bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of the effects of recombinant interleukin 6 and recombinant interleukin 1 on nonspecific resistance to infection
Authors: Van Der Meer Jos W. M. , Helle Maarten , Aarden Lucien 
Published: March 2007

AbstractInterleukin 1 (IL 1) is a potent enhancer of nonspecific resistance to infection in mice. Since IL 1 also induces interleukin 6 (IL 6), we tested the hypothesis that IL 6 mediates the effect of IL 1 on nonspecific resistance. In a lethal Pseudomonas aeruginosa infection in granulocytopenic mice, in which 80 ng of recombinant human IL 1α protects against death, IL 6 appeared to be much less effective. Dosages of 8 ng, 80 ng and 320 ng IL 6 did not differ from the control, whereas 800 ng had a marginal protective effect (0.05 < p < 0.1). IL 1 and IL 6 did not potentiate each other in animals treated with suboptimal dosages of both cytokines. Numbers of bacteria cultured from the blood, thigh muscle, liver, spleen, and kidney were similar in animals treated with 800 ng IL 6 and in control animals, arguing against activation of microbicidal mechanisms. The serum concentration profile of IL 6 after an i.p. injection of 80 ng IL 1 was similar to that after 80 ng IL 6 i.p. Only minute amounts of IL 1 were detected in serum after an i.p. injection of IL 6. Taken these data together, it appears that increased resistance to infection induced by IL 1 is not mediated by IL 6.
Role of interferon‐gamma in the modulation of the IgE response by 2,4‐dinitrophenyl‐Bordetella pertussis vaccine in the mouse
Authors: Hagen Michael , Essani Naeem A. , Strejan Gill H. 
Published: March 2007

AbstractImmunization of mice with 2,4‐dinitrophenyl‐Bordetella pertussis (DNP‐BP) failed to induce anti‐DNP IgE responses. Administration of DNP‐BP induced, however, the formation of anti‐DNP IgE B memory cells, as demonstrated by adoptive transfer. Furthermore, mice pretreated with DNP‐BP and primed with 2 μg DNP‐ovalbumin (OA) in alum 2 weeks later produced high day‐7 anti‐DNP IgE levels. These subsided to near undetectable levels by day 12–14. The transient expression of serum IgE levels was accompanied by normal levels of anti‐DNP IgG. The anti‐OA response induced as a result of priming with DNP‐OA in alum was not affected by pretreatment with DNP‐BP. IgG subclass analysis revealed that mice pretreated with DNP‐BP had elevated levels of IgG2a and reduced levels of IgG1 as compared to control (TNP‐keyhole limpet hemocyanin‐pretreated) mice. Treatment of mice with an anti‐interferon‐γ monoclonal antibody, shortly after immunization with DNP‐BP, not only reduced anti‐DNP IgG2a levels, but prevented the sharp anti‐DNP IgE decline that occurred after priming with DNP‐OA in alum. These results suggest that DNP‐BP‐induced interferon‐γ production modulates Ig isotype expression in vivo in an antigen‐specific manner.
Demonstration by class I gene transfer that reduced susceptibility of human cells to natural killer cell‐mediated lysis is inversely correlated with HLA class I antigen expression
Authors: Shimizu Yoji , Demars Robert 
Published: March 2007

AbstractHLA antigen‐loss mutants and class I gene transferents were used to analyze the influence of class I expression on natural killer (NK) cell‐mediated lysis. Only HLA antigen‐loss mutants that had lost expression of either HLA‐A and HLA‐B antigens (mutant .184) or of HLA‐A, B and C antigens (mutant .221) were distinctly susceptible to NK‐mediated lysis. Mutants with reduced expression of class II antigens but unaltered expression of class I antigens remained resistant to NK lysis. A direct demonstration of the effect of class I antigen expression on human cells was made by analyzing a variety of gene transferents of the HLA‐A, B, C null mutant .221 expressing only one transferred HLA‐A, B or C gene. These results specifically show that expression of class I antigens, with a possible preferential effect of HLA‐B expression, reduces the susceptibility of mutant .221 to NK‐mediated lysis.
In vitro and in vivo effects of interleukin 2 on the protozoan parasite leishmania
Authors: Mazingue Christine , Cottrez‐Detoeuf Françoise , Louis Jacques , Kweider Mahmud , Auriault Claude , Capron André 
Published: March 2007

AbstractT cells can have either resistance‐promoting or disease‐promoting effects in murine cutaneous leishmaniasis. It is known that the adoptive transfer of parasite‐specific helper T cells led to an exacerbation of Leishmania‐induced lesions. This work presents evidence that lymphokines produced by activated T cells could be involved in this exacerbating process by directly stimulating the parasite growth. In the presence of activated T cell supernatants, the in vitro growth of Leishmania mexicana amazonensis promastigotes was greatly enhanced. This effect was reproduced by addition of recombinant interleukin 2 (IL 2). An anti‐IL 2 antibody partially reversed the stimulatory effect of IL. An in vivo in situ treatment of infected mice with IL 2 led to an exacerbation of the lesions. The increase in footpad swelling after IL 2 treatment was correlated with a higher number of parasites per lesion. The protective effect of cyclosporin A against the development of Leishmania infection was abolished by IL 2 treatment. As we observed that IL 2 has a stimulatory effect on the in vitro Leishmania growth, we speculate that exacerbation of the lesions observed in vivo after IL 2 treatment could be partially related with a direct effect of IL 2 on the parasite growth.
Terminal deoxynucleotidyl transferase‐positive B cell precursors in fetal lymph nodes and extrahemopoietic tissues
Authors: Cattoretti Giorgio , Parravicini Carlo , Bonati Antonio , Buscaglia Mauro , Zuliani Guglielmo , Plebani Anna , Delia Domenico , Rilke Franco 
Published: March 2007

AbstractTerminal deoxynucleotidyl transferase (TdT)‐positive B cell precursors populate fetal lymph nodes (LN) of mid‐term (16th–22th week) fetuses. These cells have a B cell phenotype (HLA‐DR, CD45R, CD22, μ) and lack mature differentiation antigens (CD1c, CD20, L26). TdT cells are also present in the extranodal mesenteric mesenchyme, pancreas and LN primordia. Extranodal TdT cells are found among proliferating (i.e. Ki‐67) B cells and lack leukocyte function‐associated antigen (LFA‐1) and HLA‐DQ; these latter molecules are acquired by nodal TdT elements. Adult LN, adult and fetal spleen contain less TdT cells than fetal LN. The fetal LN contains the full range of the B cell differentiation compartment, from the TdT precursor cell to the mature B lymphocyte.
Specific immune responses restored by alteration in carbohydrate chains of surface molecules on antigen‐presenting cells
Authors: Boog Claire J. P. , Neefjes Jacques J. , Boes Jolande , Ploegh Hidde L. , Melief Cornelis J. M. 
Published: March 2007

AbstractTwo class I major histocompatibility (MHC) mutant mouse strains, H‐2bm14 and H‐2bm6, differ from the strain of origin C57BL/6 (B6, H‐2b) in one and two amino acids of the H‐2Db and H‐2Kb molecule, respectively. The bm14 Db mutation results in specific failure of female bm14 mice to generate a cytotoxic T lymphocyte (Tc) response to the male‐specific antigen H‐Y. The allospecific Tc response of CD8 B6 T cells against bm6 Kb mutant spleen cells, in contrast to that against other Kb mutants, is absolutely CD4 T helper cell dependent. Purified CD8 T cells completely fail to respond. We now report that the inability to mount these specific immune responses is restored by the use of dendritic cells (DC) as antigen‐presenting cells (APC). Comparison of MHC expression on various types of APC by cytofluorimetry and quantitative immunoprecipitation showed very high expression of class I and class II MHC molecules on DC. Strikingly, examination of class I and class II molecules by isoelectric focusing revealed qualitative differences as well. We show that the surface MHC class I molecules of DC are present in greater quantity and carry on average fewer sialic acids than the same molecules isolated from other APC types such as spleen cells, lipopolysaccharide blasts or concanavalin A blasts. That sialic acids on cell surface molecules, including MHC, may play a role in antigen presentation is suggested by our finding that removal of sialic acids, by neuraminidase, can restore specific responses to nonresponder APC as well.
Molecular control of tissue‐specific expression at the mouse TNF locus
Authors: Victor Jongeneel C. , Shakhov Alexander N. , Nedospasov Sergei A. , Cerottini Jean‐Charles 
Published: March 2007

AbstractWe have examined the patterns of mRNA accumulation and transcription of the tandemly linked genes for tumor necrosis factor (TNF)‐β and TNF‐α. In spite of their tandem arrangement and close linkage, the two TNF genes utilize separate promoters. Our results show that, while levels of mRNA correlate with patterns of TNF‐α and TNF‐β secretion by lymphocytes and macrophages, the transcriptional levels of the corresponding genes do not. The TNF‐α gene is transcribed much more heavily than the TNF‐β gene in T lymphocytes, even though the TNF‐β mRNA is more abundant. Resting T lymphocytes and macrophages, which do not accumulate any TNF mRNA, nevertheless transcribe the TNF‐α gene actively. On the other hand, the TNF‐β gene is transcriptionally silent in macrophages. Our results are consistent with a model where tissue specificity is controlled transcriptionally, whereas post‐transcriptional events differentially control mRNA abundance.
T cells recognize both conformational and cryptic determinants on the insulin molecule
Authors: Thomas James W. , George‐Gattner Hans , Danho Waleed 
Published: March 2007

AbstractT lymphocytes from strain 2 guinea pigs were studied for recognition of isolated insulin A and B chains. Insulin‐immune T cells require intact conformation of the interchain disulfide bond that forms the A chain loop but do not require the B chain. In addition, strain 2 T cells were unexpectedly found to recognize unique epitopes on isolated insulin B chain that are not generated by presentation of native insulin. These data show that the T cell repertoire of strain 2 guinea pig for insulin includes both conformational and cryptic determinants.
Granzyme A expression by normal rat natural killer (NK) cells in vivo and by interleukin 2‐activated NK cells in vitro
Authors: Velotti Francesca , Palmieri Gabriella , Morrone Stefania , Piccoli Mario , Frati Luigi , Santoni Angela 
Published: March 2007

AbstractGranzyme A (TSP‐1) is a serine esterase expressed in cytotoxic T and natural killer (NK) cell lines. Its presence in in vivo primed T cells is disputed at present. Here we show that normal rat NK cells contain granzyme A in vivo and that its expression is augmented by their short‐term in vitro treatment with IL2. Granzyme A expression in a NK cell population with LAK activity has also been examined.
Neonatal induction of allogeneic tolerance prevents T cell‐mediated autoimmunity in NOD mice
Authors: Bendelac Albert , Boitard Christian , Bach Jean‐François , Carnaud Claude 
Published: March 2007

AbstractDiabetes in the NOD mouse strain is a genetically programmed T cell‐mediated autoimmune process that is directed against an as yet unknown antigen target(s) on pancreatic β cells. To investigate whether the course of the autoimmune disease could be altered by immune manipulations of the T cell repertoire, we have induced allogeneic tolerance by injecting F1 semiallogeneic spleen cells into NOD neonates. This procedure resulted in a significant protection against both insulitis and diabetes. However, although it requires the induction of tolerance, as shown by the failure of non‐tolerizing irradiated cells to prevent autoimmunity, protection appeared to be independent of the major histocompatibility complex haplotypes of the F1 spleen cells injected at birth, e.g. (C57BL/6 x NOD)F1, (CBA/Ca x NOD)F1 or (BALB/c x NOD)F1 cells. In addition, a similar degree of protection was induced, whether the tolerant state, as assessed by mixed lymphocyte reaction studies in vitro, was of short duration, ∼6 weeks, or lasted for more than 12 weeks. Putative veto or suppressor functions of chimeric T cells were ruled out, since mice tolerized with T cell‐depleted F1 spleen cells were equally protected.We conclude that the expression of spontaneous T cell‐mediated autoimmunity can be modulated by immune manipulations at birth. Whether the protection observed in the present experiments resulted from the production of one or several specific holes in the autoimmune T cell repertoire, i.e. cross‐tolerance, or whether it resulted from nonspecific disturbances of the emerging T cell repertoire remains to be elucidated.
Rearranging sequence located in the intron of the human T cell receptor γ chain gene constant region
Authors: Chen Zhu , Loiseau Pascale , Bories Jean Christophe , Bensussan Armand , Sigaux FrançOis 
Published: March 2007

AbstractHuman T cell rearranging γ genes encode membrane proteins which are expressed by a minor subset of T cells. Extensive studies have shown that TcR γ gene rearrangements result from Vγ‐Jγ recombinations. Here we analyze an unusual rearrangement involving a non‐translatable sequence flanked by heptamer and nonamer signals in a Ti α/β‐positive T cell clone (JF1). This sequence, designated here as IγRS, is distinct from V, D or J elements. It is located in the first intron of the first constant region (Cγ1) and homologous sequences are conserved in Cγ2 introns. In JF1 cells the IγRS is juxtaposed to the Jγ2 segment downstream to a Vγ10‐Jγ1 rearrangement. The use of a cryptic splicing site induced JF1 cells to produce an aberrant large‐sized transcript containing the IγRS 3′ to the first exon of Cγ1. Such a rearrangement occurring downstram to an inframe Vγ‐Jγ junction may induce premature arrest of translation and lack of the C‐terminal part of Cγ involved in γ‐protein assembly.
Masking of veto function in vivo by activated CD4+ T lymphocytes
Authors: Rammensee Hans‐Georg , Hügin Daniela 
Published: March 2007

AbstractDonor CD8+ T lymphocytes injected into recipient mice incompatible at major histocompatibility complex (MHC) class I genes induce donor‐specific CTL nonresponsiveness, attributed to the veto function of donor cells. Here we show that conditions leading to strong activation of CD4+ T cells, namely the presence in the recipient of foreign MHC class II determinants, lead to the apparent loss of veto function of donor cells. This ‘masking’ of veto function is dependent on the dose of foreign MHC class II present. Veto function can be partially restored by treatment of recipients in vivo with CD4‐specific antibody, a measure which has been shown to eliminate the function of CD4+ T cells in vivo. We conclude that CD4+ T cells activated by contact with antigen can interfere with the veto function of CD8+ T cells. Consequences of this finding are: (a) veto function of a sample cell population can be overlooked when activation of CD4+ T cells occurs simultaneously. (b) The balance between veto function of recipient cells and its abrogation might be responsible for the kind of graft‐vs.‐host reaction generated (CD8+ T cell‐mediated and frequently lethal or CD4+ T cell‐mediated and not lethal) when parental T cells are injected into recipients incompatible at MHC class I and class II genes, (c) A possible contribution of veto cells should be considered in several protocols in which donor hemopoetic cells were used in conjunction with CD4‐specific antibodies to induce transplantation tolerance, (d) Veto function in vivo does not require a contribution of CD4+ T cells.
Marginal zone macrophages and their role in the immune response against T‐independent type 2 antigens: modulation of the cells with specific antibody
Authors: Kraal Georg , Hart Hennie Ter , Meelhuizen Constantijn , Venneker Gerard , Claassen Eric 
Published: March 2007

AbstractMarginal zone macrophages are strategically positioned in the marginal zone of the spleen and are thought to play an important role in the initiation of the immune response to T‐independent type 2 responses. The cells are characterized by high phagocytic activity and by the selective uptake of neutral polysaccharides. In the mouse marginal zone macrophages react specifically with the monoclonal antibody ER‐TR9. Injection of the antibody resulted in a complete abrogation of the uptake of neutral polysaccharides by the cells in vivo, although the cells were still capable of taking up latex and carbon particles. The complete blockade of the polysaccharide uptake did not result in an altered humoral immune response against this antigen. When the antibody ER‐TR9 was coupled to the toxin gelonin a complete elimination of the marginal zone macrophages could be established in vivo. However, complete elimination did not result in changes of the immune responses against 2,4,6‐trinitrophenylated Ficoll, suggesting that the marginal zone macrophages are either not involved in this type of response, or that their function can be taken over by other cells. The possible role of these cells and the importance of the spleen in the immune response against bacterial antigens is discussed.
Identification of a human monocyte antigen (Mo3e) associated with cellular activation and lymphokine responsiveness
Authors: Liu David Y. , Ree Joy Y. , Douglas Trochelman R. , Todd, Iii Robert F. 
Published: March 2007

AbstractA murine monoclonal IgM antibody recognizes an antigen (Mo3e) found on the surface of human peripheral blood monocytes stimulated with phorbol 12‐myristate 13‐acetate (PMA), lipopolysaccharide and muramyl dipeptide and blocks the monocyte response to migration inhibitory factor (MIF). We utilized Western blot and immunoprecipitation analyses of whole cell lysates to investigate the biochemical nature of this monocyte antigen. Two distinct bands (75 kDa and 50 kDa) were detected by anti‐Mo3e after monocyte lysates were resolved by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) and transblotted onto nitrocellulose paper. Stimulation of monocytes with PMA resulted in a marked increase in the amount of the 50‐kDa species. Immunoprecipitation of Mo3e from lysates of surface‐iodinated cells demonstrated one broad band at 55–80 kDa which increased after PMA stimulation. The epitope identified by anti‐Mo3e was resistant to 2‐mercaptoethanol and heat treatment (100°C/5 min) and was sensitive to trypsin or papain treatment. Two‐dimensional SDS‐PAGE analysis revealed that the 75‐kDa species has an isoelectric point of 7.0 and the 50‐kDa species is more acidic with an isoelectric point of 5.3. These results indicate that anti‐Mo3e antibody defines unique monocyte proteins that may play a role as suggested by previous studies, in monocyte activation and responsiveness to MIF.
Most human CD3+WT31− clones with T cell receptor Cγ1 rearrangements show strong non‐MHC‐restricted cytotoxic activity in contrast to those with Cγ2 rearrangements
Authors: Christmas Stephen E. 
Published: March 2007

AbstractClones expressing CD3 in the absence of WT31 expression were obtained by growing highly purified WT31− cells in the presence of interleukin 2 and phytohemagglutinin. Most clones showed rearrangements of T cell receptor (TcR) γ genes on both chromosomes involving all five currently identified Jγ segments. About a third of these clones had a rearranged 12 kb Kpn I band with the Jγ probe, consistent with a V9JPCγ1 rearrangement. All clones with both chromosomes rearranged to Cγ2 had low or intermediate cytotoxic activity while most of those with at least one chromosome rearranged to Cγ1 had high cytotoxic activity against both natural killer‐sensitive and natural killer‐resistant targets. This applied both to clones with and without the V9JPCγ1 rearrangement. Of three clones with both Cγ1 and Cγ2 rearrangements two had high activity and the other was only weakly cytotoxic. In addition, most clones showed rearrangement of TcR β genes. Some clones were capable of secreting levels of interferon‐γ and tumor necrosis factor‐α which were as high as those produced by CD3+4+WT31+ T cell clones. The results suggest that most human CD3+WT31− clones expressing a disulfide‐linked Cγ1/δ heterodimer are capable of mediating strong non‐major histocompatibility complex‐restricted cytotoxicity whereas those expressing non‐disulfide‐linked Cγ2/δ heterodimers are not.
Functional characterization of the CD45R (2H4) molecule on CD8 (T8) cells in the autologous mixed lymphocyte reaction system
Authors: Takeuchi Tsutomu , Rudd Christopher E. , Tanaka Shinsuke , Rothstein David M. , Schlossman Stuart F. , Morimoto Chikao 
Published: March 2007

AbstractIn the present study, we have investigated the molecular basis for the immunoregulatory function of CD8 cells after autologous mixed lymphocyte reaction (AMLR) activation. We demonstrated that the CD8+CD45R+, but not the CD8+CD45R− subset of cells effected suppression following AMLR activation. In contrast, cytotoxic activity against alloantigens resided in both the CD8+CD45R+ and CD8+CD45R− subsets of cells. Biochemical analysis showed that on CD8 cells, the 220‐kDa isoform of the LCA/T200 antigen family was better represented than the 200‐kDa isoform, when compared to CD4 cells. The density of the CD45R antigen increased on CD8 cells following activation in AMLR and treatment of AMLR‐activated CD8 cells with either anti‐CD45R antibody or anti‐CD3 antibody abolished the suppressor function of these cells. In contrast, treatment of AMLR‐activated CD4 cells with anti‐CD45R, but not anti‐CD3 antibody, abolished the suppressor/inducer function of these cells. The results suggest that the CD45R antigen as well as CD3 T cell receptor complex have an important role in the suppressor function of AMLR‐activated CD8 cells.
In vivo depletion of BoT4 (CD4) and of non‐T4/T8 lymphocyte subsets in cattle with monoclonal antibodies
Authors: Howard Christopher J. , Sopp Paul , Parsons Keith R. , Finch Julie 
Published: March 2007

AbstractThe effect on certain immune responses of depleting two distinct lymphocyte subpopulations in vivo by inoculating calves with monoclonal antibodies (mAb) was examined. An mAb directed against the BoT4 antigen (the bovine homologue of CD4) effectively removed the BoT4+ lymphocytes from peripheral blood mononuclear cells (PBM). Compared to controls, treated calves showed a reduced antibody response to human O red blood cells and to ovalbumin. PBM prepared from BoT4‐depleted animals also had a significantly reduced ability to respond in vitro to the mitogens phytohemagglutinin, concanavalin A and pokeweed mitogen. An mAb directed against a second numerically large bovine lymphocyte subpopulation i.e. BoT2−, BoT4−, BoT8− (CD2−, CD4−, CD8−), that may be homologous to the CD4−, CD8− cells in man and rodents that synthesize the γ/δ+ T cell receptor, was also used for in vivo depletion. Compared to controls, calves depleted of this subpopulation showed an enhanced antibody response. The proliferative response of PBM to pokeweed mitogen was also significantly increased but responses to concanavalin A and phytohemagglutinin remained unchanged. The results suggest this lymphocyte subpopulation has a nonspecific suppressor activity acting on B cell responses either directly or through an effect on T helper cells. The non‐T4/T8 cells are found extensively in the epithelium and lamina propria of the mucosa of the alimentary tract but not in T cell areas of the lymph nodes, tonsil and spleen. These non‐T4/T8 cells may thus be, or contain, an intraepithelial lymphocyte population with a suppressor function.