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PubMedDate not supplied

Expression of proliferation and differentiation antigens in response to modulation of membrane fluidity in chronic lymphocytic leukemia lymphocytes.

Isolated lymphocytes from patients with chronic lymphocytic leukemia (CLL) and from healthy controls were investigated for cell membrane fluidity and lipid phase separation. Expression of surface immunoglobulins, OKB7 and HLA-DR antigen, transferrin and interleukin-2 receptor was determined in relation to modulation of membrane lipid composition in each individual case. Structural and functional changes of membrane lipids and impaired lipid-protein interactions could be demonstrated in CLL lymphocytes. However, there is no simple correlation of membrane fluidity and receptor expression. This interaction poses a complex physicochemical problem, which must consider the original structural and functional state of the lipid bilayer. Disturded lipid-protein interactions are discussed in terms of defective transmembrane signalling and cell-cell interaction, allowing uncoupling of the leukemic cell from the network of growth and differentiation factors.

Antigens, Differentiation↗
PubMed1989

Transient modulation of Schwann cell antigens after peripheral nerve transection and subsequent regeneration.

Schwann cells within the distal portion of a transected nerve undergo a series of poorly understood events in response to injury and loss of axonal contact. These events may influence the regeneration of PNS neurons. In this study we examined the alteration of antigens located in the basal lamina, plasma membrane and cytoplasm of Schwann cells within the distal nerve stump: (a) after a complete transection of the sciatic nerve, and (b) subsequent to reestablished contact between regenerating axons and dedifferentated Schwann cells separated from contact with neurons. Visualization of laminin and heparan sulphate proteoglycan molecules at various intervals after nerve transection always revealed intact basal lamina channels. In response to loss of axonal contact, vimentin expression by Schwann cells within the distal nerve stump increased, becoming a predominant intermediate filament protein of the cytoskeleton while glial fibrillary acid protein (GFAP) expression decreased. This reversal in the prominence of intermediate filament protein was maintained until the onset of axonal reinnervation, at which point expression of GFAP increased and vimentin decreased. Expression of the Schwann cell plasma membrane associated protein, C4, closely mimicked GFAP expression during axon degeneration and subsequent reinnervation. In the normal uninjured nerve, tissue plasminogen activator (tPA) and S-100 were localized in the region near the Schwann cell-axon interface and the outer Schwann cell plasma membrane. In response to loss of axonal contact, the S-100 and tPA immunoreactivity associated with the Schwann cell-axon interface was lost while that localized around the outer Schwann cell plasma membrane remained unchanged. The results of this study demonstrate that Schwann cells modulate a portion of their antigenic repertoire in response to a loss of axonal contact and after contact with regenerating axons.

Animals↗
PubMed1997

T-cell antigen receptor transmembrane peptides modulate T-cell function and T cell-mediated disease.

This study describes a novel method of inhibiting T-cell function by the use of peptides rationally designed from the T-cell antigen receptor (TCR) alpha-chain transmembrane sequence involved with TCR receptor assembly. The most effective peptide (core peptide, CP) modulating in vitro and in vivo T-cell function contained nine amino acids two of which, lysine and arginine, were hydrophilic and separated by four hydrophobic amino acids. CP without chemical modification or conjugation was able to enter non-T and T cells. Conjugation of CP at the carboxyl terminus with palmitic acid resulted in a greater inhibition of T-cell interleukin-2 (IL-2) production in vitro than peptide alone. When examined for effects in vivo, CP reduced clinical signs of inflammation in three T cell-mediated disease models including adjuvant-induced arthritis, experimental allergic neuritis, and cyclophosphamide-induced diabetes in NOD/Lt(F) mice. This peptide or its analogues has potential as a therapeutic agent in human inflammatory and autoimmune disorders.

Amino Acid Sequence↗
PubMed1987

Functional and phenotypical characterization of activated T cells from intra-articular sites in inflammatory joint diseases. Possible modulation of the CD3 antigen.

The presence of activated T lymphocytes bearing interleukin 2 (IL-2) receptors and HLA class II (Ia) antigens accompanied by impaired T cell functions such as a decreased mitogenic responsiveness are characteristic findings, especially in intra-articular sites in chronic inflammatory joint diseases. The objective of the present study was to further characterize these in vivo activated T cells by the investigation of IL-2 production and a possible T cell receptor modulation. IL-2 receptors were found to be expressed primarily in the CD4+ subset. The Ia+ subset expressing both DR and DQ antigens showed a weaker mitogen-induced response as compared to the Ia- fraction. A decreased mitogen-induced IL-2 production and a lower response to anti-CD3 monoclonal antibodies was observed with synovial T lymphocytes as compared to peripheral blood T cells. The density of the CD3 molecule, known to be closely associated with the T cell receptor, was significantly lower in intra-articular sites, while other T cell-specific surface molecules were expressed to a similar extent in both compartments. The decreased synovial T cell mitogenesis was not restored by the addition of lymphokines (IL-1 and IL-2) or blood monocytes, nor by removing CD8+ T cells. These data present further evidence for a significant T cell activation in intra-articular sites in chronic inflammatory joint diseases. The decreased expression of the CD3 glycoprotein suggests a modulation by so far unidentified antigen(s), which could also be responsible for the weak T cell response elicited by polyclonal mitogens.

Antibodies, Monoclonal↗
PubMed1999

Identification of a cycle-modulated 200-kDa endometrial antigen by a monoclonal antibody LDS60.

We have developed a mouse monoclonal antibody, LDS60, against a cycle-dependent antigen by immunising (MF1 x BALB/c)F1 mice with a human endometrial membrane preparation. In formalin fixed paraffin embedded sections, LDS60 identified an epithelial specific antigen which exhibited a specific pattern of expression during the menstrual cycle. It was only occasionally expressed during the proliferative phase. During the early-secretory phase, there was intracytoplasmic staining in about half of the glands examined. This was in the form of small microvesicles, either near the base of the cell or supranuclear. In the mid-secretory phase the same proportion of glands exhibited staining in the form of micro-vesicles that were noted to accumulate nearer to the cell apices. In the late-secretory phase, there was no intracytoplasmic staining and the antigen was localised to the luminal border of the glandular epithelium and some staining appeared within the gland lumen of approximately 20% of glands. It is also diffusely expressed in some mucous secreting cells in the tongue, stomach and colon, as well as lung pneumocytes. The antigen has a molecular weight of approximately 200 kDa as identified by immunoblotting. This antigen exhibits similarities to MUC-1 which is involved in uterine receptivity and could therefore have a similar role. Its cycle modulation suggests that it could be used to monitor the uterine response to steroids.

Animals↗
PubMed2006

Expansion of mesenchymal stem cells isolated from pediatric and adult donor bone marrow.

The enormous plasticity of mesenchymal stem cells (MSCs) suggests an improvement of a standard protocol of isolation and ex vivo expansion for experimental and clinical use. We isolated and expanded MSCs from bone marrow (BM) of pediatric and young adult donors, to analyze the growth kinetic, immunophenotype, telomere length, karyotype during ex vivo expansion. Seventeen BM samples were collected from young adult donors and 8 from pediatric donors. MSCs isolated from two groups showed no morphological differences while their cell growth was strictly related to the donor's age. The MSCs isolated from pediatric donors reached a cumulative PD almost twice as high as MSCs isolated from young adult donors after 112 days (10.2 +/- 1.9 versus 5.5 +/- 3.7). Furthermore, we analyzed the modulation of antigen expression in the MSCs isolated from two groups until 10th passage (77 days) and there was no significant difference between the modulation of antigen expression. In particular, at the first passage, MSCs showed a low contamination of hemopoietic cells which became insignificant in the following passages. There was a high expression of CD90, CD29, CD44 and CD105 and variable and moderate expression of CD166 and CD106 at the start of MSC culture and at each passage during expansion. No chromosomal alteration or evidence of cellular senescence were observed in all analyzed samples. All these data suggest that MSCs can be isolated and expanded from most healthy donors, providing for an autologous source of stem cells.

Adult↗
PubMed2002

Rap1 functions as a key regulator of T-cell and antigen-presenting cell interactions and modulates T-cell responses.

Activation of T cells by antigen requires adhesive interactions with antigen-presenting cells (APC) in which leukocyte function-associated antigen 1 (LFA-1) and intercellular adhesion molecules (ICAMs) are important. However, it is not well understood what signaling molecules regulate this process and how the modulation of adhesive events influences T-cell activation. Here we show that Rap1 is activated in T cells in an antigen-dependent manner and accumulated at the contact site of T-cell and antigen-loaded APC. Inhibition of Rap1 activation by a dominant-negative Rap1 or SPA-1, a Rap1 GTPase-activating protein, abrogates LFA-1-ICAM-1-mediated adhesive interactions with antigen-pulsed APC and the subsequent T-cell-receptor triggering and interleukin-2 production. Conversely, augmented antigen-dependent Rap1 activation by the expression of wild-type Rap1 enhances these responses but culminates in apoptosis by Fas and FasL. Thus, Rap1 functions as a key regulator of T-cell and APC interactions and modulates T-cell responses from productive activation to activation-induced cell death by regulating the strength of adhesive interactions. Moreover, constitutive Rap1 activation rendered T cells unresponsive with accumulation of p27(Kip1). Our study indicates that the activation state of Rap1 has a decisive effect on the T-cell response to antigen.

Antigen-Presenting Cells↗
PubMed1975

Modulation of HL-A antigens by anti-HLA antiserum: effects on the cytotoxicity assay and mixed leukocyte reaction.

Modulation of human leukocyte antigen (HLA) was attempted by treating leukocytes with specific anti-HLA antiserum or by their passage through columns coated with anti-HLA or a double layer of HLA-anti-HLA. The modulated cells were resistant to the cytotoxic effects of the anti-HLA, and they were poor stimulators and good responders to allogeneic cells in the unidirectional mixed leukocyte reaction. Modulated cells regained their HLA 16 hr after modulation if kept in cell suspension alone. The proliferative responses of modulated cells to mitogens were as good as non-modulated cells, indicating that modulation was probably not caused by depletion of lymphoid cells. Supernatants of modulated cells that were incubated overnight or preformed HLA-anti-HLA complexes were capable of suppressing and enhancing the MLR of specific cells depending on the dose used. The similarities of modulation of HLA to other lymphocyte receptors and the limitation of application of the modulation phenomenon to transplantation of allogeneic cells are discussed.

Antibody Specificity↗
PubMed1991

Differential modulation of leucocyte surface antigens by various inducers on the T-cell line MOLT-4.

Pretreatment of MOLT-4 T-cell line with 12-0-tetradecanoylphorbol 13-acetate (TPA) potentiated the interferon alpha-induced cell surface expression of class I HLA. Simultaneous combined action of TPA and rIFN-alpha resulted in a synergistic effect upon the up-regulation of class I HLA. Neither TPA nor rIFN modulated the cell surface expression of HLA class II (DR and DP) antigens. Leucocyte common antigen (CD45) cell surface expression was quantitatively increased on MOLT-4 cells by TPA induction, unaltered by rIFN and up-regulated by combined action of TPA and rIFN. CD8 antigen was down-regulated by both TPA and rIFN.

Antigens, CD↗
PubMed1989

Co-cross-linking of surface immunoglobulin Fc gamma receptors on B lymphocytes uncouples the antigen receptors from their associated G protein.

Cross-linking of surface Ig receptors (sIg) by mitogenic forms of anti-Ig antibodies (e.g. F(ab')2 fragments of rabbit anti-Ig) causes the rapid, and prolonged breakdown of phosphatidylinositol 4,5-bisphosphate. This response involves an unidentified guanine nucleotide regulatory protein (termed Gp), which couples sIg to the polyphosphoinositide-specific phosphodiesterase. Intact (IgG) rabbit anti-Ig antibodies, which co-cross-link sIg and Fc gamma receptors on B cells, only induce short-lived inositol phospholipid breakdown and abortive B cell activation. We show here that in permeabilized B cells intact anti-Ig inhibits the reconstituted breakdown of inositol phospholipids given by a combination of F(ab')2 anti-Ig and the non-hydrolyzable GTP analogue guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S), but not the basal stimulation of Gp induced by GTP gamma S alone. These results therefore indicate that co-cross-linkage of sIg and Fc gamma receptors on B cells uncouples the antigen receptors from the associated G protein, but does not affect coupling between Gp and the phosphodiesterase. These observations therefore provide further insight into the mechanisms whereby engaging Fc receptors on B cells, by antigen-antibody complexes for example, could modulate antigen-induced B cell activation.

Animals↗
PubMed2005

Rhesus macaques with high levels of vaccine induced IFN-gamma producing cells better control viral set-point following challenge with SIV239.

HIV-1 specific cellular immune responses play a significant part in controlling HIV-1 viral replication and are an important component of an HIV-1 vaccine induced immune response. We reported earlier that recombinant DNA vaccine delivered intramuscularly, and recombinant Listeria monocytogenes, delivered orally induced CD8+ and CD4+ T cell immune responses in rhesus macaques and that this vaccine protocol showed partial protection against an SIV239 challenge. In this paper, we have analyzed the SIV antigen-specific immune responses at the time of challenge and during the subsequent infection course. We find that the immune status of the animals, as measured by the frequency of antigen-specific IFN-gamma secreting peripheral blood mononuclear cells, at the time of challenge correlates more strongly with viral loads at set point than peak viral loads. The correlation between the immune response and viral load was strongest early, as viral set-point was just being established and disintegrates overtime. This study demonstrates the cellular immune response to SIV at the time of challenge of a nonhuman primate is able to impact on viral set-point following SIV239 challenge. Further, this study demonstrates that as virus replicates the T cell immune response to SIV antigens induced by the vaccine is modulated by antigen encountered by immune cells during viral replication.

Animals↗
PubMed1995

Marked prolongation of incompatible class I deficient heart allografts: paradoxical effects between primarily and secondarily vascularized allografts.

These studies argue strongly against the widespread use of skin grafts for rejection testing. Primarily vascularized grafts of a clinically grafted organ would seem to be much more relevant to future studies. These results suggest that the elimination of either class I or class II antigens in grafts or techniques to modulate these antigens or reduce the degree of incompatibility of these antigens by tissue typing should be actively pursued for solid organ grafting in the future.

Animals↗
PubMed1995

Internalization of human macrophage surface antigens induced by monoclonal antibodies.

Drugs intended to be endocytosed by macrophages may be transported by MAbs directed against these cells. Twenty MAbs were investigated for this purpose. The binding of these MAbs to macrophages obtained from a 7 day culture of blood monocytes showed that anti-CD11b and anti-CD14 recognized the highest number of cell surface antigen sites. Further assays determined that anti-CD63, Mo5 and anti-CD33 were the MAbs that induced the strongest modulation of the corresponding antigens, the highest rate being with anti-CD63. Endocytosis of antigen-antibody complexes was evidenced by the presence of MAbs in the cytoplasm. Anti-CD63 MAbs induced the highest internalization in this assay. For most MAbs, however, the density of antigen sites and the intensity of antigen modulation were not predictive of the amount of MAb detected in the cytoplasm.

Antibodies, Monoclonal↗
PubMed2000

Modulation of human leukocyte antigen and intracellular adhesion molecule-1 surface expression in malignant and nonmalignant human thyroid cells by cytokines in the context of extracellular matrix.

Interactions between malignant cells and their environment are achieved via cell-surface receptors and adhesion molecules. The extracellular matrix (ECM) and ECM-bound cytokines modulate the expression of cell-surface molecules on target malignant cells, which may lead to changes in their susceptibility to cytolysis, in their ability to present antigens, and in the induction of local immune-cell activation and patrol. Eventually, these alterations may culminate in either the destruction, or escape and proliferation, of the tumor. We studied the effects of the ECM and its components in a "naive" form or following binding of the inflammatory cytokines interferon gamma (IFNgamma) and tumor necrosis factor alpha (TNFalpha) on the surface expression of human leukocyte antigen (HLA) class-I, HLA class-II (HLA-DR), and intracellular adhesion molecule-1 (ICAM-1), on nonmalignant and malignant thyroid cells. The basal expression of HLA class-I molecules was not significantly changed either by naive ECM and its components or by ECM-bound cytokines. ECM synergized with IFNgamma and TNFalpha in inducing HLA-DR molecules on nonmalignant and malignant thyrocytes, with higher HLA-DR levels on the malignant cells. The laminin component, in particular, synergized with IFNgamma. Basal ICAM-1 expression on nonneoplastic cells was not significantly affected by the cytokines when grown in the absence of ECM, but was significantly upregulated when cells were cultured on ECM. In contrast, in malignant thyrocyte cultures, ECM significantly attenuated IFNgamma- and TNFalpha-mediated enhancement of ICAM-1 expression. We concluded that signals derived from ECM-embedded cytokines participate in the regulation of key thyroid cell surface molecules and, thus, may affect the final outcome of human thyroid malignancies.

Animals↗
PubMed1987

Modulation of class-II antigen expression in human thyroid epithelial cell cultures.

The modulation of HLA-D expression of thyroid epithelial cells (TEC) was studied in vitro by means of immunofluorescence. Under serum-free culture conditions, TSH and TSH-receptor antibodies induce HLA-D on TECs derived from GD-patients. Serum-free culture conditions provide a higher availability of TSH-receptors by a 'right side right' polarity of the cellular morphology. There was no evidence for IFN-gamma producing cell contaminations on GD-TECs. TSH in contrast to IFN-gamma does not induce HLA-DQ on TECs. HLA-DQ is not displayed by spontaneously class-II antigen expressing GD-TECs. Methimazole as well as perchlorate do not suppress HLA-D expression of TECs.

Cells, Cultured↗
PubMed1987

Modulation of CD4 by antigenic activation.

Cell surface expression of CD4, an invariant membrane glycoprotein, is characteristic of the MHC class II-restricted T cell helper/inducer subset. Although the specificity and restriction patterns of T lymphocytes are determined by the T cell receptor for antigen, CD4 might represent an additional "interaction" molecule that is required to strengthen the interaction between T cells, antigen, and antigen-presenting cells. In this manuscript, we have shown that the cell surface expression of CD4 is correlated with activation of T cells. Data presented in this paper have demonstrated, for the first time, that antigenic stimulation of human T cell clones caused a decrease in the expression of the CD4 marker (as well as to the CD3 marker) to about 50% of the constitutive level. As previously demonstrated, PMA caused modulation of CD4 and CD3, which suggested that phosphorylation by protein kinase C played a crucial role in the regulation of the expression of both markers. The parallel down-regulation of CD3 and CD4 after antigen stimulation suggested that both markers might be members of a multimolecular complex mediating T cell activation.

Antigens, Differentiation, T-Lymphocyte↗
PubMed2000

My4+/LeuM3- molecule and CD19 antigen are down-modulate by low affinity Fc gamma receptor II (CD32) stimulation on CD56-positive B-lymphoma cells.

My4+/LeuM3- molecule is recognized by My4, but not by LeuM3, both well known mAbs to CD14. In a previous study we showed that the My4+/LeuM3- molecule on a human monoblastic cell line, U937, is not CD14, but another cell surface antigen. The roles and functions of the My4+/LeuM3- molecule remained unknown. We now report that specific stimulation of Fc gammaR with aggregated IgG or anti-Fc gammaRII antibody down-modulated the My4+/LeuM3- molecules, as well as CD19, in a case of CD56-positive B cell lymphoma. Stimulation of Fc gammaR with anti-mu antibody, which induced concomitant stimulation of sIg, did not induce down-modulation of either molecule. Stimulation of CR2 (CD21), a protein which is functionally or physically associated with CD19, with anti-CR2 (CD21) mAbs also had no effect. The modulation occurred specifically on CD56-positive B-lymphoma cells, since My4+/LeuM3(-)-positive, CD56-negative B-lymphoma cells did not respond to the stimulation. These results suggest that CD19 and My4+/LeuM3- molecules are functionally or physically associated with Fc gammaR II on CD56 positive B-lymphoma cells defined as being at a terminal B cell differentiation stage.

Antibodies, Monoclonal↗