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Results for “Leukocyte L1 Antigen Complex”

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At least 19 recordsLinked to original sources
PubMed1992

Expression and function of the neural cell adhesion molecule L1 in mouse leukocytes.

The neural cell adhesion molecule L1 is a cell surface glycoprotein of the immunoglobulin superfamily which mediates adhesion between neural cells. The possibility that similar cell-cell recognition mechanisms may be shared by the nervous and immune systems prompted us to study the expression and function of L1 in cells of the hematopoietic system. Immunofluorescence analysis using monoclonal L1 antibody revealed that the molecule is expressed in the bone marrow, spleen, and thymus of the mouse. This observation was confirmed by amplifying cDNA derived from these organs by the polymerase chain reaction with L1-specific oligonucleotide primers. Two-color fluorescence analysis indicated that bone marrow lymphoid and granulocyte precursor cells express low and high levels of L1, respectively. In the thymus L1 is primarily expressed by mature cells that have a strong expression of CD3 and in the spleen both B cells and T cells express L1. The possible function of L1 in lymphoid cells was studied using subcloned ESb-MP lymphoma cells having high or low densities of L1 on the cell surface as well as activated splenic B lymphoblasts. Parental and subcloned ESb-MP cells that strongly expressed L1 could form homotypic aggregates in the presence of low Ca2+ levels, whereas subcloned ESb-MP cells with a weak expression of L1 did not aggregate, suggesting that L1 mediates the Ca(2+)-independent aggregation of the parental ESb-MP cells. Furthermore, the aggregation of activated B lymphoblasts under physiological concentrations of Ca2+ and Mg2+ was inhibited by 30% in the presence of Fab fragments of polyclonal L1 antibodies, implying that L1 also mediates adhesion among normal lymphoid cells. A possible role of L1 on lymphocytes in stimulating the innervation of lymphoid organs is discussed.

Animals↗
PubMed1993

L1 adhesion molecule on mouse leukocytes: regulation and involvement in endothelial cell binding.

L1 is a cell surface glycoprotein of the immunoglobulin superfamily which was initially shown to mediate adhesion between neural cells. Recently we have reported that L1 is expressed by bone marrow cells and the majority of mature lymphocytes (Kowitz et al., Eur. J. Immunol. 1992. 22: 1199-1205). To analyze the function of L1 on leukocytes we studied its regulation following cell activation. In vitro activation of B lymphocytes with lipopolysaccharide or T lymphocytes with phorbol 12-myristate 13-acetate/Ca2+ ionophore, concanavalin A or anti-CD3 monoclonal antibody as well as in vivo activation of V beta 8+ T cells with staphylococcal enterotoxin B (SEB) revealed a down-regulation of L1 within 48 h. A rapid loss of L1 expression was seen when mouse neutrophils were activated with PMA alone. This rapid loss paralleled the shedding of L-selectin. We also studied a possible role of L1 in the binding of leukocytes to endothelial cells. ESb-MP lymphoma cells with a high expression of L1 (L1hi) could bind to bend3 endothelioma cells without prior activation with inflammatory cytokines. The interaction was inhibited by anti-L1 antibodies. In contrast, ESb-MP cells with low L1 expression (L1lo) were only marginally bound. Latex beads coated with affinity-isolated L1 antigen were also able to bind to the endothelioma cells in a specific fashion. The binding of ESb-MP lymphoma cells required Ca2+ and Mg2+ ions and was sensitive to cold temperature. Since the endothelioma cells did not express L1 the binding mechanism studied here is distinct from the established L1-L1 homotypic interaction. It is possible that the novel L1-mediated adhesion pathway involves an unidentified ligand and could play a role in leukocyte migration.

Animals↗
PubMed1995

The leucocyte protein L1 (calprotectin): a putative nonspecific defence factor at epithelial surfaces.

The L1 protein occurs at high concentrations in neutrophils, monocytes, certain reactive tissue macrophages, squamous mucosal epithelia, and reactive epidermis. It constitutes in fact about 60% of the neutrophilic cytosol protein fraction. The two L1 chains (L1H and L1L) are referred to by a bewildering collection of names, various authors having different preferences (MRP-8 and MRP-14; CFA or calgranulin A and B). The most recent proposal is calprotectin because of its calcium-binding properties and antimicrobial effect shown in vitro. L1 belongs to the S-100 protein family and may be involved in the regulation of keratinocyte proliferation and differentiation. It exists at high levels in blood and interstitial tissue fluid in several infectious, inflammatory, and malignant disorders, and it is released abundantly in foci of granulocytes and macrophages. The C-terminal sequence of the L1H chain has been shown to be identical to the N-terminus of peptides known as neutrophil immobilizing factors. Such an activity of L1 could be important for the accumulation of vital granulocytes, while L1 released from neutrophils, macrophages and epithelial cells might exert antimicrobial activity, perhaps by depriving microorganisms of zinc. The minimum inhibitory concentrations of L1 in vitro were found to be 4-32 mg/l for Candida albicans, 64 mg/l for Staphylococcus aureus, 64-256 mg/l for S. epidermidis, and 256 mg/ml for Escherichia coli and Klebsiella spp. Killing was observed at 2-4 times higher concentrations. In patients with HIV infection, those who developed oral candidiasis had significantly lower parotid L1 levels than those who did not (67 micrograms/l vs. 216 micrograms/l).

AIDS-Related Opportunistic Infections↗
PubMed2001

Wound healing response in the presence of stromal irregularities after excimer laser treatment.

PURPOSE: To trace the fate of stromal irregularities after excimer laser treatment and to increase our knowledge of the reasons why surface irregularities in the ablation bed cause inferior postoperative results. METHODS: Twelve New Zealand White rabbits received a transepithelial photoablation to a preset depth of 60 microm. An electron microscopy specimen grid was then placed on the denuded stroma and another 20 microm ablation was applied in order to produce surface irregularities. Another six rabbits received a plano transepithelial photoablation to a preset depth of 80 microm. The treated corneas were harvested at various timepoints and differentially further processed for microradiography, hematoxylin-eosin -, hyaluronan (HA)- and leukocyte protein L1 staining. RESULTS: In the grid treated corneas the subepithelial mesh pattern is clearly discernible after 1 week, and after 4 weeks it is replaced by a subepithelial layer containing HA and water. The thinning of this layer between 1 and 12 weeks is statistically significant (p<0.05). After 4 and 8 week the plano treated corneas only exhibit some subepithelial HA- and water accumulation. After 1 day the grid treated corneas show an extensive stromal infiltration of leukocytes. In the plano treated corneas the leukocytes mainly remain on the surface. CONCLUSIONS: During the healing process stromal irregularities are flattened, leaving a homogeneous zone with increased water content. This subepithelial layer is rarefying as new subepithelial tissue is forming. Postablational irregularities induce a more pronounced healing reaction when compared to a smooth ablation surface. Leukocyte infiltration seems to play a role in this process.

Animals↗
PubMed1984

Plasma levels of the leucocyte L1 protein in febrile conditions: relation to aetiology, number of leucocytes in blood, blood sedimentation reaction and C-reactive protein.

Plasma levels of a novel leucocyte protein (L1) were determined in a series of 176 febrile patients and compared with CRP, BLC, and BSR. Among 82 patients with bacterial infection, 81 had L1 levels above the 0.95 interval. Levels of 40 to 130 times the normal mean were seen frequently during life-threatening infections like septicaemia, meningitis, or pneumonia. In contrast, 23 of 27 patients with viral infections had normal L1 levels. A poor correlation was found between L1 levels, CRP, BLC, and BSR, suggesting that these parameters reflect different aspects of the response to tissue damage and inflammation. L1 and CRP seem equal in distinguishing between bacterial and viral infections. Low or normal L1 levels argue strongly against a bacterial infection, while elevated L1 levels discriminate poorly between bacterial and non-infectious inflammatory or malignant diseases.

Adolescent↗
PubMed2000

[Host defense mechanisms against fungal infections].

Recent advances in the research on host defense mechanisms against infections with Candida and Aspergillus were reviewed. Modes of the defense mechanisms were divided into three phases by thedifferent physiological circumstances surrounding the fungi: 1, the exocrine fluid in which fungi exist on the mucosal membranes; 2, the tissues invaded by fungi with the circulating blood; and 3, the limited lesions where fungi continue to be alive with a restricted blood flow. In each defense mechanism, theroles of the endogenous antifungal substances such as lactoferrin, defensins and calprotectin and leukocytes were discussed.

Aspergillosis↗
PubMed2005

Fecal leukocyte proteins in inflammatory bowel disease and irritable bowel syndrome.

UNLABELLED: The aim of this prospective study was to compare five different leukocyte proteins in feces of patients with chronic inflammatory bowel disease (IBD), irritable bowel syndrome (IBS) and healthy persons who underwent prophylactic colonoscopy. METHODS: The leukocyte proteins calprotectin, lactoferrin, lysozyme, myeloperoxidase, and PMN-elastase were determined with immunoassays in fecal samples of three consecutive feces (e.g. three days) in 40 healthy persons, 39 patients with chronic IBD (of these 21 with Crohn's disease and 18 with ulcerative colitis), and 40 patients with IBS. RESULTS: ROC curves calculated for healthy persons and patients with IBD yielded the following areas under the curves (AUCs): PMN-elastase 0.916, calprotectin 0.872, myeloperoxidase 0.750, lysozyme 0.726, and lactoferrin 0.693. The AUCs of PMN-elastase and calprotectin were not significantly different (p = 0.327), whereas PMN-elastase or calprotectin vs. the other proteins were significantly different (p < 0.001). PMN-elastase and calprotectin correlated with the endoscopically classified severity of inflammation. All fecal leukocyte markers in IBS were found in the range of the healthy persons. Data on storage stability of leukocyte proteins in fecal supernatants are given. CONCLUSION: Fecal PMN-elastase and calprotectin support the differentiation of chronic IBD from IBS and correlate with the severity of inflammation.

Adult↗
PubMed1993

Calprotectin and complement activation during major operations with or without cardiopulmonary bypass.

Plasma concentrations of the granulocyte cell marker calprotectin were assessed during operation and 24 hours postoperatively in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass, abdominal aneurysmectomy with implantation of an aortic graft, or thoracotomy without implantation of synthetic material. The concentration of calprotectin increased significantly (p < 0.01) in all three groups. Ten of the 30 patients in the group undergoing cardiopulmonary bypass received methylprednisolone at the start of the operation. No difference in calprotectin concentration was seen between the two subgroups (p > 0.05). Plasma concentration of calprotectin was shown to increase rapidly in patients undergoing cardiopulmonary bypass and aneurysmectomy, in whom complement activation also took place. However, the calprotectin concentration increased slowly during the operation and the postoperative period in patients undergoing a thoracotomy, in whom complement was not activated. At wound closure the calprotectin concentration was significantly elevated in the cardiopulmonary bypass and aneurysmectomy groups compared with the thoracotomy group (p < 0.05). The calprotectin concentration remained elevated during the postoperative period in all three groups. Our results indicate that calprotectin may serve as a suitable cellular marker when the biocompatibility of artificial surfaces is studied.

Adult↗
PubMed1994

Reduced complement and granulocyte activation with heparin-coated cardiopulmonary bypass.

Plasma concentrations of the complement activation products C3b, iC3b, and C3c; the terminal C5b-9 complement complex; and the granulocyte proteins calprotectin, myeloperoxidase, and lactoferrin were assessed in two groups of patients undergoing aortocoronary bypass procedures. In 10 patients operated on, the bypass circuits were coated by the Carmeda Bio-Active Surface and systemic heparinization was reduced to 1.5 mg/kg; in another 10, the systems were uncoated and the dosage of systemic heparinization was 4 mg/kg. In both groups, significant complement activation was observed after the onset of cardiopulmonary bypass, but the maximum levels of C3b, iC3b, and C3c and the terminal C5b-9 complement complex were significantly lower in the heparin-coated group. In both groups, a significant increase in calprotectin, myeloperoxidase, and lactoferrin release was observed by the end of operation. The maximum myeloperoxidase levels were significantly lower in the heparin-coated group than those in the uncoated group (p = 0.03). There was a correlation of borderline significance between the formation of terminal C5b-9 complement complex and lactoferrin release, as well as between the formation of terminal C5b-9 complement complex and myeloperoxidase release (p = 0.05). The postoperative blood loss did not differ significantly between the two groups. We conclude that coating by end point-attached and functionally active heparin allows a significant reduction in the amount of systemic heparinization, and significantly reduces complement and granulocyte activation.

Aged↗
PubMed2000

The human neural cell adhesion molecule L1 functions as a costimulatory molecule in T cell activation.

L1 is a neural cell adhesion molecule (CAM) known to be important for normal neurological development. Despite being described as a neural CAM, we have documented L1 expression by antigen-presenting cells of myelomonocytic origin. Here we demonstrate that L1 can function as a costimulatory molecule in T cell activation. A monoclonal antibody that abrogates L1-L1 homophilic binding significantly reduced mixed leukocyte responses initiated by allogeneic L1+ dendritic cells. Autologous T cell activation in response to phytohemagglutinin was also inhibited by blockade of L1. In accordance with these results, transfection of human L1 into a murine myeloma cell line significantly increased the capacity of these cells to stimulate xenogeneic T cell responses. As a costimulatory ligand L1 could represent a novel target for immunotherapeutic intervention and may act as an important intermediary in neuroimmunological processes and disease.

Animals↗
PubMed1998

Expression of major histocompatibility complex class II antigen in neoplastic cells of canine cutaneous histiocytoma.

Forty five cases of canine cutaneous histiocytoma (CCH) were examined by immunohistology for expression and distribution of major histocompatibility complex (MHC) class II antigen in neoplastic cells. In addition, expression of lysozyme and calprotectin (leucocyte protein L1) in neoplastic cells was investigated. Furthermore, B and T lymphocytes were demonstrated by antibodies against the CD3 antigen, IgG, and IgM. Neoplastic cells showed two staining patterns for MHC class II antigen: focal juxtanuclear cytoplasmic staining and/or rim-like staining along the cell periphery. In 24 cases, a predominant or exclusive focal juxtanuclear cytoplasmic MHC class II antigen reaction in neoplastic cells, and the presence of few diffusely distributed infiltrating CD3 antigen-positive T lymphocytes were observed. Tumors with numerous neoplastic cells exhibiting staining for MHC class II antigen along the cell periphery (n = 21) showed increased inflammatory alterations, represented by disseminated and nodular infiltrations of mainly CD3 antigen-positive T cells. B cells, plasma cells, exudate macrophages, and neutrophils were rarely seen disseminated between neoplastic cells whereas their number increased within focal inflammatory infiltrates. The focal cytoplasmic reaction for MHC class II antigen in neoplastic cells might represent newly synthesized MHC class II molecules stored in vesicles, whereas staining of the cell periphery might occur due to accumulation of MHC class II molecules along the plasma membrane. The increasing expression of MHC class II molecules on the cell surface might be the decisive factor for onset and progression of tumor regression. However, the exact mechanism of priming and activation of T cells by neoplastic cells and the nature of the presented antigen are not yet known.

Animals↗
PubMed1991

Calprotectin in cerebrospinal fluid of the HIV infected: a diagnostic marker of opportunistic central nervous system infection?

The calprotectin level in the cerebrospinal fluid (CSF) of 15 HIV positive patients with symptoms from the central nervous system (CNS) was measured. All 5 patients with opportunistic infections had levels above the reference range and all 10 patients with HIV associated encephalopathy had levels within the reference range. Thus, the calprotectin level in CSF can be of diagnostic value in differentiating between HIV associated encephalopathy and opportunistic infection in the HIV positive patient with symptoms from the CNS.

AIDS Dementia Complex↗
PubMed1994

Roller and centrifugal pumps compared in vitro with regard to haemolysis, granulocyte and complement activation.

A Biomedicus centrifugal pump and a Polystan roller pump were compared in vitro with regard to differences in haemolysis, granulocyte and complement activation. Six circuits of tubing and oxygenators were connected to each pump. Heparinized fresh human blood was circulated for 72 hours in the systems. Blood samples were drawn at defined intervals. Haemolysis was assessed by determination of lactate dehydrogenase (LD) and potassium, and granulocyte activation by quantification of the granulocyte proteins calprotectin, lactoferrin and myeloperoxidase. Complement activation was assessed by measuring C3 activation products (C3b, iC3b and C3c), and the terminal C5b-9 complement complex (TCC). The results indicate more haemolysis and complement activation in the roller pump group, revealed by significantly higher concentrations of LD, potassium, C3 activation products and TCC. Calprotectin, lactoferrin and myeloperoxidase were all significantly increased in both groups, but the rise appeared earlier in the roller pump group. The concentrations of LD and potassium both correlated significantly with C3 activation products, indicating that complement activation may at least partly be responsible for the haemolysis.

Cell Adhesion Molecules, Neuronal↗
PubMed2004

Immunohistochemical localization of macrophage CD68+, HLA-DR+, L1+ and CD44+ subsets in uterine endometrium during different phases of menstrual cycle.

Different tissue macrophage subsets were immunohistochemically examined in normal endometrial samples collected from proliferative (n=4), peri-ovulatory (n=6) and secretory (n=8) phases of menstrual cycles in women. The different macrophage subsets, namely CD68 (pan macrophage marker), CD44 (transmembrane adhesion molecule), HLA-DR (transmembrane heterodimeric protein involved in antigen presentation) and L1 (calprotectin)-positive cells, as well as, CD45 (common leucocytic antigen)-positive cells were examined on the basis of immunohistochemical staining, and areas of immunoprecipitation were analyzed morphometrically using computer-assisted video imaging system. The stage-specific distribution of receptors for estrogen (ER) and progesterone (PR) in endometrial cells were examined and morphometrically analyzed. There was an increase in the number of CD45+ cells (P < 0.01) and CD68+ cells (P < 0.05) in secretory phase endometrium compared with proliferative and peri-ovulatory phases. There was no remarkable cycle dependent pattern in HLA-DR+ and L1+ cells. However, there was an increase in CD44 immunopositive area in peri-ovulatory (P < 0.05) and in secretory (P < 0.01) phases of endometrium compared with proliferative phase endometrium. A higher (P < 0.01) degree of immunopositivity for ER was observed during peri-ovulatory phase, and for PR, during peri-ovulatory (P < 0.05) and secretory (P < 0.01) phases compared with proliferative phase of cycle. Positive correlations between areas occupied by (i) CD68+ cells and PR (P < 0.01), (ii) HLA-DR+ and L1+ cells (P < 0.05), (iii) CD45+ and CD68+ cells (P < 0.01), (iv) CD45+ and L1+ cells (P < 0.05), and (v) PR and L1+ cells (P < 0.05) were obtained. It appears that the recruitment of different macrophage subsets in human endometrium involves a complex set of endocrine and paracrine factors.

Antigens, CD↗
PubMed1992

L1 substrate enhances outgrowth of tyrosine hydroxylase-immunoreactive neurites in mesencephalic cell culture.

We have evaluated neurite outgrowth from mesencephalic tyrosine hydroxylase-positive neurons grown in vitro on different substrates. Cultures of ventral mesencephalon from rat embryos (E13) were plated on plastic dishes coated with the following substrates: L1, L2/HNK-1 "residual" (mainly J1/160 but also tenascin), MAG antigens from mouse brains, laminin, fibronectin, poly-L-lysine, RGD peptide, and plastic alone. After 3, 4, and 6 days in vitro, the cultures were stained using an antibody against tyrosine hydroxylase (TH), and the length of TH-positive neurites was measured by computer-assisted image analysis in a double-blind fashion. L1 antigen had a significant positive effect on neurite outgrowth compared to the other substrates studied. Laminin and fibronectin were also favorable substrates. In cultures treated with cytosine arabinoside to prevent mitoses and glial proliferation, the positive effect of L1 was abolished, but laminin still had a stimulatory effect. These data indicate that L1 may be indirectly involved in differentiation or axonal elongation of substantia nigra dopaminergic neurons and suggest a complex effect involving both neurons and glia on dopaminergic neurite development.

Animals↗
PubMed2002

Functional binding interaction identified between the axonal CAM L1 and members of the ERM family.

A yeast two-hybrid library was screened using the cytoplasmic domain of the axonal cell adhesion molecule L1 to identify binding partners that may be involved in the regulation of L1 function. The intracellular domain of L1 bound to ezrin, a member of the ezrin, radixin, and moesin (ERM) family of membrane-cytoskeleton linking proteins, at a site overlapping that for AP2, a clathrin adaptor. Binding of bacterial fusion proteins confirmed this interaction. To determine whether ERM proteins interact with L1 in vivo, extracellular antibodies to L1 were used to force cluster the protein on cultured hippocampal neurons and PC12 cells, which were then immunolabeled for ERM proteins. Confocal analysis revealed a precise pattern of codistribution between ERMs and L1 clusters in axons and PC12 neurites, whereas ERMs in dendrites and spectrin labeling remained evenly distributed. Transfection of hippocampal neurons grown on an L1 substrate with a dominant negative ERM construct resulted in extensive and abnormal elaboration of membrane protrusions and an increase in axon branching, highlighting the importance of the ERM-actin interaction in axon development. Together, our data indicate that L1 binds directly to members of the ERM family and suggest this association may coordinate aspects of axonal morphogenesis.

Actins↗
PubMedDate not supplied

An immunohistochemical study of histiocytic ulcerative colitis in boxer dogs.

Histiocytic ulcerative colitis (HUC) is an inflammatory bowel disease (IBD) that occurs predominantly in dogs of the boxer breed. The lesions are characterized by mucosal ulceration and mixed inflammatory cell infiltrate that includes the presence of periodic acid-Schiff (PAS)-positive macrophages. However, the phenotype of the inflammatory cells has not been characterized further. In the present study, immunohistochemistry and computer-aided morphometric analysis were used to define populations of leucocyte subsets in the colon of 14 boxer dogs with HUC. Biopsies from six of these dogs included both lesional and non-lesional regions. Colonic tissue from 11 dogs of various breeds without evidence of gastrointestinal disease served as controls. In HUC lesions there were significantly more IgG(+), IgG3(+), IgG4(+)plasma cells, CD3(+)T cells, MHC class II(+)cells, L1(+)cells and PAS(+)cells in the lamina propria than in both control colon and non-lesional colonic regions of affected dogs. In the epithelial compartment, goblet cells were significantly decreased in HUC lesions compared to both control and non-lesional HUC colon, and intensity of enterocyte MHC class II expression was significantly increased. These observations are similar to those documented in human IBD, especially ulcerative colitis, and suggest an important role for the mucosal immune system in the pathogenesis of canine HUC.

Animals↗