bluuebunny/crossref_metadata_2025_split huggingface dataset:
Granulocyte‐macrophage colony‐stimulating factor‐cultured bone marrow‐derived macrophages reveal accessory cell function and synthesis of MHC class II determinants in the absence of external stimuli
Authors: Fischer Hans‐Georg , Opel Beate , Reske Konrad , Reske‐Kunz Angelia B. 
Published: March 2007

AbstractThe antigen‐mediated activation of a number of T cell clones by bone marrow (BM) cells cultivated in the presence of various colony‐stimulating factor (CSF) preparations was investigated. BM macrophages (BMMϕ,) grown in L929 cell supernatant as a crude source of macrophage colony‐stimulating factor (M‐CSF) as well as BM cells propagated in the presence of recombinant M‐CSF exhibited transient antigen presentation potential to some T cell clones, being maximal on day 7 and having declined to a low level by day 19 of in vitro culture. Treatment of these long‐term‐cultivated BMMϕ, populations with recombinant interferon‐γ (IFN‐γ) resulted in predominant antigen presentation capacity. In contrast, BM cells differentiated in the presence of recombinant granulocyte (G)M‐CSF developed highly efficient accessory cell function to all T cell clones examined. This function became apparent earlier, was retained during the time period tested (up to day 19 of continuous culture) and did not require prior stimulation by IFN‐γ. The functionally competent cells were shown to belong to the monocyte/macrophage lineage. These findings are consistent with the demonstration of substantial levels of major histocompatibility complex (MHC) class II molecules synthesized by GM‐CSF‐cultured BM cells in the absence of exogenous IFN‐γ. In contrast, M‐CSF grown BM cells synthesized only minute amounts of Ia antigens unless they were stimulated by IFN‐γ. Because GM‐CSF‐cultivated BM cells proved clearly superior to M‐CSF‐grown and IFN‐γ‐activated BM cells with respect to antigen‐presenting capacity but exhibited lower levels of MHC class II molecules, other properties acting in addition to surface Ia antigens might be responsible for their pronounced T cell accessory function.
The role of suppression in immunoregulation: in vivo analysis using a monoclonal antibody to T suppressor factors
Authors: Ferguson Thomas A. , Ptak Wlodzimierz , Michael Iverson G. , Flood Patrick 
Published: March 2007

AbstractWe have used a monoclonal antibody (mAb)‐specific for murine T suppressor (Ts) cells (mAb 14‐12) to study the role of T cells in tolerance and immunoregulation. We demonstrate that mAb 14‐12 can block in vivo T, cell activity in a variety of experimental systems. It prevents the induction of Ts cells induced by i.v. injection of the water‐soluble hapten 2,4,6‐trinitrobenzene sulfonic acid, and the protein antigen bovine serum albumin. When 14‐12 mAb is given prior to the i.v. injection of Tstrinitro phenyl‐conjugated spleen cells (TNP‐SC) it blocks the induction of T, cells and sufficiently overcomes suppression so that TNP‐SC is able to induce immunity. mAb 14‐12 can convert nonresponder mice into responders for the Ir gene‐controlled response to the random terpolymer L‐glutamic acid60‐L‐alanine30‐L‐tyrosine10 (GAT), and can substitute for cyclophosphamide in overcoming a suppressor barrier in the adoptive transfer of contact sensitivity. Administration of 14‐12 mAb just prior to immunization results in the augmentation of contact sensitivity, antibody and plaque‐forming cell responses. These results demonstrate the versatility of this reagent for the study of Ts cell activity.
Frequency analysis of functional Ig Cε gene expression in the presence and absence of interleukin 4 in lipopolysaccharide‐reactive murine B cells from high and low IgE responder strains
Authors: Savelkoul Huub F. J. , Termeulen Jacqueline , Coffman Robbert L. , Van Der Linde‐Preesman Rianne A. 
Published: March 2007

AbstractNonresponder SJL mice produce low levels of antigen‐specific IgE after immunization, compared to responder strains. Young athymic BALB/c nude mice are unable to produce antigen‐specific or total IgE in their serum. These mice also have very low numbers of background IgE‐secreting cells in their lymphoid organs. High‐responder BALB/c mice do have substantial numbers of background IgE‐secreting cells while low‐responder AKR mice show intermediate numbers. Similar differences were found when analyzing lipopolysaccharide (LPS)‐reactive B cells in cell suspensions of spleen and bone marrow in limiting dilution cultures. Limiting dilution analysis of T cell‐depleted splenic B cell cultures revealed that the defective IgE production in SJL mice is not due to an intrinsic B cell defect. This defect can be substantially overcome by addition of exogenous interleukin 4 (IL4) to these cultures. Furthermore, it was shown in limiting dilution cultures that SJL thymocyte feeder cells were able to suppress IgE production by LPS‐activated high‐responder BALB/c B cells. The addition of IL4 or neutralizing antibodies against IL4 or interferon‐y to these cultures helped to overcome this suppressive effect to a large extent. We conclude that different IgE responder types are caused, at least in part, by a defective IL4 production or by a defect in the TH2 system that is functionally detectable at the level of thymocytes.
Species conservation of the T cell lymphocyte CD2 cell surface antigen
Authors: Brown Marion H. , Sewell William A. , Mason David Y. , Rothbard Jonathan B. , Crumpton Michael J. 
Published: March 2007

AbstractA rabbit polyclonal antiserum was raised against a synthetic peptide, termed CD2‐300, comprizing 18 amino acid residues which are conserved among the cytoplasmic domains of the human, rat and mouse CD2 antigens. Cross‐depletion experiments showed that the CD2 monoclonal antibody OKTl1 and purified CD2‐300 antibodies (Ab) precipitated the same molecules from the surface of human T lymphoblasts. The results of immunoprecipitation analyses indicated that the purified CD2‐300 Ab were specific for human and mouse CD2, and that the CD2‐300 peptide competitively and specifically inhibited precipitation by CD2‐300 Ab in both species. When employed to stain murine tissues, the CD2‐300 Ab gave the anticipated pattern of distribution for the CD2 antigen, although there was some nonspecific labeling of non‐T cells.
Aggravation of experimental cutaneous leishmaniasis in mice by administration of interleukin 3
Authors: Feng Zhu Yun , Louis Jacques , Kindler Vincent , Pedrazzini Thierry , Eliason James F. , Behin Reza , Vassalli Pierre 
Published: March 2007

AbstractPrevious studies from our laboratory have shown that some in vitro maintained Leish‐mania major‐specific L3T4+ T cells were capable of exacerbating cutaneous leishmaniasis after adoptive transfer to normal syngeneic mice. Results presented in this report show that these cells released substantial amounts of interleukin 3 (IL 3) and granulocyte‐macrophage colony‐stimulating factors after specific stimulation in vitro. In order to assess the involvement of such lymphokines in the exacerbation of cutaneous leishmaniasis by these L3T4+ T cells, the effect of the administration of important doses of IL 3 on the course of infection with L. major was investigated. The treatment of genetically susceptible B ALB/c mice with IL 3 resulted in an enhancement of the size of lesions and favored the multiplication of parasites at anatomical sites distant from the primary lesion. Although IL 3 did not modify the development of lesions in genetically resistant CBA mice, this lymphokine promoted the growth of Leishmania in lymph node draining the lesion. Finally, the addition of IL3 to macrophages parasitized in vitro enhanced the survival of intracellular Leishmania major.
A map of VH genes located next to the DH region in the Igh locus of two congenic Igh‐recombinant mouse strains
Authors: Lehle Georg , Kolb Cornelia , Kappen Claudia , Schü Ralph , Weiler Eberhardt , Krawinkel Ulrich 
Published: March 2007

AbstractA new congenic mouse strain (C57BL16‐Igh‐Vb‐Ca) with a recombinant chromosome 12 is described. It carries the Igh‐la allele, but shows the serological characteristics of C57BL/6 when analyzed for idiotype expression with respect to the antigens dextran and (4‐hydroxy‐5‐iodo‐3‐nitrophenyl)acetyl (NIP). We analyzed liver DNA from one animal for restriction fragment length polymorphism by hybridization to probes detecting members of nine VH gene families and DH segments, and compared it to DNA from animals carrying the nonrecombinant haplotypes Igh2 and Ighb, respectively. The breakpoint of recombination maps to the region carrying members of VH gene families VGAM3.8, PC7183 and Q52. The CB8KN strain which according to the serological analysis carries a recombinant Igh locus (Igh‐Va‐Cb) on BALB/c background was also analyzed. In this strain the breakpoint of recombination again maps to the region carrying members of VH gene families VGAM3.8, PC7183 and Q52. Our results show that the VH genes of families PC7183 and Q52 are interspersed and map to the region next to the DH locus. At least one gene from the VGAM3.8 family also maps to this region in the Igha and the Ighb haplotype.
Increased bactericidal macrophage activity induced by immunological stimuli is dependent on interferon (IFN)‐Γ
Authors: Leist Thomas P. , Heuchel Rainer , Zinkernagel Rolf M. 
Published: March 2007

AbstractDuring generalized immune responses such as the acute phase of graft‐vs.‐host reaction (GvHR) or many systemic viral infections the macrophage‐monocyte system of mice is activated as demonstrated by their increased bactericidal capacity against Listeria monocytogenes. To study the effect of interferon (IFN)‐γ in maintainance of macrophage activity, lymphocytic choriomeningitis virus (LCMV) primed C57BW6 mice or (C57BL/10 × B10.BR) F1 mice undergoing a GvHR were treated with polyclonal specific sheep anti‐IFN‐γ antiserum. In both cases injection of anti‐IFN‐γ resulted in inhibition of the stimulatory effects on macrophages as detected by reduced bactericidal activity when compared to mice treated with normal serum. Treatment with a polyclonal sheep anti‐IFN‐α, β antiserum on the other hand did not interfere with the activation status of the macrophages. The findings suggest that IFN‐α is produced both early in a GvHR and during the acute phase of an systemic infection with LCMV, and that it is involved in in vivo modulation of the increased activity of mononuclear phagocytes in immunologically stimulated mice.
Infection of B lymphocytes by the human immunodeficiency virus and their susceptibility to cytotoxic cells
Authors: Malkovsk Miroslav , Philpott Karen , Dalgleish Angus G. , Mellor Andy L. , Patterson Steve , Webste A. David B. , Edwards Andrew J. , Maddon Paul J. 
Published: March 2007

AbstractThe T4 molecule (CD4) is an important component of the human immunodeficiency virus (HIV) receptor. As yet, no other component has been demonstrated. We report here that two cell lines, a B lymphoblastoid cell line (Gupta) and a glial cell line (HEB) derived from human embryonal brain tissue, are productively infectable with two distinct isolates of HIV as judged by electron microscopy and immunological and virological studies. These two cell lines do not display detectable surface CD4 glyco‐protein. However, using S1 nuclease analysis, we have found that both cell lines do express low levels of CD4 mRNA. Neither of them produced syncytia formation upon HIV infection, a recognized feature of HIV‐infected cells strongly expressing the CD4 glycoprotein. It is conceivable that the CD4 mRNA is translated, resulting in meager surface expression of CD4 molecules undetectable by conventional techniques. Therefore, infection with HIV may be one of the most sensitive methods of demonstrating low levels of CD4 expression by human cells. Furthermore, HIV‐infected Gupta cells have here been shown to be more susceptible to the lytic activity of natural killer (NK) cells than their uninfected counterparts. These phenomena may be important for pathogenesis of HIV‐associated disorders.
Thymocyte clones from 14‐day mouse embryos II. Transcription of T3γ gene may precede rearrangement of TcRδ and expression of T3δ, T3ε and T11 genes
Authors: Pelkonen Jukka , Tunnacliffe Alan , Palacios Ronald 
Published: March 2007

AbstractWe have studied the state of TcRδ gene and the expression of T3δ, T3ε, T3γ and T11 (CD2) genes in the fetal thymocyte (FT) clones A2, G15, H5, E10, D5, H12, F1 and D11 obtained from a 14‐day B10.BR mouse fetal thymus. The eight FT clones contain the TcRδ gene in the germ‐line configuration as determined by Southern blot analysis. With the exception of clones E10 and D5, the other six FT clones express normal sized transcripts for T3δ gene and none of the eight FT clones produced detectable RNA transcripts for T3δ, T3ε and T11 genes as assessed by Northern blot analysis. Together with our previous work showing that all eight FT clones contain the TcRδ and the TcRβ gene clusters in the germ‐line configuration, the data indicate that the FT clones represent the earliest stage of T cell development identified within the thymus. Our results provide evidence that (a) the T3γ gene is the first of the genes that encode components of a TcR/T3 complex to be expressed in ontogeny within the thymus; (b) the T3 (δ, E, γ) genes are switched on asynchronously and their expression must be differentially regulated, and (c) the T11 gene product may not be involved in early stages of T cell development within the thymus.
Interferon‐alpha can synergize with interleukin 2 for human in vitro antibody response
Authors: Delfraissy Jean‐Fragois , Wallon Christine , Galanaud Pierre 
Published: March 2007

AbstractWe tested the effect of interferon (IFN)‐α on the specific anti‐2,4,6‐trinitrophenyl (TNP) response induced by TNP‐conjugated polyacrylamide beads in cultures of purified human B cells. IFN‐α alone had no effect. Interleukin 2 (IL2) alone had a restorative effect which could be considerably (10 x) enhanced by IFN‐α. This reflected a true synergy most apparent with IL 2 concentrations of 10 U/ml and IFN‐α concentrations of 103‐105 U/ml. The highest concentrations of IFN‐α were not inhibitory. In contrast, IFN‐α did not enhance the effect of an IL2‐free T cell‐derived supernatant able to support the B cell differentiation. Sequential incubations showed that IFN‐α acted earlier than IL2 on B cell response. The effect of IFN‐α was dependent on an efficient interaction between IL2 and its receptor which could be inhibited by a monoclonal antibody toward the CD25 antigen. Thus, IFN‐α can positively interact with a well defined interleukin, IL2, at a pre or post receptor level to potentiate antibody response.
Evidence that protein kinase C differentially regulates the human T lymphocyte CD2 and CD3 surface antigens
Authors: Cantrell Doreen A. , Verbi Winston , Davies Adelina , Parke Peter , Crumpton Michael J. 
Published: March 2007

AbstractThe purpose of the present study was to explore the effects of protein kinase C (PKC) stimulation on two cell surface receptors that regulate T cell growth: the T cell antigen receptor/CD3 complex and the CD2 antigen. The data show that PKC differentially regulates the expression and functions of CD2 and CD3 molecules. Thus, activation of PKC induced a decrease in cell surface levels of CD3 molecules but an increase in the expression of CD2 antigens. Additionally, prolonged stimulation of PKC inhibited subsequent T cell activation via CD3 but promoted activation via CD2 molecules. These results suggest that the CD2 cellular activation pathway would be preferred in T cells which have been exposed to stimulators of PKC. The molecular basis for the regulatory effects of PKC on CD3 and CD2 molecules and its physiological significance are discussed.
The preferential accumulation of helper‐inducer T lymphocytes in inflammatory lesions: evidence for regulation by selective endothelial and homotypic adhesion
Authors: Pitzalis Costantino , Kingsley Gabrielle , Haskard Dorian , Panayi Gabriel 
Published: March 2007

AbstractThe mechanisms which lead to the accumulation of T lymphocytes into inflammatory lesions are not clearly understood. We have previously shown that synovial CD4 T lymphocytes are mostly CDw29UCHL1 (helper‐inducer cells) and very few carry the CD45R antigen which identifies the suppressor‐inducer subset. Synovial CD8 cells are also CDw29UCHL1CD45R−. In the present study, lymphocytes from pleural and peritoneal inflammatory infiltrates were shown to have a similar phenotypic pattern. Furthermore, it was demonstrated that the CDw29UCHL1 subset had a greater ability than CD45R cells to adhere to endothelial cells and to form homotypic clusters. Differential surface expression of LFA‐1 on the two subsets was also shown, but this could not account for the demonstrated adhesion differences. Differences in adhesion between CDw29/UCHL1 and CD45R cells may explain the preferential accumulation of CDw29/UCHL1 cells in inflammatory infiltrates and underlie some of the functional differences between cells taken from sites of chronic inflammation and those from peripheral blood.
Maturation of the delayed‐type hypersensitivity response in SJL mice: absence of effector cell induction
Authors: Matsushima Glenn K. , Stohlman Stephen A. 
Published: March 2007

AbstractImmunization of young adult SJL mice (6 weeks of age) with a wide variety of particulate and soluble antigens does not elicit a delayed‐type hypersensitivity (DTH) response. Young adult SJL lack a DTM response through 8 weeks of age but attain the mature adult level of responsiveness at 10 weeks of age. Nylon wool‐enriched TDTH effectors and an antigen‐specific T cell clone both elicited DTH responses when transferred into 6‐week‐old SJL. Thus, the cascade of events at the local site appears to be functionally intact in 6‐week‐old SJL. However, T cells from immunized 6‐week‐old SJL fail to transfer DTH responsiveness to naive 6‐week‐old SJL recipients unless macrophages from 12‐week‐old SJL supplemented the immunization. Thus, the unresponsiveness of 6‐week‐old SJL appears to be due to a lack of induction of TDTH effectors. In addition, SJL mice immunized at 6 weeks of age and challenged with antigen at the DTH responsive age of 12 weeks did not mount a DTH response. Immunized 6‐week‐old SJL, supplemented with macrophages from 12‐week‐old SJL, and 1Zweek‐old SJL did respond to a second antigenic challenge when held for an equivalent 6‐week period. Thus, 6‐week‐old SJL fail to induce Tom effectors and to generate memory TDTH cells. Finally, antigen‐pulsed macrophages from 12‐week‐old SJL transferred DTH responsiveness into naive 6‐week and 12‐week‐old SJL recipients, while antigen‐pulsed cells from 6‐week donors were unable to transfer DTH responsiveness. These data indicate that the maturational deficit in the DTH responsiveness of 6‐week‐old SJL resides in the inability of macrophages to induce TDTH effectors.
B cell memory to thymus‐independent antigens type 1 and type 2: the role of lipopolysaccharide in B memory induction
Authors: Zhang Jun , Liu Yong‐Jun , Maclennan Ian C. M. , Gray David , Lane Peter J. L. 
Published: March 2007

AbstractSeveral studies have indicated that thymus‐independent (TI) antigens, unlike their thymus‐dependent (TD) counterparts, are poor at generating memory antibody responses (Immunol. Today 1981.3: 217). In contrast to this view, the present report shows that the TI type 1 (TI‐1) antigen, 2,4,6‐trinitrophenyl‐lipopolysaccharide (TNP‐LPS), elicits good secondary responses in rats. These secondary antibody responses are not only greater in magnitude than the primary responses, but display a different pattern of Ig classes with more IgG and IgA antibodies produced. In transfer experiments between congenic strains of rats which differ in their kappa light chain Ig allotype, it is shown that this memory is attributable to persistent B cell clones. The TI‐2 antigen, 2,4‐dinitrophenyl‐hydroxyethyl starch (DNP‐HES), given alone did not elicit B cell memory. However, when DNP‐HES is presented to the immune system in association with LPS, the pattern of the anti‐DNP response is similar to that elicited by TNP‐LPS.The capacity to generate TI memory is associated with the appearance of hapten‐specific B cells in the marginal zones of the spleen. Hapten‐binding cells were induced in the marginal zones following immunization with TNP‐LPS, but not by DNP‐HES. However, concurrent immunization with DNP‐HES and LPS which were not covalently linked was found to induce DNP‐binding cells in the marginal zone. There is complete correlation between the appearance of hapten‐binding memory B cells in the marginal zone and the capacity of these antigens to induce secondary responses.
Long‐lasting thymus‐independent immune responses to anti‐idiotype lipopolysaccharide conjugates require continuous B cell renewal
Authors: Burlen Odile , Coutinho António , Freitas Antonio A. 
Published: March 2007

AbstractIn the present investigation, we have studied the antibody response of both C57BLJ6 lipopolysaccharide‐responder mice (B6 LPS‐R) and C57BLAOScCr LPS‐nonrespon‐der mice (B10.Cr LPS‐NR) upon immunization with copolymers of LPS and either Ac38 or Ac46 anti‐idiotypes. As both strains of mice studied are of the Ighb allotype the antibody response obtained was quantified by estimating the serum levels of the complementary idiotype, B1–8, in immunized mice. The results show that while the injection of the LPS‐R strain B6 with copolymers of LPS anti‐idiotype resulted in a long‐lasting idiotype response the immunization of the LPS‐NR strain, B10.Cr, resulted in virtually no response. This finding allowed us to perform cell transfer experiments to study the response of isolated cells from B6 mice transferred into LPS‐NR hosts. Using such a cell transfer model, the results obtained suggest that long‐lasting idiotype responses observed in the LPS‐R strain require continuous B cell production in bone marrow. The relevance of this finding to the understanding of the long‐lasting (fluctuating) antibody responses to nondegradable thymus‐independent polysaccharides is discussed.
Phenotypic characteristics of cells involved in induced suppression to murine experimental autoimmune thyroiditis
Authors: Parish Nicole M. , Roitt Ivan M. , Cooke Anne 
Published: March 2007

AbstractSuppression of induced experimental autoimmune thyroiditis can be consistently transferred with spleen cells to syngeneic recipients, provided they are first treated with 200 rads irradiation. Treatment with anti‐Thy‐1 in vivo immediately prior to transfer abrogates the suppression, while depleting B cells has no effect.The in siru induced tolerance can be prevented by treatment with monoclonal antibodies to the Ly‐1 or L3T4 molecules either prior to or post tolerization. Anti‐Ly‐2 treatment has no effect. In the transfer, again treatment of donors with anti‐L3T4 prior to transfer prevents the demonstration of suppression in the recipients, while anti‐Ly‐2 does not affect suppression. These data suggest that the suppression is being mediated either by a CD4− T suppressor cell or a CD4 suppressor inducer cell. Preliminary experiments do not support the possiblity of a CD8 suppressor cell being activated in the recipient.