bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cross‐linking of the surface immunoglobulin on lymphocytes from the bursa of Fabricius results in second messenger generation
Authors: Ratcliffe Michael J. H. , Tkalec Lydia 
Published: March 2007

AbstractThe bursa of Fabricius represents the major site of B lymphocyte development in avianspecies. Although the vast majority of bursal lymphocytes express cell surface immunoglobulin (sIg), it is generally considered that the bursa does not represent a significant site of antigen‐induced B cell maturation to Ig secretion. However, the question as to whether antigen, either exogenous or self, can induce positive or negative selection of bursal lymphocytes in such a way as to modify the peripheral B cell repertoire remains open. Clearly, such intrabursal selection would require that bursal lymphocyte sIg have the molecular machinery to transduce signals into the cell as a consequence of its interaction with antigen.In this report we demonstrate that exposure of bursal lymphocytes to antibodies directed against sIg induced a rapid increase in cytosolic free calcium ion concentrations [Ca2+]i. Furthermore, such antibodies also induced a rapid increase in intracellular phosphatidic acid concentrations followed by a rise in intracellular phosphatidylinositol. Increased [Ca2+]i, phosphatidic acid and phosphatidylinositol levels required the cross‐linking of sIg and were not induced by antibodies to other bursal cell surface antigens. Thus, cross‐linkingof the sIg on bursal lymphocytes results in second messenger generation, demonstrating that bursal sIg is a functional signal transduction element.
Induction of germ‐line immunoglobulin heavy chain transcripts by mitogens and interleukins prior to switch recombination
Authors: Severinson Eva , Fernandez Carmen , Stavnezer Janet 
Published: March 2007

AbstractIt has recently been postulated that immunoglobulin class switching is preceded by transcription from unrearranged heavy chain genes. In this report, we have investigated the conditons under which RNA transcribed from unrearranged Cγ3, Cγ1, Cγ2b, Cγ2a, Cϵ and Cα genes are induced in normal spleen cells by mitogens and/or interleukin (IL)4, IL5 and interferon‐γ. Lipopolysaccharide (LPS) plus IL4 induced germ‐line γ1 and ϵ transcripts. LPS induced γ2b and γ3 transcripts and high doses of IL4 suppressed these LPS‐induced transcripts. Interferon‐γ induced low levels of germ‐line γ2a transcripts and profoundly suppressed the γ1 and ϵ transcripts induced by LPS and IL4. IL5 alone or in combination with IL4 and/or LPS did not induce germ‐line α transcripts. Spleen cells of the partially immunodeficient mice CBA/N and C3H/HeJ, which do not express IgG3 could be induced, however, by polyclonal activators to express germ‐line γ3 and γ2b transcripts. The data indicate that the capacity of a ligand to induce/suppress transcription of a particular unrearranged heavychain gene is a good indicator of its capacity to induce switching to the corresponding Ig isotype. However, it is also clear that control of switching can be carried out at other levels.
Correlations of autoimmunity with H2 and T cell receptor β chain genotypesin (NZB x NZW) F2 mice
Authors: Noonan Daniel J. , McConahey Patricia J. , Cardenas Gustavo J. 
Published: March 2007

AbstractAccelerated autoimmunity as expressed by the classical autoimmune strain mouse (NZB XNZW)F1 is thought to be the result of major histocompatibility complex (MHC)‐associated NZW genes acting on a genetic predisposition for autoimmunity as expressedby the NZB mouse. To evaluate more accurately both H2 and T cell receptor (TcR) β chain involvement in F1 disease, we studied the segregation of NZB (H2d, TcRB) and NZW (H2w, TcRW) haplotypes of these genetic elements and the development of autoimmunity in (NZB X NZW)F2 generation mice. F2 mice with the H2d/z genotype lived shorter average life‐spans and expressed elevated levels of antibodies to gp70, ssDNA and dsDNA, while those with the TcRW/W genotype (homozygous for the NZW TcR deletion) expressed elevated levels of autoantibodies but had relatively long life‐spans. On the other hand, mice with the TcRB/B genotype (homozygous for the NZB TcR) produced consistently low levels of autoantibodies but died at an early age. The most severely affected F2 population were the mice carrying both the TcRB/B and H2d/z alleles. These mice died on an average within the first 5 months of life, but produced the lowest levels of antibodies to gp70, single‐stranded DNA and double‐stranded DNA. These data confirm the contribution of NZW H2linked genes to accelerated autoimmunity in the F1 hybrid and, furthermore, define NZB TcR‐linked components as primary developers of this phenomenon. They also suggest a limited, if any, contribution of both the NZW TcR deletion and traditional autoantibodies to F1 accelerated autoimmunity.
Eosinophil cytotoxicity enhancing factor: purification, characterization and immunocytochemical localization on the monocyte surface
Authors: Elsas P. Xavier , Capella Elsas M. I. Gaspar , Dessein Alain J. 
Published: March 2007

AbstractThe monokine eosinophil cytotoxicity enhancing factor (ECEF) increases antibody‐dependent cytotoxicity of eosinophils towards helminth larvae. A monokine biochemicallyindistinguishable from ECEF increases the release of leukotriene C4 and other arachidonicacid metabolites by eosinophils. We have developed monoclonal antibodies (mAb) to these monokines by immunizing mice with ECEF made by the U‐937 histiocytic lymphoma cell line. mAb 81.10.C9 (IgG2b) and 9A6G (IgG1) inhibit the effect of the monokine on release of A A products. Both mAb bind ECEF, which appears after affinity chromatography purification as a major 13—14‐kDa and a minor 62‐kDa component (13—14 kDa and 52 kDa after reduction) in silver‐stained gels. An additional component of 30 kDa is detectable after radioiodination of the immunopurified material. The specificity of both mAb was studied in several ways. In immunoprecipitation, bothrecognize the 13—14‐kDa and the 30‐kDa components, while the 62–(52)‐kDa protein is not significantly precipitated. Both mAb react in enzyme‐linked immunosorbent assay with products secreted by peripheral blood mononuclear cells and monocytes, as well as with those secreted by phorbol 12‐myristate 13‐acetateand lipopolysaccharide‐stimulated U‐937 cells and with the immunopurified proteins. These were separated in sodium dodecyl sulfate‐polyacrylamide gel electrophoresis, electroeluted and assayed for ECEF activity. Activity was associated with the 13—14‐kDa and the 30‐kDa fractions, as seen by increased eosinophil antibody‐dependent adherence to schistosomula and cytotoxicity. Granulocyte‐monocyte‐colony‐stimulating factor and interleukin 1, but not tumor necrosisfactor, could be detected in crude U‐937 supernatants. However, active immunopurified ECEF has no activity in assays for granulocyte‐monocyte‐colony‐stimulating factor, interleukin 1 or tumor necrosis factor. Immunocytochemical localization of ECEF employing the mAb shows strong surface staining of viable monocytes and U‐937 cells, suggesting that ECEF is associated to the cell surface. These properties distinguish ECEF from other monokines previously reported to activate eosinophils.
A novel pathway of human B cell activation initiated by CK226 surface antigen
Authors: Poggi Alessandro , Maggi Enrico , Biagiotti Roberta , Giudizi Maria Grazia , Almerigogna Fabio , Pella Nicoletta , Caligaris‐cappio Federico , Romagnani Sergio , Moretta Lorenzo 
Published: March 2007

AbstractIn this study we analyzed the effect of CK226 monoclonal antibody (mAb) on human B cell activation and proliferation. This mAb was shown to recognize a 75‐kDa surface molecule expressed on both T and B lymphocytes and to mediate T lymphocyte activation andproliferation. Flow cytometry analysis of B cell populations isolated from peripheral blood, tonsil and spleen showed that CK226 surface antigen is highly expressed on 40—80% of surface Ig+ cells. When purified B cells were cultured in the presence of CK226 mAb, up‐regulation of major histocompatibility complex class II and CD23 surface structures and the de novo expression of CD25 antigen could be detected within 48 h. In addition, B cells underwent proliferation ([3H] thymidine uptake) in the absence of either T cells or exogenous lymphokines. Proliferation was potentiated by the addition of suboptimal concentrations (0.5 ng/ml) of phorbol 12‐myristate 13‐acetate (PMA). Cells recovered at day 5 were surface Ig+ and no CD3+ cells could be detected. CK226‐induced proliferation (either in the presence or in the absence of PMA) was not inhibited by anti‐CD25 mAb. Addition of exogenous interleukin 2 to CK226‐stimulated B cells resulted in further increase of B cell proliferation. On the other hand, CK226 mAb did not display a co‐stimulatory effect with submitogenic concentrations of either anti‐Ig antibody or Staphylococcus aureus Cowan strain I bacteria. In addition proliferation induced by mitogenic concentrations of the above stimuli was inhibited in a dose‐dependent fashion by CK226 mAb.
T cell receptor‐bearing cells among rat intestinal intraepithelial lymphocytes are mainly α/β+ and are thymus dependent
Authors: Vaage John Torgils , Dissen Erik , Ager Ann , Roberts Ian , Fossum Sigbjørn , Rolstad Bent 
Published: March 2007

AbstractRearrangement of both the β and γ chain T cell receptor (TcR) genes was detected in intestinal intraepithelial lymphocytes (IEL) from normal euthymic rats. Flow cytometric analyses showed that about 73% of the IEL were CD3+ (1F4) and that67% were TcR α/β+ (R73). About 5% of the IEL were found to be CD3+, TcR α/β− in double‐labeling experiments suggesting that a small fraction of IEL in the rat express the alternative TcR γ/δ. More than 70% of the IEL were granular implying that many CD3+ IEL are granular. In IEL from athymic nude rats no rearrangement of either the TcR β or γ chain genes or surface expression of CD3 or TcR α/β was detected despite the fact that about 95% of the cells were granular and morphologically similar to those in normal rats. Taken together our data suggest that the majority of IEL in the rat express the conventional TcR α/β and that TcR‐bearingcells in the gut epithelium are thymus dependent.
Cytofluorometric and cytomorphologic analysis of human bone marrow cells derived fromstromal cultures stimulated by granulocyte‐macrophage colony‐stimulating factor, interferon‐γ and splenopentin pentapeptide
Authors: Maciejewski Jaroslaw , Wächter Marlies , Elstner Elena , Weber Harald , Diezel Wolfgang , Seiler Friedrich R. , Volk Hans‐dieter 
Published: March 2007

AbstractWe studied the influence of human recombinant granulocyte‐macrophage colony‐stimulating factor (hrGM‐CSF), human recombinant interferon‐γ (hrIFN‐γ) and splenopentin pentapeptide (Sp‐5), either alone or in combination, on the proliferation and differentiation of human bone marrow cells in modified Dexter's cultures. After 10, 14 and 21 days cells were analyzed by classical staining according to Pappenheim and by cytofluorometry with a set of different monoclonal antibodies. IFN‐γ inhibited the proliferation of progenitor cells and provided signals promoting monocytic differentiation, whereas GM‐CSF induced the proliferation of blastoid elements which expressed HLA‐DR and M2 (VIM‐2 monoclonal antibody), but progressively lost surface CD34. Furthermore, an increase of CD15+ cells was also observed. When GM‐CSF was tested in combination with IFN‐γ, it abolished the inhibitory effect of IFN‐γ and both cytokines synergized to promote the expression of CD11c, CD14 and M2 surface antigens. Sp‐5 alone had only a marginal activity, but it potentiated the effects of GM‐CSF. These findings suggest that GM‐CSF may induce the transition from stem cells to committed myeloid progenitors. In contrast to IFN‐γ, Sp‐5 can serve as an additional proliferative signal with negligible effects on cell maturation.
Study of the thymocyte cell cycle by bivariate analysis of incorporated bromodeoxyuridine and DNA content
Authors: Baron Christophe , Pénit Claude 
Published: March 2007

AbstractThe in vivo cell cycle of normal murine thymocytes was studied by bivariate analysis of bromodeoxyuridine and total DNA content in the 24 h following a single injection of the thymidine analogue. Bromodeoxyuridine incorporation was strictly limited to cells in S phase and 98% of S phase cells were labeled, demonstrating high efficiency and specificity. Cell‐cycle parameters were determined by measuring the DNA content of bromodeoxyuridine‐labeled cells, related to their distribution in the different phases. The changes of this distribution as a function of time reflected the progression of the cells along the cell cycle. The duration of total cycle, S phase, and both G2/M and G1 was 10 h, 6.5 h and 1.5 h, respectively. All thymocytes labeled inS phase entered G2/M, divided and returned to the G0/G1. Seventy percent of them remained in the resting state, and the other 30% reentered a second S phase. Cell‐cycle parameters of isolated CD4−CD8− cells were also determined. No evidence of cell loss during S or G2/M phase was found, suggesting that intrathymic cell death is not directly linked to the proliferative phases of differentiation.
Allergen‐directed expression of Fc receptors for IgE (CD23) on human T lymphocytes is modulated by interleukin 4 and interferon‐γ
Authors: Prinz Jörg C. , Baur Xaver , Mazur Gertraud , Peter Rieber E. 
Published: March 2007

AbstractT lymphocytes bearing Fc receptors (FcR) for immunoglobulins are known to have immunoglobulin class‐specific regulatory functions. Here we report that expression on T cells of the low‐affinity FcR for IgE (FcϵRII/CD23) is preferentially induced by stimulation with antigens that cause an IgE response. T cells from eight patientsallergic to the hemoglobin of Chironomus thummi thummi mosquito larvae (CHIT I) were analyzed for reactivity with the anti‐FcERII/CD23 monoclonal antibody (mAb)M‐L25 under various conditions. No FcϵRII/CD23+ T cells were observed among freshly isolated, resting peripheral blood mononuclear cells (PBMC). Stimulation of PBMC with CHIT I, however, induced a marked although transient FcϵRII/CD23 expression on a large portion of the allergen‐activated T lymphocytes. It reached a maximum of 37.2 ± 4.6% FcϵRII/CD23+ T cell blasts on day 5 of culture. The selectivity of this expression became evident when compared to non‐allergenic control antigens: after stimulation of PBMC with tetanus toxoid or purified protein derivative from tuberculin a maximum of 4.6% ± 1.4% and 4.2% ± 1.1% T cell blasts was found to express FcϵRII/CD23, respectively. Activation by an anti‐CD3 mAb was insufficient to induce FcϵRII/CD23 on T cells. The allergen‐stimulated FcϵRII/CD23+ T cells exclusively belonged to the CD4+CD29+ helper inducer T cell subset.Using a cDNA probe coding for the B cell FcϵRII/CD23, Northern blot analysis revealed a 1.7‐kb FcϵRII/CD23 mRNA in extracts of highly purified allergen‐stimulated T cells. It was of the same size as FcϵRII/CD23 mRNA of the lymphoblastoid B cell line WI‐L2.Of several cytokines tested [interleukin (IL) 1 to IL 6, interferon‐γ (IFN‐γ), tumor necrosis factor‐α] only IL 4 and IFN‐γ significantly modified allergen‐induced FcϵRII/CD23 expression onT cells. The latter was enhanced nearly twofold in the presence of IL 4, and was almost completely abrogated by IFN‐γ. IL 4, however, could not increase the number of FcϵRII/CD23+ T lymphocytes either alone or in combination with an anti‐CD3 mAb. Taken together, the selective induction of FcϵRII/CD23 onT cells by allergen and its inclusion in the regulatory network of cytokines point to an important role of FcϵRII/CD23+ T lymphocytes in the human IgE response.
Polymorphism of age‐related changes in interleukin (IL) production: differential changes of T helper subpopulations, synthesizing IL 2, IL3 and IL4
Authors: Kubo Masato , Cinader Bernhard 
Published: March 2007

AbstractInbred mice were examined for strain differences in age‐associated changes in the capacity to synthesize interleukin (IL), i.e. IL2, IL3 and IL4 after stimulation with phorbol myristate acetate (PMA) and calcium ionophore (A23187). Production of IL2remains constant in A/J, DBA/1 and DBA/2 mice and decreases with age in one of the strains examined (C57BL/6J). Strain differences in age‐associated changeof synthesis did not show the relation between youthful synthetic capacity and magnitude of later decrease (“economic correction”) which is observed in several other systems. This difference between different types of polymorphisms is attributed to an age‐associated defect in intrinsic capacity to synthesize IL2 which may occur in onlyone of the tested strains, C57BL/6J. In contrast to IL 2 production, the quantities of IL3 and IL4 increase progressively, with advancing age, in mice of the three strains tested. T cells from old mice contain a greater frequency of cells producing IL3, than do those of young mice. In addition, synthesis of IL3 is induced at a relatively lower concentration of PMA in cells from old animals and this may be a consequence of different signal requirements of the two subsets of the T helper cells, but also a change in intrinsic properties of these cells. Since IL3 and IL4 production, but not IL2 production, increaseswith age, it is reasonable to conclude that this reflects an expansion of a T helper cellpopulation which secretes IL3 and IL4, but not IL2, presumably TH2.
Paradoxical lessening of autoimmune processes in non‐obese diabetic mice afterinfection with the diabetogenic variant of encephalomyocarditis virus
Authors: Hermitte Laurence , Vialettes Bernard , Naquet Philippe , Atlan Catherine , Payan Marie‐josé , Vague Philippe 
Published: March 2007

AbstractIn order to gain insight into the interaction between autoimmunity and viral infection in the onset of insulin‐dependent diabetes, non‐obese diabetic (NOD) micewhich spontaneously develop autoimmune diabetes were inoculated with the diabetogenic variant of the encephalomyocarditis virus (EMCV‐D) before the onset of the disease. The pre‐diabetic period was divided into two phases: the early phase (days 88 to 116) during which development of spontaneous diabetes is rare and the late phase (day 123 to 200) during which the incidence of spontaneous diabetes is high. As controls ICR mice of common ancestry were also inoculated. During the early phase diabetes was observed in 4/10 inoculated, 0/13 control NOD and 7/13 inoculated ICR males vs. 6/12 inoculated, 1/11 control NOD and 0/15 inoculated ICR females. However, in NOD female, virus‐induced diabetes prevalence was variable from one experiment to another. In parallel the flow cytometric analysis showed a high percentage of L3T4+ T lymphocytes in the pancreas of inoculated female NOD mice 10 days after the infection. At this time a large proportion of both L3T4+ and Ly‐2+ cells expressed the interleukin 2 receptor. During the late phase no new case of diabetes occurred in inoculated NOD mice but one case was observed in control NOD males and five in control NOD females. This prevention of autoimmune diabetes was constantly found in other experiments. Insulitis was milder in inoculated NOD mice of both sexes than in control NOD. Adoptive transfer of diabetes into irradiated 8‐week‐old males by splenocytes from 28‐week‐old females was successful in five out seven attempts with control splenocytes and in zero out of six attempts with splenocytes from inoculated mice. This immunosuppression was specific as the ability of lymphocytes to respond to soluble or allogeneic antigens was preserved.In the early phase EMCV‐D precipitated the onset of diabetes in females NOD mice by amplifying L3T4+ T lymphocyte‐mediated immune mechanisms. During the late phase viral infection had lessened immune processes in animals which had resistedor recovered from virus‐induced diabetes.
Major histocompatibility complex regulation of the class of the immune response: the H‐2d haplotype determines poor interferon‐γ response to several antigens
Authors: Asherson Geoffrey L. , Dieli Francesco , Gautam Yvonne , Khai Siew L. , Zembala Marck 
Published: March 2007

AbstractThe lymph node cells of CBA (H‐2k), but not BALB/c (H‐2d) mice, release interferon (IFN)‐γ into the supernatant when immunized with picryl chloride epicutaneously and then exposed to antigen (haptenized cells) in vitro 4 days later. The failure in IFN‐γ production maps to the major histocompatibility complex (MHC; H‐2d) in the congenic BALB/c, BALB/k and BALB/b mice. The evidence that this is an MHC regulation of the class of response to a range of antigens and not a classical Ir gene effect is (a) the difference is seen with several antigens including picryl chloride, “oxazolone” and purified protein derivative of tuberculin and (b) BALB/c mice, which fail to produce IFN‐γ, show excellent contact sensitivity to picryl chloride. It was also found that the crosses between responder and nonresponder strains (CBA × BALB/c)F1 respond to antigen on responder cell but not on nonresponder cells. This influence ofMHC on the class of the immune response is a possible basis for some of the associations of MHC with disease.
Partial tolerance in β‐galactosidase‐transgenic mice
Authors: Theopold Ulrich , Köhler Georges 
Published: March 2007

AbstractA transgenic mouse line was produced which allowed the expression of E. coli β‐galactosidase (β‐Gal) under the regulatory elements of the immunoglobulin heavy chain locus. Expression of the transgene is found in spleen and bone marrow. Upon immunization of the transgenic mice with β‐Gal, a reduced but clearly detectable antibody response was obtained. Affinity purification with sera from immunized transgenic mice suggests that they contain lower affinity antibodies as compared to normal littermates.Transgenic and nontransgenic mice immunized with bovine serum albumin (BSA) alone or as amixture with β‐Gal gave comparable anti‐BSA responses. Immunization with a chemically cross‐linked (Gal‐BSA)‐protein, however, showed a 10‐ to 30‐fold difference in the anti‐BSA response. Partial unresponsiveness to β‐Gal in the transgenic mice is best explained by a dominant, peripheral suppression mechanism linked to the antigen‐presenting potential of B cells.
Distribution, inducibility and biological function of the cloned and expressed human βFc receptor II
Authors: Engelhardt Waltraud , Geerds Christina , Frey Jürgen 
Published: March 2007

AbstractA cDNA encoding the human βFcγ receptor II (FcRII) was isolated from a placental cDNA library. Analysis of the predicted amino acid sequence indicates that this receptor is synthesized with a 42‐amino acid leader sequence. The mature protein consists of 249 amino acids. The leader sequence and the cytoplasmic domain are strikingly different from the CDw32 antigen but show great homology to the mouse β2FcR. RNA blot analysis of human cells using CDw32 and βFcRII‐specific DNA fragments demonstrated one βFcRII transcript (1.7 kb) in B cells and in HL‐60 cells which were induced to differentiate along a monocyte‐macrophage pathway by phorbol 12‐myristate 13‐acetate treatment. Under these conditions the CDw32 transcripts (2.5 and 1.7 kb) are induced to a minor extent in HL‐60 cells. In contrast, the 2.5‐kb CDw32 transcript is strongly induced in HL‐60 cells which have been induced to differentiate into granulocytes by exposure to dimethylsulfoxide. To determine the biological properties of the βFcRII, we expressed the antigen in FcR− hamster cells. Only immune complexes but not monomeric human IgG were bound significantly. Bound ligand was efficiently internalized within 15 min and it was then found in vesicular structures. Thus the low‐affinity βFcRII is able to internalize ligands without cooperation with any other FcR.