bluuebunny/crossref_metadata_2025_split huggingface dataset:
The HML-1 antigen of intestinal lymphocytes is an activation antigen.
Authors: Schieferdecker H L , Ullrich R , Weiss-Breckwoldt A N , Schwarting R , Stein H , Riecken E O , Zeitz M 
Published: December 2022

Abstract
The Ag recognized by the mAb HML-1 is expressed on more than 90% of human intestinal intraepithelial lymphocytes, whereas in other lymphoid tissues it is rarely or not expressed. In the present study, we have investigated the percentage of HML-1-positive cells in the human intestinal lamina propria and the coexpression of HML-1 with different T cell subset markers. In addition, we studied the inducibility of HML-1 on PBL which normally are HML-1-negative. Flow cytometric analysis of isolated intestinal lamina propria lymphocytes (LPL) showed that about 40% of the cells expressed HML-1, the majority belonging to the CD8-positive subpopulation. Virtually all LPL expressed CD45RO, whereas the percentage of CD29-positive cells was only about 50%, similar to PBL. There were only few cells expressing CD45RA or Leu-8 in the lamina propria. HML-1-positive cells were almost exclusively CD45RA-negative, but were found in both the CD29-positive and the CD29-negative subpopulation of LPL. In vitro stimulation of PBL showed that the expression of HML-1 was inducible on T cells by mitogens, phorbolester, Ag, and rIL-2. Expression of HML-1 was induced with a different time course and with differences in the response to the investigated stimuli compared with CD25. Activated HML-1-positive PBL were also predominantly CD45RA-negative. The findings show that HML-1 is an Ag, which is expressed in vivo on a specific subset of previously activated T cells in the unique environment of the intestinal mucosa, and which can be induced in vitro by different activation signals on PBL.
Induction of proliferation of human follicular (B type) lymphoma cells by cognate interaction with CD4+ T cell clones.
Authors: Umetsu D T , Esserman L , Donlon T A , DeKruyff R H , Levy R 
Published: December 2022

Abstract
We examined stimuli which are required for the induction of in vitro proliferation of follicular lymphoma cells, a low grade non-Hodgkin's B cell lymphoma characterized by a specific chromosomal translocation, t(14;18)(q32;q21), and by in vivo growth of the lymphoma cells in germinal center-like follicles infiltrated with CD4+ T cells. The purified follicular lymphoma cells, which are morphologically uniform, small, and dense, did not respond to stimulation with soluble lymphokines in the absence of T cells. Vigorous in vitro proliferation of follicular lymphoma cells was induced, however, when the follicular lymphoma cells were cultured with a CD4+ T cell clone which recognized alloantigens expressed by the lymphoma cells. This response required B-T cell contact, and was inhibited by anti-class II but not by anti-class I MHC mAb, indicating that these neoplastic B cells behaved as normal B cells and responded to normal activation and differentiation signals from T cells. After the cognate B lymphoma-T cell interaction occurred in culture, addition of IL-2 or IL-4 enhanced the proliferation of the tumor cells. These results, with a monoclonal and homogeneous population of B cells, affirm the idea that cognate interaction between B cells and Th cells is required for the effective activation of resting B cells. Moreover, these results suggest that a critical host-tumor interaction occurs in vivo, and that the polyclonal CD4+ T cells that infiltrate follicular lymphomas play a role in sustaining rather than inhibiting tumor growth in vivo. If so, therapies directed not only against the neoplastic cell but also against specific T cells and their cognate interactions with tumor cells may have a rationale.
A role for cytokines in antigen presentation: IL-1 and IL-4 induce accessory functions of antigen-presenting cells.
Authors: Aiello F B , Longo D L , Overton R , Takacs L , Durum S K 
Published: December 2022

Abstract
Fixation of APC with 1-ethyl-3-(3-dimethylamino-propyl)carbodiimide (ECDI) eliminates their ability to stimulate proliferation of alloreactive T cells or the D10 T cell clone, although a partial response, IL-4 production, was measured. However, if APC were activated before fixation, they could be ECDI-fixed and retain the ability to induce T cell proliferation. IL-1, IL-4 or LPS were capable of activating APC in this way, whereas IFN-gamma was not. This activation step occurred in 6 h, required protein synthesis, and was distinct from increases in Ia or IL-1. This suggests resting APC lack structures that are essential for inducing T cell proliferation.
IL-6 activity in feline infectious peritonitis.
Authors: Goitsuka R , Ohashi T , Ono K , Yasukawa K , Koishibara Y , Fukui H , Ohsugi Y , Hasegawa A 
Published: December 2022

Abstract
Involvement of IL-6 in the development of vasculitis and polyclonal gammopathy in feline infectious peritonitis (FIP) was investigated, by using the proliferative responses of two IL-6-dependent murine hybridoma cell clones, B3B1 and MH60.BSF-2 cells. A significant IL-6 activity was found in sera and ascitic fluids of cats with FIP, whereas no IL-6 activity was detected in sera from healthy cats. In these FIP cats, IL-6 activity in ascitic fluids was significantly higher than that in sera. Peritoneal exudate cells from FIP cats were also found to release a high level of IL-6 to the culture supernatant. The ascitic IL-6 activity was eluted into the fractions corresponding to the m.w. of 30,000 to 40,000 in gel filtration, and into the fractions at the salt concentration from 0.2 to 0.3 M NaCl in anion exchange chromatography. The level of ascitic IL-6 activity was inversely correlated to serum albumin/globulin ratio in these FIP cats. These findings indicate that IL-6 accumulated in the ascites might leaked into the systemic circulation, and be linked to systemic alterations such as enhanced synthesis of Ig and acute phase proteins.
Antiidiotypic antibody mimicry of a bluetongue virus neutralizing antigen.
Authors: Grieder F B , Schultz K T 
Published: December 2022

Abstract
Syngeneic antiidiotypic (Anti-Id) mAb were produced to the Bluetongue virus (BTV) serotype 17 neutralizing mAb. Three anti-Id mAb had the characteristics of an internal image of the Id as demonstrated by 1) the internal image anti-Id mAb were capable of mimicking BTV by blocking the neutralizing activity of the idiotypic neutralizing mAb and 2) the anti-Id mAb bound specifically to the surface of BTV susceptible cells in indirect binding experiments as determined by immunocytochemistry and flow cytometric analysis. The potential application of these internal image anti-Id mAb in this arbovirus system is discussed.
Cyclosporin A inhibits degranulation of rat basophilic leukemia cells and human basophils. Inhibition of mediator release without affecting PI hydrolysis or Ca2+ fluxes.
Authors: Hultsch T , Rodriguez J L , Kaliner M A , Hohman R J 
Published: December 2022

Abstract
Cyclosporin A (CSA) inhibits IgE receptor-mediated exocytosis from rat basophilic leukemia (RBL) cells and human peripheral blood basophils in a dose-dependent manner over the therapeutic range of CSA concentrations achieved in vivo. Half-maximal inhibition was observed at 0.2 micrograms/ml CSA. The effect of CSA on several biochemical parameters involved in receptor-mediated activation of RBL cells was examined. Maximum inhibition of secretion occurred when CSA was added 5 min before activation, and inhibition was nearly maximum when the drug was added 2 min before the cells were triggered. The same results were observed when RBL cells were stimulated with A23187, a calcium ionophore. These results suggest a mechanism other than inhibition of protein synthesis is involved. Inhibition by CSA of release by either secretagogue persisted, even if CSA was removed from the buffer before the cells were triggered. No inhibition was observed of either receptor-mediated phosphatidylinositol hydrolysis, 45Ca2+ uptake, or the rise in the intracellular concentration of free Ca2+ under the same conditions that produced greater than 80% inhibition of serotonin release. These results demonstrate that the early events in signal transduction are not affected, and suggest that the intracellular target for CSA participates in a later stage of exocytosis. Furthermore, the data suggest that CSA suppresses cells other than T lymphocytes and predict that patients on CSA therapy may have altered response to allergens.
Stimulation of the respiratory burst in peripheral blood monocytes by lipoteichoic acid. The involvement of calcium ions and phospholipase A2.
Authors: Tarsi-Tsuk D , Levy R 
Published: December 2022

Abstract
Lipoteichoic acid (LTA) from Streptococcus faecalis stimulates the respiratory burst in peripheral blood monocytes (mon), as measured by cytochrome C reduction. The effect of LTA was time and dose dependent. LTA stimulated the respiratory burst in a biphasic manner within a range of 1 to 1000 ng/ml.10(6) mon, with maximal activity at 50 ng/ml. At this concentration LTA increased the activity from 0.97 +/- 0.2 to 4.88 +/- 0.2 nmol.10(6) mon/20 min. The role of calcium ions in the effect of LTA in stimulating respiratory burst was studied by changing the availability of calcium ions in the medium, and by measuring the effect of LTA on 45Ca2+ uptake and on intracellular Ca2+ levels. Removal of extracellular calcium ions in the presence of the calcium chelator EGTA, abolished the LTA-stimulated respiratory burst. LTA (50 ng/ml) was found to increase 45Ca2+ uptake into monocytes within seconds (from 2200 +/- 242 in the untreated cells to 4642 +/- 365 cpm/min in the LTA-treated mon). At this concentration, LTA stimulated an immediate rise in the intracellular free Ca2+ concentration to 155 +/- 15 nM as compared with 120 +/- 14 nM in the unstimulated monocytes. LTA caused a specific release of arachidonic acid indicating the involvement of phospholipase A2 in the transduction signal stimulating the respiratory burst by LTA.
Effects of lipopolysaccharide on phospholipase A2 activity and tumor necrosis factor expression in HL-60 cells.
Authors: Mohri M , Spriggs D R , Kufe D 
Published: December 2022

Abstract
LPS has been identified as a potent activator of mononuclear phagocytes. This activation is associated with TNF gene expression. The intracellular signaling mechanisms responsible for this effect, however, are unknown. The present studies demonstrate that LPS induces TNF transcripts in HL-60 promyelocytic leukemia cells. Because previous studies have demonstrated that eicosanoids are involved in the regulation of TNF gene expression in these cells, we examined the effects of LPS on activation of the arachidonic acid cascade. The results demonstrate that LPS stimulates phospholipase A2 activity and the hydrolysis of both 1,2-dipalmitoyl phosphatidylcholine and 1-steroyl 2-arachidonoyl phosphatidylcholine. In contrast, there was no detectable effect of LPS on activation of protein kinase C. We also demonstrate that inhibition of phospholipase A2 activity with bromophenacyl bromide or quinacrine blocks the induction of TNF transcripts by LPS. These findings suggested that LPS induces TNF gene expression through formation of arachidonic acid metabolites. Indeed, similar results were obtained with mellitin, a known activator of phospholipase A2 and eicosanoid production. Previous studies have also suggested that TNF mRNA levels are increased in HL-60 cells by the 5-lipoxygenase pathway and, in the present work inhibitors of this enzyme blocked LPS-induced TNF expression. Moreover, the cyclooxygenase metabolite, PGE2, as well as dibutyryl cAMP, inhibited the induction of TNF transcripts by LPS. Taken together, these results suggest that LPS induces TNF gene expression through activation of phospholipase A2 and that the level of this induction is regulated by activity of the 5-lipoxygenase and cyclooxygenase pathways.
V region gene usage and somatic mutation in the primary and secondary responses to influenza virus hemagglutinin.
Authors: Clarke S H , Staudt L M , Kavaler J , Schwartz D , Gerhard W U , Weigert M G 
Published: December 2022

Abstract
Most (80 to 90%) primary antibodies specific for the Sb site of influenza virus (A/PR/8/34) hemagglutinin share an Id (designated C4). Secondary antihemagglutinin(Sb) antibodies also exhibit the C4 Id although less frequently (10 to 15%). We have analyzed the V region nucleotide sequences of primary and secondary antibodies with the C4 Id. Primary C4 antibodies are encoded by the same Vk gene, belonging to the Vk8 group, usually rearranged to Jk5. The H chains are diverse, encoded by VH genes belonging to at least four different VH families, a variety of DH genes, and either JH2, JH3, or JH4. There is only one somatic mutation among seven Vk and two VH genes encoding primary C4 antibodies. Secondary C4 antibodies are also encoded by the same Vk8-Jk5 gene segment and by diverse VH genes. Additional heterogeneity in the secondary response is caused by somatic mutation.
Anti-CD3 antibodies induce T cells from unprimed animals to secrete IL-4 both in vitro and in vivo.
Authors: Flamand V , Abramowicz D , Goldman M , Biernaux C , Huez G , Urbain J , Moser M , Leo O 
Published: December 2022

Abstract
Recently, functional heterogeneity among Th cells has been recognized. Based on pattern of lymphokine secretion, two mutually exclusive subsets of CD4+ cells have been defined and designated Th1 (secreting IL-2 and IFN-gamma) and Th2 (secreting IL-4 and IL-5). Identification of these subsets was mostly based on the study of long term cultured T cell lines and clones, and little is known about the Th heterogeneity in vivo. In particular, it has been suggested that IL-4 producing cells cannot be detected in vivo or in primary stimulations in vitro unless responder cells had been previously primed. Our data however, indicate that anti-CD3 mediated stimulation can induce T cells isolated from unprimed animals to IL-4 production. An assay system based on the ability of IL-4 to increase Ia expression of B cells present in the environment of activated T cells was found to be more sensitive than detection of secreted IL-4 in the supernatant by conventional bioassays and was used to study IL-4 production by unprimed lymphocytes polyclonally stimulated in vivo and in vitro by anti-CD3 mAb. The results obtained indicate that CD4+ CD8- T cells able to produce IL-4 upon receptor-specific stimulation exist in the preimmune pool of adult animals. Remarkably, these cells can also be stimulated in vivo by treating animals with anti-CD3 mAb, as indicated by the in vivo induction of IL-4 specific mRNA and hyper-Ia expression on B cells. These results indicate that the inability to detect IL-4 in primary cultures is not due to different activation requirements of Th2 cells but may simply result from their lower frequency in unprimed animals.
CD8+ T cells inhibit HIV replication in naturally infected CD4+ T cells. Evidence for a soluble inhibitor.
Authors: Brinchmann J E , Gaudernack G , Vartdal F 
Published: December 2022

Abstract
This study describes the inhibitory effect exerted by activated CD8+ T cells on the replication of HIV in naturally infected CD4+ T cells. Highly purified CD4+ T cells from asymptomatic HIV seropositive individuals were stimulated with anti-TCR mAb-coated beads in the presence of IL-2. HIV was subsequently reproducibly isolated in cell supernatants from all study participants (53 cultures from 42 individuals). Both autologous and allogeneic CD8+ T cells from asymptomatic HIV seropositive and healthy HIV seronegative individuals inhibited the replication of HIV in these cultures in a dose-dependent manner. CD8+ T cells from patients with AIDS showed reduced or no such inhibitory activity. The inhibitory effect was not dependent on direct cell-cell contact: an inhibitory effect was exerted by CD8+ T cells across a semipermeable membrane, and an inhibitory activity was also exerted by the cell-free supernatants from activated CD8+ T cells. These results suggest that activated CD8+ T cells secrete a soluble inhibitor of HIV replication.
VH and VL gene usage by murine IgG antibodies that bind autologous insulin.
Authors: Ewulonu U K , Nell L J , Thomas J W 
Published: December 2022

Abstract
To assess the recognition structures of antibodies that bind a self-Ag, we used mRNA analysis to identify the V region genes of IgG antibodies that bind autologous insulin. Four anti-insulin mAb from primary immunization of BALB/c mice use different combinations of H and L chain V region genes. Two VH genes are from the V-gam 3-2 and V-gam 3-8 families that are infrequently expressed in adult BALB/c mice, and two VH genes are members of the J558 family. Each anti-insulin antibody uses a different Vk gene family. Two antibodies express common Vk genes (Ox1 and Vk21C), whereas two other Vk genes are unusual in BALB/c mice. One Vk gene may represent a BALB/c equivalent of the VkOx2 subfamily and another is identical to a Vk used by anti-idiotypic antibodies from C57Bl/6 mice. When compared with known germ-line counterparts, all of the Vk sequences are close to germ-line configuration. In contrast, the germ-line counterparts for the anti-insulin VH genes are not known, however, they differ only in five to seven predicted amino acids from VH of other expressed antibodies. One antibody (mAb 123) differs in one amino acid in complementarity-determining regions 1 and 2 from the VH of the murine tumor BCL1, and another (mAb 126) employs an unmutated DFL16.1 germ-line D segment. These data suggest that antibodies binding autologous insulin use V gene components that are not extensively mutated, even when derived by immunization with heterologous insulin.
Molecular events in B lymphocyte differentiation. Inducible expression of the endogenous mouse mammary tumor proviral gene, Mtv-9.
Authors: King L B , Lund F E , White D A , Sharma S , Corley R B 
Published: December 2022

Abstract
We have previously shown that the steady state levels of transcripts encoded by an endogenous mouse mammary tumor virus (MMTV) increase during LPS-induced differentiation of both normal B lymphocytes and an inducible B cell lymphoma, CH12. A large body of evidence suggests that MMTV expression is primarily limited to mammary tissues and that expression in cell lines from nonmammary tissues is accompanied by viral amplification and alterations in the transcriptional control regions of the viral long terminal repeat. We have, therefore, carefully characterized MMTV expression in CH12 cells and in other cells of the B lineage in order to determine if the expression of MMTV transcripts in differentiating B cells results from the "abnormal" transcriptional regulation seen in other nonmammary tissue. In this manuscript, we present evidence that MMTV transcripts are expressed in a variety of cells of the B lineage and that the levels of constitutive expression vary among the different cells. On the other hand, T cell lymphomas lacking amplified MMTV do not contain proviral transcripts, suggesting that MMTV transcription may be preferentially expressed in B lymphocytes. We demonstrate that MMTV transcripts are up-regulated during cytokine-mediated as well as LPS-mediated differentiation, and that most, if not all, expression is due to the activity of a single proviral gene, Mtv-9, in CH12 cells. Furthermore, the expression of MMTV transcripts in CH12 cells neither requires nor is accompanied by amplification of the provirus. Sequence analysis demonstrates that the U3 region of the expressed Mtv-9 long terminal repeat contains neither deletions nor insertions, and the well-characterized enhancer and promoter sites in the glucocorticoid response element which are known to be involved in transcriptional regulation of MMTV in mammary tissues have not been disrupted. These data suggest that the Mtv-9 locus behaves as a normal somatic gene which is differentially regulated during B cell development and differentiation. Unlike the events which lead to MMTV expression in other nonmammary tissues, B cells may express transcription factor(s) which are capable of inducing expression of endogenous MMTV proviral genes during the natural course of differentiation. Analysis of the mechanisms which control the expression of this gene should be useful in characterizing the molecular events which govern B cell differentiation.
Mapping the fine specificity of a cytolytic T cell response to HIV-1 nef protein.
Authors: Koenig S , Fuerst T R , Wood L V , Woods R M , Suzich J A , Jones G M , de la Cruz V F , Davey R T , Venkatesan S , Moss B 
Published: December 2022

Abstract
Epitope mapping of a MHC class I-restricted cytotoxic T cell response to nef, a regulatory protein of HIV, was performed with fresh PBMC from HIV-seropositive donors and target cells pulsed with a panel of overlapping peptides of the nef protein. These nef-specific CTL recognized a synthetic peptide of 10 residues derived from a nonamphipathic, highly conserved region of the nef protein in association with the HLA A3.1 molecule. Using human cell transfectants expressing mutations of the A3 molecule, we demonstrated that the amino acid at position 152 of the A3.1 molecule appears to be critical for detection of this response. Thus, rapid analysis of the epitopes of HIV proteins stimulating CTL responses can be achieved using a combination of fresh donor PBMC and target cells pulsed with synthesized peptides.
T lymphocyte recognition of a celiac disease-associated cis- or trans-encoded HLA-DQ alpha/beta-heterodimer.
Authors: Lundin K E , Sollid L M , Qvigstad E , Markussen G , Gjertsen H A , Ek J , Thorsby E 
Published: December 2022

Abstract
The HLA-associated susceptibility to develop celiac disease may to a large extent be attributed to the combination of particular DQA1 and DQB1 genes, i.e., the DQA1*0501 and DBQB1*0201 alleles, located either in cis position (on the DR3DQw2 haplotype) or in trans position (DR5DQw7/DR7DQw2 heterozygous individuals). We report three alloreactive T lymphocyte clones that recognize an HLA-DQ alpha/beta heterodimer both when the DQA1*0501 and DQB1*0201 alleles are located in cis or in trans position. Thus, the celiac disease associated DQA1 and DQB1 genes encode a functionally expressed DQ alpha/beta heterodimer.
Local production of tumor necrosis factor and IFN-gamma in tuberculous pleuritis.
Authors: Barnes P F , Fong S J , Brennan P J , Twomey P E , Mazumder A , Modlin R L 
Published: December 2022

Abstract
TNF and IFN-gamma are thought to be involved in the immune response to mycobacterial infection because they exhibit antimycobacterial effects in vitro. To investigate the roles of these cytokines in vivo at the site of disease activity in human tuberculosis, we evaluated local cytokine production in patients with tuberculous pleuritis. Both TNF and IFN-gamma were selectively concentrated 5- to 30-fold in pleural fluid, compared to blood of the same patients. Messenger RNA for both cytokines was detected in pleural tissue by in situ hybridization, suggesting that selective cytokine concentration is due to local cytokine production. Two Mycobacterium tuberculosis cell wall components, the protein-peptidoglycan complex and lipoarabinomannan, caused dose-dependent release of TNF by pleural fluid mononuclear cells and may constitute the stimuli for TNF production in the pleural space. In contrast to results obtained for TNF release, the protein-peptidoglycan complex, but not lipoarabinomannan, stimulated IFN-gamma release by pleural fluid mononuclear cells. The clinical manifestations of tuberculous pleuritis, such as fever, exudative pleural effusion, and tissue necrosis, may be due to the effects of elevated local TNF concentrations, produced in response to mycobacterial cell wall components.