (EC) monolayers is observed after stimulation of the EC with interleukin 1 (IL 1). To determine whether new protein synthesis was required for this effect of IL 1, EC were incubated with IL 1 in the presence of cycloheximide or puromycin. Three different effects of these protein synthesis inhibitors on T-EC binding were observed. First, preincubation of the EC with both IL 1 and an inhibitor blocked the increase in binding if the inhibitor was present during both the preincubation and the 1 hr duration of the T-EC binding assay, suggesting that new protein synthesis is required for the enhancement of T-EC adhesion by IL 1. Second, preincubation of the EC with low doses of the inhibitors (0.1 to 1 microgram/ml) in the absence of IL 1 consistently increased T-EC binding, even if the inhibitors were present during the T-EC adhesion assay; in addition, the inhibitors additionally increased the stimulatory effect of IL 1 if the EC were washed free of the inhibitor before the assay step. The binding-enhancing effect of low concentrations of cycloheximide could be inhibited by an antibody to the CDw18 complex on the T cell, suggesting an up-regulation of the ligand on the EC involved in CDw18-dependent T cell adhesion. Third, higher concentrations of the inhibitors (3 to 10 micrograms/ml) were toxic for the EC in the presence of IL 1, possibly due to the combined blocking effect of IL 1 and inhibitors on EC protein synthesis.