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PubMed1999

Effects of single intravenous doses of recombinant human interleukin-10 on subsets of circulating leukocytes in humans.

Recombinant human interleukin-10 (rhIL-10) is a potent and specific immunomodulatory agent which inhibits endotoxin-stimulated pro-inflammatory cytokine production by monocytes, blocks T-lymphocyte activation by antigen presenting cells, and modulates T(H)1/T(H)2 balance in immune responses. In previous clinical trials, rhIL-10 administered to healthy volunteers induced rapid and transient elevations of neutrophil and monocyte counts and reductions of lymphocyte counts in addition to suppression of endotoxin-stimulated whole blood cytokine synthesis. We sought to better characterize the effects of rhIL-10 on immunophenotypically defined subsets of circulating leukocytes that could be relevant to its immunomodulatory effects. Healthy volunteers were given single doses of 10 microg/kg rhIL-10 (n = 8) or equivalent placebo (n = 4) by intravenous injection. Significant changes of circulating leukocytes included transiently increased neutrophils and monocytes with parallel increases of CD33+ and CD14+ cells. Total lymphocytes as well as total CD3+, CD3+/CD4+ and CD3+/CD8+ cells transiently decreased. Mean fluorescence intensity of CD11a (integrin alpha-chain subunit of lymphocyte function antigen-1, LFA-1) on lymphocytes transiently but significantly decreased, suggesting a mechanism for transient alteration of lymphocyte trafficking. In addition, mean fluorescence intensity of HLA-DR (major histocompatibility class II) on CD14+ cells (predominantly monocytes) transiently but significantly decreased, implying a possible alteration of antigen presenting function. Further study will be required to elucidate the immunomodulatory roles and potential clinical significance of these hematologic changes in therapeutic trials of rhIL-10 in patients with chronic inflammatory and autoimmune diseases.

Adult↗
PubMed2002

Characterization of a feline homologue of the alphaE integrin subunit (CD103) reveals high specificity for intra-epithelial lymphocytes.

The characteristics of a feline homologue of the alphaE integrin (CD103), defined by two murine monoclonal antibodies, Fe7.1B8 (IgG1) and Fe7.2D8 (IgG1), are described. These antibodies recognized 75% of intra-epithelial (range 59-88%) and 40% of lamina proprial (range 28-46%) T cells of the intestinal mucosal tissue of the small intestine in contrast with approximately 2% of peripheral blood lymphocytes. Both antibodies immunoprecipitated a 180 kDa protein from biotinylated feline intra-epithelial mucosal leukocytes consistent with the alphaE integrin subunit in conjunction with a 120 kDa protein consistent with the beta7 subunit. The nucleotide sequence of feline alphaE integrin, generated from molecular cloning of the feline alphaE encoding cDNA, is also reported. This feline molecule shares 72% sequence homology with human and 69% homology with murine and rat counterparts. Homology includes the presence of an X (extra) domain, that appears unique to alphaE molecules as described for human, rat and mouse, as well as areas of homology common to other alpha integrins. Of note is a typical I (inserted) domain, the presence of seven repeat regions, and highly conserved sequences in the cytoplasmic tail. Transfection studies demonstrated that both antibodies recognized an extracellular component which encompassed the X and I domains of the cloned alphaE integrin subunit. These studies demonstrate that the pattern of tissue distribution, biochemical characteristics, and cDNA sequence of the feline alphaE integrin subunit are largely similar to that described for other species.

Amino Acid Sequence↗
PubMed1994

Cellular adhesion antigen modulation in purpura pigmentosa chronica.

BACKGROUND: Purpura pigmentosa chronica is an inflammatory skin disorder probably caused by an allergic reaction. Delayed-type hypersensitivity or immunocomplex vasculitis has been considered as a possible mechanism. OBJECTIVE: Detailed analysis of cell adhesion molecule (CAM) modulation may give further insights into the pathogenesis and underlying immune reaction of this disease. METHODS: By immunohistochemical techniques we investigated the in situ expression of integrins, selectins, and CAMs of the immunoglobulin superfamily. RESULTS: Infiltrating lymphocytes expressed LFA-1, LFA-2, VLA-4, and VLA-5, whereas some of the macrophages were also positive for p150/95 and MAC-1. VLA-1 was found on lymphocytes near the basement membrane of the epidermis. Compared with uninvolved or healthy skin endothelial cells showed upregulation of ICAM-1, VCAM-1, and, focally, E-selectin. Some fibroblasts were positive for ICAM-1. ICAM-1 was also upregulated on lesional keratinocytes that also expressed alpha 2, alpha 3, and alpha 6 integrin chains on basal and suprabasal epidermal layers. CONCLUSION: Our findings demonstrate characteristic modifications in the expression of CAMs in purpura pigmentosa chronica and indicate the involvement of the epidermis in this disease. This modulation shows close parallels to those described for chronic delayed-type immune reactions of the skin.

Cell Adhesion Molecules↗
PubMed2003

Developmental and regional differences in the consolidation of long-term potentiation.

The alpha5beta1 integrin is present in high concentrations in the apical dendrites of pyramidal neurons in adult rats but is virtually absent in the basal dendrites. Moreover, alpha5beta1 does not appear in apical dendritic branches until the third post-natal week. Given that integrins contribute to the consolidation of synaptic plasticity, these results raise the possibility of developmental and regional differences in the stability of long-term potentiation (LTP). The present study tested this point using a LTP reversal paradigm in field CA1 of hippocampal slices. In accord with earlier reports, low-frequency afferent stimulation (5 Hz) introduced 30 s after theta burst stimulation (TBS) completely reversed LTP but was ineffective 30 min and 60 min later in slices from adult rats. The same low-frequency trains caused a partial reversal of LTP when applied 30 and 60 min post-TBS in slices from 21-day-old rats and a complete reversal at all time points in slices from 10-day-old rats. LTP in the basal dendrites of adult rats did not fully consolidate; i.e. potentiation was partially reversed by low-frequency stimulation even after delays of 30 or 60 min. Moreover, spaced (10 min) applications of 5- Hz pulses beginning at 30 min post-TBS completely erased LTP. The reversal effect in both apical and basal dendrites was blocked by N-methyl-D-aspartic acid receptor antagonists but an integrin antagonist had differential effects across the two dendritic domains. These results constitute evidence that the stability of LTP increases with age in the apical dendrites but remains incomplete even in adulthood in the basal dendrites. The possibilities that the developmental and regional variations in LTP consolidation are correlated with integrin expression and linked to different types of memory processing are discussed.

Animals↗
PubMed2001

The Haspin gene: location in an intron of the integrin alphaE gene, associated transcription of an integrin alphaE-derived RNA and expression in diploid as well as haploid cells.

Haspin is a serine/threonine kinase, recently identified in mice, that is thought to regulate cell cycle and differentiation of haploid germ cells. Here, the haspin gene is identified within an intron of the integrin alphaE gene. Transcription occurs from a bi-directional CpG island-associated promoter that also generates an alternatively spliced integrin alphaE derived RNA. Remarkably, the human and murine haspin genes lack introns, and have features of retroposons. The human haspin cDNA reveals that the human and murine proteins are 83% identical in the C-terminal kinase domain, but only 53% identical in the N-terminal region. The haspin kinase domain has structural features that distinguish it from previously characterized proteins and suggest that haspin is a member of a new family of protein kinases. Although formerly thought to be expressed selectively in the testes, haspin is also transcribed at lower levels in thymus, bone marrow, fetal liver and other fetal tissues, and in all proliferating cell lines tested. Thus haspin is likely to be important in regulation of diploid as well as haploid cell differentiation in a variety of tissues.

Alternative Splicing↗
PubMed2003

CD103+ intraepithelial lymphocytes--a unique population in microsatellite unstable sporadic colorectal cancer.

Colorectal cancers with microsatellite instability (MSI) typically show increased numbers of intraepithelial lymphocytes (IEL) in comparison to microsatellite stable (MSS) cancers. The aim of this study was to determine the phenotype of this unique lymphocyte population in MSI and MSS colorectal cancers. Twenty-four individuals with sporadic colorectal cancer (17 MSI, 7 MSS) were included in this study. Intraepithelial and stromal lymphocytes were detected using immunohistochemistry with anti-CD8 and anti-CD103 antibodies, and two observers independently quantified the numbers of lymphocytes. CD103+ (alpha E beta 7+) IELs detected within tumour tissue co-expressed CD8+ while the stromal lymphocytes were phenotypically heterogeneous, with respect to CD8+ and CD103+ expression. MSI colorectal cancers harboured increased numbers of CD8+ CD103+ IELs, as well as CD8+ CD103- and CD8+ CD103+ stromal lymphocytes, when compared with MSS colorectal cancers. CD103+ IELs were found at 27-fold greater numbers in the tumour epithelium than in normal epithelium from the same patient (P = 0.001, Wilcoxon matched pairs test). From our findings, we have proposed a mechanism for the homing of these alpha E beta 7+ lymphocytes to tumour tissue in MSI and MSS colorectal cancers.

Aged↗
PubMed2001

Regulation of alpha7 integrin by mechanical stress during skeletal muscle regeneration.

The continuity of the tendon-myofibre-tendon units disrupted by shearing injury must be re-established during regeneration. We have previously demonstrated in freely moving rats that transected myofibres reinforce their lateral integrin-mediated adhesion, with the maximum around days 5-7. After day 14, most integrin molecules are redistributed to the newly formed myotendinous junctions, by which the ends of regenerating myofibres attach to the scar between the stumps. Here, we analyzed the effects of mechanical stress (free and forced mobilization vs. immobilization and denervation separately and in combination) on the expression of alpha7 integrin and merosin in regenerating myofibres using quantitative in situ hybridization and immunohistochemistry. In all groups, alpha7 integrin expression was upregulated at mRNA level, whereas increased protein accumulation in lateral sarcolemma occurred only in the mobilized groups. The accumulation of merosin was not affected by the stress level. The results demonstrate that active mechanical stress reinforces early lateral integrin-mediated adhesion; molecules may at the same time mediate signals from matrix to cells for adaptation to the altered biomechanical status.

Animals↗
PubMed2003

Expression of mouse agrin in normal, denervated and dystrophic muscle.

Agrin is a heparan sulfate proteoglycan that is required for the development of postsynaptic specializations at the neuromuscular junction. An alternatively spliced isoform of agrin that lacks this activity is found in basement membranes of several tissues including embryonic muscle. Overexpression of a miniaturized form of this agrin isoform ameliorates the severe muscle dystrophy of laminin alpha2-deficient mice, a mouse model for merosin-deficient congenital muscle dystrophy. Several lines of evidence indicate that this amelioration is based on the high-affinity binding of the mini-agrin to the laminins and to alpha-dystroglycan. Here, we used antibodies raised against mouse agrin to evaluate protein expression in adult muscle of normal and dystrophic mice. We find that expression of agrin in non-synaptic region varies greatly between different muscles in wild-type mice and that its levels are altered in dystrophic muscle.

Agrin↗
PubMed1998

Essential role of alpha 6 integrins in cortical and retinal lamination.

Extracellular matrix (ECM) is believed to play important roles in many aspects of nervous system development [1]. The laminins are ECM glycoproteins expressed in neural tissues and are potent stimulators of neurite outgrowth in vitro [1-3]. Genetic approaches using Drosophila and Caenorhabditis elegans have demonstrated a role for laminin and a laminin receptor in vivo in axon pathfinding and fasciculation, respectively [4,5]. In higher organisms, however, the role of laminins in the development of the nervous system is poorly understood. Integrins alpha 6 beta 1 and alpha 6 beta 4 are major laminin receptors. A role for the alpha 6 integrin in neurulation has been reported in amphibians [6]. We previously described mice lacking integrin alpha 6; these mice died at birth with severe skin blistering [7]. Detailed analyses of integrin alpha 6-/- mice reported here revealed abnormalities in the laminar organization of the developing cerebral cortex and retina. Ectopic neuroblastic outgrowths were found on the brain surface and in the vitreous body in the eye. Alterations of laminin deposition were found in mutant brains. Thus, this study provides evidence for an essential role of integrin-laminin interactions in the proper development of the nervous system. These observations are particularly significant given the recent report that human patients suffering from epidermolysis bullosa can carry mutations in ITGA6, the gene encoding the alpha 6 integrin chain [8,9].

Animals↗
PubMed2002

CD4(+)CD25(+) immunoregulatory T cells: gene expression analysis reveals a functional role for the glucocorticoid-induced TNF receptor.

CD4(+)CD25(+) immunoregulatory T cells represent a unique lineage of thymic-derived cells that potently suppress both in vitro and in vivo effector T cell function. We analyzed CD4(+)CD25(+) and CD4(+)CD25(-) T cells by DNA microarray, identifying 29 genes differentially expressed in the resting subpopulations, and 77 that were differentially expressed following activation. Most of these genes were elevated in the CD4(+)CD25(+) population, suggesting a previously activated phenotype. Among these were a number of genes that antagonize signaling, including members of the SOCS family, which may contribute to their anergic phenotype. Multiple cell surface receptors also had increased expression in CD4(+)CD25(+) cells, including GITR, a member of the TNF receptor superfamily. Importantly, antibodies to GITR abrogated suppression, demonstrating a functional role for this receptor in regulating the CD4(+)CD25(+) T cell subset.

Animals↗
PubMed1991

Fibronectin and VLA-4 in haematopoietic stem cell-microenvironment interactions.

The self-renewal and differentiation of haematopoietic stem cells occurs in vivo and in vitro in direct contact with cells making up the haematopoietic microenvironment. In this study we used adhesive ligands and blocking antibodies to identify stromal cell-derived extracellular matrix proteins involved in promoting attachment of murine haematopoietic stem cells. Here we report that day-12 colony-forming-unit spleen (CFU-S12)5 cells and reconstituting haematopoietic stem cells attach to the C-terminal, heparin-binding fragment of fibronectin by recognizing the CS-1 peptide of the alternatively spliced non-type III connecting segment (IIICS) of human plasma fibronectin. Furthermore, CFU-S12 stem cells express the alpha 4 subunit of the VLA-4 integrin receptor, which is known to be a receptor for the CS-1 sequence, and monoclonal antibodies against the integrin alpha 4 subunit of VLA-4 block adhesion of CFU-S12 stem cells to plates coated with the C-terminal fibronectin fragment. Finally, polyclonal antibodies against the integrin beta 1 subunit of VLA-4 inhibit the formation of CFU-S12-derived spleen colonies and medullary haematopoiesis in vivo following intravenous infusion of antibody-treated bone marrow cells.

Animals↗
PubMed2000

Discriminative immunophenotype of bronchoalveolar lavage CD4 lymphocytes in sarcoidosis.

The diagnosis of pulmonary sarcoidosis relies in part on the observation of alveolar CD4+ lymphocytosis. However, this criterion is not fully discriminative because this anomaly is also found in other types of lung diseases. Among other possible distinctive criteria, we investigated the expression of lymphocyte-addressing molecules, which could differ according to the pathophysiology of lung diseases. We investigated CD103 (alpha(E)beta7 integrin, CD103-beta7), reported to be both expressed on intra-epithelial lymphocytes in mucosal areas, including bronchi, and possibly involved in the recruitment of alveolar lymphocytes. The expression of CD103 was examined on bronchoalveolar lavage lymphocytes from 93 consecutive patients, including 34 patients with CD4+ lymphocytosis. For all patients, the expression of CD19, CD3, CD4, CD8, CD57, LFA1, DR, and CD103 was assessed by flow cytometry. Sarcoidosis seemed remarkably characterized by the lack of CD103 expression on the predominant CD4+ subset. Statistically significant differences were found between patients with sarcoidosis, with other types of CD4+ lymphocytosis, and with other lung disorders in the CD103+ cell levels and in the CD103/CD4 ratio. Combined use of the CD4/CD8 ratio (> 2.5) and the CD103/CD4 ratio (< 0.31) to assess bronchoalveolar lavage lymphocytes is a promising new tool for the diagnosis of sarcoidosis.

Adult↗
PubMed2004

TIA-1 expression in hairy cell leukemia.

We measured T-cell intracellular antigen-1 (TIA-1) expression in neoplastic cells from patients with hairy cell leukemia. Five of nine cases were positive for cytoplasmic TIA-1, with a small, dot-like, granular expression pattern. However, neoplastic cells were granzyme B- and perforin- negative in all cases. Other positive markers were CD20 in 9/9 cases, CD19 in 9/9 cases, DBA44 in 8/9 cases, LeuM5(CD11C) in 8/9 cases, IL-2R(CD25) in 7/9 cases, CD103 in 7/9 cases, FMC7 in 6/9 cases, and tartrate- resistant acid phosphatase in 5/7 cases. We also analyzed TIA-1 expression in 94 B cell lymphomas, including 19 diffuse, large cell lymphomas, 19 mantle cell lymphomas, six follicular lymphomas, two extranodal marginal zone B-cell lymphomas, 13 nodal marginal zone B-cell lymphomas, one mediastinal large-cell lymphoma, 19 diffuse small-cell lymphomas, 14 myelomas, and one splenic lymphoma with villous lymphocytes. All cases were negative for TIA-1 expression. Based on these findings, TIA-1 expression in neoplastic cells of low-grade B-cell lymphomas may be a good diagnostic marker for hairy cell leukemia. Moreover, TIA-1 reactivity in lymphomas does not necessarily indicate a T- or NK-cell derivation.

Adult↗
PubMed1997

Absence of integrin alpha 7 causes a novel form of muscular dystrophy.

Integrin alpha 7 beta 1 is a specific cellular receptor for the basement membrane protein laminin-1 (refs 1,2), as well as for the laminin isoforms -2 and -4 (ref. 3). The alpha 7 subunit is expressed mainly in skeletal and cardiac muscle and has been suggested to be involved in differentiation and migration processes during myogenesis. Three cytoplasmic and two extracellular splice variants that have been described are developmentally regulated and expressed in different sites in the muscle. In adult muscle, the alpha 7A and alpha 7B subunits are concentrated in myotendinous junctions but can also be detected in neuromuscular junctions and along the sarcolemmal membrane. To study the potential involvement of alpha 7 integrin, during myogenesis and its role in muscle integrity and function, we generated a null allele of the alpha 7 gene (Itga7) in the germline of mice by homologous recombination in embryonic stem (ES) cells. Surprisingly, mice homozygous for the mutation are viable and fertile, indicating that the alpha 7 beta 1 integrin is not essential for myogenesis. However, histological analysis of skeletal muscle revealed typical symptoms of a progressive muscular dystrophy starting soon after birth, but with a distinct variability in different muscle types. The observed histopathological changes strongly indicate an impairment of function of the myotendinous junctions. These findings demonstrate that alpha 7 beta 1 integrin represents an indispensable linkage between the muscle fibre and the extracellular matrix that is independent of the dystrophin-dystroglycan complex-mediated interaction of the cytoskeleton with the muscle basement membrane.

Animals↗
PubMed2005

Invasive and noninvasive uveal melanomas have different adhesive properties.

AIMS: To establish if invasive and noninvasive uveal melanomas have differences in expression of adhesion molecules, and whether their adhesive interactions with the extracellular matrix (ECM) and endothelium vary. METHODS: Cells from an invasive and noninvasive uveal melanoma cell line and hepatic and dermal microvascular endothelial cells were assessed by flow cytometry for adhesion molecule expression. Tumour cell adhesion to ECM substrates (collagens I and IV, fibronectin, laminin, and vitronectin) and endothelial cells was also investigated using a commercially available assay or a fluorescence-based in vitro assay, respectively. The significance of results comparing cell lines was determined using a Student's t-test, whereby P-values of less than 0.05 were taken as significant. RESULTS: alpha1- and alpha4-integrins were not expressed by noninvasive cells, but were detected on invasive cells. The invasive cell line also expressed higher levels of other integrins than the noninvasive line. Correspondingly, invasive cells adhered in higher numbers to ECM substrates and endothelial cells, and for the latter, the difference was highly significant (P<0.001). No preference in adhesion of invasive cells for the hepatic endothelium was observed. CONCLUSIONS: Successful attachment to and migration through the ECM, basement membrane, and endothelium are vital processes involved in malignant progression. Differential expression of alpha1- and alpha4-integrins by invasive and noninvasive cells infers a role for these receptors in invasion, while the ability of invasive cells to adhere more efficiently to the endothelium suggests that this is a critical factor in uveal melanoma invasion.

Cell Adhesion↗
PubMed2005

Tenascin-W is found in malignant mammary tumors, promotes alpha8 integrin-dependent motility and requires p38MAPK activity for BMP-2 and TNF-alpha induced expression in vitro.

Tenascins represent a family of extracellular matrix glycoproteins with distinctive expression patterns. Here we have analyzed the most recently described member, tenascin-W, in breast cancer. Mammary tumors isolated from transgenic mice expressing hormone-induced oncogenes reveal tenascin-W in the stroma around lesions with a high likelihood of metastasis. The presence of tenascin-W was correlated with the expression of its putative receptor, alpha8 integrin. HC11 cells derived from normal mammary epithelium do not express alpha8 integrin and fail to cross tenascin-W-coated filters. However, 4T1 mammary carcinoma cells do express alpha8 integrin and their migration is stimulated by tenascin-W. The expression of tenascin-W is induced by BMP-2 but not by TGF-beta1, though the latter is a potent inducer of tenascin-C. The expression of tenascin-W is dependent on p38MAPK and JNK signaling pathways. Since preinflammatory cytokines also act through p38MAPK and JNK signaling pathways, the possible role of TNF-alpha in tenascin-W expression was also examined. TNF-alpha induced the expression of both tenascin-W and tenascin-C, and this induction was p38MAPK- and cyclooxygenase-dependent. Our results show that tenascin-W may be a useful diagnostic marker for breast malignancies, and that the induction of tenascin-W in the tumor stroma may contribute to the invasive behavior of tumor cells.

Bone Morphogenetic Protein 2↗
PubMed2003

The effects of ultraviolet B treatment on the expression of adhesion molecules by circulating T lymphocytes in psoriasis.

BACKGROUND: T lymphocytes are believed to play a role in the pathogenesis of psoriasis; > 80% of T lymphocytes that infiltrate psoriatic lesions express the surface glycoprotein cutaneous lymphocyte-associated antigen (CLA), compared with < 20% in the blood. Exposure to ultraviolet (UV) B is an effective treatment for psoriasis. OBJECTIVES: To compare the effects of UVB treatment of psoriasis on the expression of CLA and several other surface markers expressed by circulating T lymphocytes. METHODS: Peripheral blood mononuclear cells from psoriatic patients were stained for adhesion molecules and stimulated with streptococcal antigens before and once weekly during 3 weeks of UVB treatment. RESULTS: A marked and progressive decrease was observed during the treatment in expression of the CLA and the very late antigen-4alpha by T cells; this decrease correlated closely with clinical improvement (Psoriasis Area and Severity Index). T-cell expression of intercellular adhesion molecule-1 was not significantly affected during the treatment and no change was observed in the activation markers CD25 and CD69 or lymphocyte proliferation after stimulation with streptococcal antigens or superantigens. CONCLUSIONS: UVB treatment is associated with a marked reduction in the expression of skin-homing molecules by circulating T cells. This may be relevant to the therapeutic effect of UVB in psoriasis.

Adolescent↗
PubMed2001

In multiple myeloma, only a single stage of neoplastic plasma cell differentiation can be identified by VLA-5 and CD45 expression.

The nature of the proliferating fraction in myeloma is still not known and understanding the characteristics of this fraction is central to the development of effective novel therapies. However, myeloma plasma cells typically show a very low rate of proliferation and this complicates accurate analysis. Although the level of CD45 and/or VLA-5 has been reported to identify proliferating 'precursor' plasma cells, there are discrepancies between these studies. We have therefore used a rigorous sequential gating strategy to simultaneously analyse cycle status and immunophenotype with respect to CD45, VLA-5 and a range of other integrin molecules. In 11 presentation myeloma patients, the proliferative fraction was distributed evenly between CD45+ and CD45- cells, however, cycling plasma cells were consistently VLA-5-. There was close correlation between the expression of VLA-5 and a range of other integrin molecules (CD11a, CD11c, CD103), as well as the immunoglobulin-associated molecules CD79a/b (Spearman, n = 10, P < 0.0001). In short-term culture, cells that were initially VLA-5-showed increasing VLA-5 expression with time. However, simultaneous analysis of the DNA-binding dye 7-amino-actinomycin D demonstrated that this was not as a result of differentiation, as VLA-5+ plasma cells were all non-viable. This was confirmed in freshly explanted plasma cells from nine patients. Discrete stages of plasma cell differentiation could not be distinguished by the level of CD45 or VLA-5 expression. The results indicate that there is a single stage of plasma cell differentiation, with the phenotype CD38+CD138+VLA-5-. These findings support the hypothesis that neoplastic bone marrow plasma cells represent an independent, self-replenishing population.

Antigens, CD↗