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At least 19 recordsLinked to original sources
PubMed2000

A novel point mutation in CD18 causing the expression of dysfunctional CD11/CD18 leucocyte integrins in a patient with leucocyte adhesion deficiency (LAD).

Leucocyte adhesion deficiency type 1 (LAD-1) is characterized by the incapacity of leucocytes to carry out their adhesion functions via their CD11/CD18 antigens, which are also referred to as the leucocyte integrins. The patients generally suffer from poor wound healing and recurrent bacterial and fungal infections. In severe cases, the infections are often systemic and life-threatening. A LAD patient (AW) of moderate phenotype has been identified but, unlike most other cases, the level of CD11/CD18 antigens on her leucocytes are uncharacteristically high for a LAD patient. Molecular analysis revealed that she is a compound heterozygote for CD18 mutations. She has inherited a D231H mutation from her father and a G284S mutation from her mother. By transfection studies, it was established that the G284S mutation does not support CD11/CD18 antigen expression on the cell surface. In contrast, the D231H mutation does not affect CD18 forming integrin heterodimers with the CD11 antigens on the cell surface. However, the expressed integrins with the D231H mutation are not adhesive to ligands.

Animals↗
PubMed1986

Expression of CD11, CDw15, and transferrin receptor antigens on human hematopoietic progenitor cells.

The expression of transferrin receptor-associated antigens and of CD11 and CDw15 antigens was investigated on myeloid committed progenitor cells (CFU-GM day 10, CFU-GM day 7, and cluster-forming cells [CFC] day 4), on erythroid committed progenitor cells (BFU-E and CFU-E), and on multilineage progenitor cells (CFU-GEMM). Both complement-dependent cytotoxicity and fluorescence-activated cell-sorting assays were performed. Complement-dependent cytotoxicity appeared to be the more sensitive assay. Transferrin receptor-associated antigens appeared to be clearly present on all myeloid and erythroid committed progenitor cells, but were found to be only weakly expressed on CFU-GEMM. CD11 antigens appeared to be strongly expressed only on mature granulocytes, monocytes, and certain lymphocytes, but not significantly on myeloid committed precursor cells. Surprisingly, CD11 antigens were weakly, but significantly, present on CFU-E. CDw15 antigens appeared to be restricted to myeloid differentiation and were increasingly expressed from CFU-GM day 10 to CFC day 4. Thus, antitransferrin receptor, CD11, and CDw15 antibodies can be used to separate hematopoietic progenitor cells and may be useful tools in the study of hematopoietic differentiation.

Antibodies, Monoclonal↗
PubMed1990

Clinical significance of standard CD assessment in acute leukemia.

The data of detailed studies of immunophenotype of blast cells in 426 patients with acute leukemias are presented. Diagnostic and prognostic significance of different marker expression has been evaluated in groups of patients with ALL and AML. Frequency distribution of T1, T2, T3, pre-B, B, common, Ia and null subvariants identified according to immunoclassification of Baryshinkov et al. was studied in 250 children with ALL. These subvariants differed both in duration of disease (p = 0.0015) and in duration of first complete remission (p = 0.0031). The use of monoclonal antibodies of VI-series in 90 patients with ALL allowed to describe an immunophenotype of the subvariants in detail. The mosaic expression of myeloid antigens CD11, CD14, CD15, CDw65 identified by MoAbs VIM-12, VIM-13, VIM-D5 and VIM-2, respectively, on blast cells of patients with AML was shown. The expression of CD11 (ICO-GM1) or CD15 (ICO-G2) was prognostically unfavorable in children with AML (p = 0.0028). The expression of T-cell markers (E-receptor, CD7, reactivity with anti-T-cell serum) on blasts was prognostically favorable in children with AML (p = 0.003). So the data of immunophenotyping are of great value for accurate diagnosis and prognosis of acute leukemias.

Antibodies, Monoclonal↗
PubMed1991

Enzyme histochemical, immuno histochemical and electron microscopic studies of two cases of leukemic malignant histiocytosis.

Two cases of leukemic malignant histiocytosis had similar morphologic and enzyme histochemical findings. Large blasts with low nuclear/cytoplasmic ratios, occasional azurophilic granules, and immature nuclei with nucleoli were seen in peripheral blood and bone marrow smears. Case 1 had occasional erythrophagocytosis, while in Case 2 it was rare. They were peroxidase negative, and very strongly positive by alpha-naphthyl butyrate esterase stain, the latter being inhibited by sodium fluoride. Acid phosphatase stains were also very strongly positive and were inhibited with tartaric acid. They were also stained granularly with PAS. Surface marker analysis revealed myeloid surface antigens, CD11+, CD13+ and HLA-DR+ in Case 1, and CD11+, CD13+, CD33+ and HLA-DR+ in Case 2. Immunoperoxidase stains of bone marrow biopsies revealed that lysozyme was positive in both cases. S-100 protein was strongly positive in Case 1, but weakly so in the skin tumor and negative in the bone marrow of Case 2. Electron microscopy showed both cases to be myeloperoxidase negative and rich in cytoplasmic organelles, such as lysosomes, mitochondria, and endoplasmic reticuli. Nuclei were irregularly shaped and nucleoli were present in virtually all the cells. These findings suggest that the malignant histiocytes in these two cases derive from bone marrow macrophages, and S-100 protein can also be detected in monocyte-macrophage derived histiocytes.

Adenocarcinoma↗
PubMed1986

Influence of minor thermal injury on expression of complement receptor CR3 on human neutrophils.

Thermal injury is well known to inhibit functions of the circulating neutrophil related to its role in host defense against infection, but the mechanism(s) of this phenomenon are not fully understood. To gain further clues to these mechanisms, the authors have studied patients with thermal injury in terms of altered expression of neutrophil cell membrane receptors for the opsonic complement-derived ligand C3bi--complement receptor Type 3, or CR3. CR3 expression was selected for study because an increase in the number of receptors on the cell surface can be stimulated by products of complement activation known to accumulate after thermal injury and because of the role of CR3 in phagocytic and adherence functions of the neutrophil. Expression of CR3 was monitored semiquantitatively by flow cytometry with the use of a murine monoclonal antibody (OKM1) specific for an antigen (CD11) associated with this receptor. Patients evaluated were limited in this study to those with minor degrees of thermal injury (second-degree burn involving less than 20% of total body surface area) so that possible confounding effects of major injury and its complications could be eliminated. It was observed that patient neutrophil CR3 becomes significantly up-regulated during the first week, as early as 1 day after injury. The maximum level of expression of CR3 averaged greater than 150% (range, 70-314%) of the respective minimum level observed for each patient. The minimum levels of expression of CR3 on patient neutrophils, reached 11-37 days after injury for 7 of 8 patients, were comparable to the level of expression of CR3 on unstimulated control neutrophils. Such temporal up-regulation of patient neutrophil CR3 suggests the early generation of stimuli of CR3 mobilization in response to thermal injury. Increased numbers of CR3 on patient neutrophils may augment microbicidal function and enhance or inhibit delivery of cells to the burn site.

Adult↗
PubMed2003

Chemotaxis of non-compressed blood polymorphonuclear leukocytes from an adolescent with severe leukocyte adhesion deficiency.

We have defined the defect in a child with severe leukocyte adhesion deficiency-1 (LAD) as resulting from a single amino acid shift in CD18 (from a C to T mutation at position 533) that prevents heterodimerization with the CD11 antigens to produce beta(2) integrins-the first reported patient homozygous for this defect. Although beset by frequent infections, the patient has survived to adolescence despite the lack of these important adhesion molecules. Consistent with his clinical course is the ability of his PMN to respond chemotactically in slide preparations, albeit with difficulty because of their poor purchase on substrate. The operant adhesins are unknown; his polymorphonuclear leukocytes (PMN) remain chemotactically responsive in the presence of antibodies to alphavbeta(3) and beta(1) integrins and to integrin-associated protein (IAP). These findings indicate that not all patients with severe LAD are candidates for early bone marrow transplantation.

Amino Acid Substitution↗
PubMed1994

Elevated expression of CD80 (B7/BB1) and other accessory molecules on synovial fluid mononuclear cell subsets in rheumatoid arthritis.

OBJECTIVE: To assess the expression of important accessory molecules such as CD80 (B7/BB1) and CD54 (intercellular adhesion molecule 1) on potential antigen-presenting cells (APC) in the synovial fluid (SF) of patients with rheumatoid arthritis (RA). METHODS: The level of expression of various accessory molecules on T cells, monocytes, and CD5+ or CD5- B cells from RA SF was compared, by multiparameter flow cytometric analysis, with the expression on peripheral blood (PB) mononuclear cells from the same patients and from normal controls. The functional significance of increased expression of these accessory molecules was assessed by the ability of the different cell populations to stimulate T cells in the mixed lymphocyte reaction. RESULTS: Monocytes, T cells, and B cells isolated from the SF of inflamed joints of patients with RA expressed significantly higher levels of CD80 and CD54 than those from the PB of RA patients or normal controls. CD11b and CD11c expression also were increased on SF B cells, while SF monocytes exhibited enhanced levels of CD40. Further, we found that the elevated CD80 and CD54 levels in RA SF cells may enhance the capacity of these cells to act as stimulatory APC. CONCLUSION: This is the first demonstration that specific cell subsets constitutively express increased levels of CD80 at a site of autoimmune pathology, which could potentially contribute to the initiation or maintenance of autoimmune disease.

Antigen-Presenting Cells↗
PubMed1995

The red cell LW blood group protein is an intercellular adhesion molecule which binds to CD11/CD18 leukocyte integrins.

Leukocyte adhesion involves the leukocyte-specific integrins CD11a/CD18, CD11b/CD18 and CD11c/CD18, which bind to intercellular adhesion molecules (ICAM). Three ICAM have been described, and are expressed on leukocytes and various other cells, but are absent from red cells. Here, we show that the red cell Landsteiner-Wiener (LW) blood group glycoprotein is an ICAM which binds to the leukocyte-specific integrins. This finding has important implications in red cell physiology.

Blood Group Antigens↗
PubMed1995

Analysis of lymphocyte costimulation in vivo using transgenic and 'knockout' mice.

The use of transgenic technologies in the functional evaluation of the contributions of costimulatory pathways to T-cell activation in vivo has recently undergone a rapid expansion. During the past two years, mice deficient in costimulatory molecules and their receptors have been generated. These mice have revealed novel and critical in vivo functions of costimulatory pathways and have provided valuable models in which to test therapeutic strategies involving costimulatory pathway blockade. Transgenic mice constitutively expressing costimulatory molecules have provided insights into their role in peripheral tolerance.

Abatacept↗
PubMed2005

Dendritic cells in germ-free and specific pathogen-free mice have similar phenotypes and in vitro antigen presenting function.

Dendritic cells (DC) can direct downstream T-cell responses. Although bacterial adjuvants are strong activators of DC in vitro, the effects of normal enteric bacteria on DC in vivo are not well defined. We used germ-free (GF) mice to determine whether enteric bacteria alter DC phenotype and ability to stimulate naïve T cells. Surface expression of CD11c, CD86, and MHCII was measured on splenic and mesenteric lymph node (MLN) DC. In addition, we tested the ability of T-cell depleted splenocytes from mice injected with LPS to stimulate allogeneic T cells, as determined by cell proliferation. The absolute numbers of CD11c+ DC were decreased in the MLN and spleen of GF mice. Freshly isolated CD11c+ DC from spleens or MLN of SPF and GF mice expressed similar levels of CD86 and MHCII by FACS analysis. Proportions of splenic DC expressing CD4 or CD8 were not different in GF versus SPF mice, although the percentage of CD8alpha-/CD11b+ DC was higher in GF MLN. Intraperitoneal injection of LPS upregulated MHCII and CD86 to a similar extent on splenic DC from GF or SPF mice. Splenic antigen-presenting cells, as well as unseparated spleen or MLN cells, from GF or SPF mice also induced similar levels of T-cell proliferation in vitro. We conclude that commensal bacterial flora do not affect co-stimulatory molecule expression of DC in the spleen or MLN, which exhibit a predominantly immature phenotype. In addition, splenic APC from GF mice are fully competent to stimulate naïve T-cell proliferation in vitro.

Animals↗
PubMed2002

Use of intraperitoneal interferon alpha-2b therapy after conservative surgery for endometriosis and postoperative medical treatment with depot gonadotropin-releasing hormone analog: a randomized clinical trial.

OBJECTIVE: To evaluate the possible therapeutic effects of interferon alpha-2b left in the peritoneum after surgery, followed by or not followed by treatment with GnRH analogs. DESIGN: A prospective, randomized clinical trial. SETTING: University hospital. PATIENT(S): Fifty-two infertile patients with moderate or severe endometriosis. INTERVENTION(S): Laparotomic conservative surgery and either interferon alpha-2b or saline alone left in the pouch of Douglas followed by administration of either GnRH analogs depot or oral indomethacin with transvaginal echography and analysis of CA-125, immunoglobulins, and lymphocyte populations. MAIN OUTCOME MEASURE(S): Recurrence of endometriosis was considered clinically, echographically, and laparoscopically. RESULT(S): Recurrence of endometriosis in four cases without interferon (15.4%) versus 11 patients (42.3%) with interferon alpha-2b. Life table analysis showed significant differences between the groups with and without interferon 21 months after conservative surgery. There were no differences in the recurrence between the groups with or without GnRH analogs. Likewise, there were no significant changes in immunoglobulins and lymphocyte populations among patients with and without recurrence of endometriosis. The patients that received GnRH analogs depot showed a decrease in the number of CD16 and an increase of CD11b cells after treatment. CONCLUSION(S): The use of interferon alpha-2b within the peritoneal cavity after conservative surgery may be inappropriate because it increased later recurrence of endometriosis. The postoperative treatment with GnRH analogs did not significantly reduce the recurrence rate. Immunoglobulins and lymphocyte populations did not change in relation to the recurrence of endometriosis.

Adult↗
PubMed2003

Expression of co-stimulatory molecules on acute myeloid leukaemia blasts may effect duration of first remission.

Many solid tumours have been shown to lack expression of either of the immune co-stimulatory molecules CD80 (B7.1) or CD86 (B7.2), which is thought to be one of the ways in which tumours may escape immune recognition. We have examined the surface expression of CD80, CD86, human leucocyte antigen (HLA) class I and II, CD11a, CD54, and CD58 on the blast cells from patients with acute myeloid leukaemia (AML) at presentation. CD80 was only rarely expressed on AML blasts and, in those leukaemic cells expressing CD80, the level of expression was low. In contrast, expression of CD86 was detected on the AML blasts in more than half of the samples tested and, in some cases, the level of expression was equivalent to that of mature monocytes and activated B lymphocytes. The percentage of leukaemic blasts expressing CD86 was higher in the M4 and M5 French-American-British (FAB) types, and expression of CD11a and HLA class II was higher in the M4 FAB type. There was no difference in expression of CD80, CD54, CD58, or HLA Class I between different FAB subgroups. There was no significant difference in duration of first remission with expression of CD80, CD86, CD11a, CD54 or HLA class II. However, when expression of CD80 and CD86 were considered together, a significantly longer duration of remission was found. We suggest that these molecules may play a role in immunosurveillance, resulting in prolonged remission in some patients treated for AML.

Acute Disease↗
PubMedDate not supplied

PD-L2+ dendritic cells and PD-1+ CD4+ T cells in schistosomiasis correlate with morbidity.

Dendritic cells (DC) are critical antigen-presenting cells for the induction and control of immune responses. PD-L2 (B7-DC) is a regulatory ligand on subpopulations of DC, and binds to the co-regulatory receptor PD-1, present on some activated T lymphocytes, leading to down-regulation. We now show that very early during experimental schistosomiasis (by 5 weeks) a significantly higher proportion of splenic CD11c+/B220- DC express PD-L2, and by 6 weeks after infection a higher proportion of splenic CD4 T cells express PD-1. In this CBA/J mouse/Schistosoma mansoni chronic infection model we have shown that most mice develop moderate morbidity (Moderate Splenomegaly Syndrome, MSS), while some parallel-infected mice express different immune characteristics and die or develop severe morbidity (Hypersplenomegaly Syndrome, HSS). We now report a positive correlation between the proportion of splenic CD11c+/B220- DC that express PD-L2 and showing MSS. In contrast, there is an inverse correlation between the proportion of splenic CD3+/CD4+ T lymphocytes that express PD-1 and showing MSS. The data demonstrate that schistosomes can induce sustained elevated percentages of PD-L2-expressing, B220-negative DC. Furthermore, when this potentially immunoregulatory environment occurs chronically, infected mice are most likely to have developed MSS, expressing moderate morbidity.

Animals↗
PubMed2003

CD45-positive cells of the retina and their responsiveness to in vivo and in vitro treatment with IFN-gamma or anti-CD40.

PURPOSE: The ability to mount antigen-specific immune reactions in the retina demonstrates local recognition of retinal antigens. However, properties of antigen-presenting cells (APCs) of the retina are uncertain. The current study was undertaken to look for evidence of CD45(+) cells with APC potential in the retina and to examine their in situ and in vitro responses to IFN-gamma and anti-CD40, two stimuli known to upregulate activities associated with antigen presentation. METHODS: Mice were pretreated with systemic or intracameral (IC) inoculations of IFN-gamma or anti-CD40. Retinas were harvested, enzymatically dissociated, positively selected with anti-CD45, and analyzed by flow cytometry with antibodies known to identify APCs. RESULTS: The most common CD45(+) retinal cells were CD11b(+), F4/80(+), CD8 alpha(+), CD80(+), and major histocompatibility complex (MHC) class II(lo), a phenotype characteristic of central nervous system (CNS) microglia (MG). There was also a small population of DEC-205(+) cells and a smaller number of CD11c(+) cells, both markers of dendritic cells (DCs). IC inoculation of IFN-gamma led to an increase in the number of CD45(+) cells and a modest upregulation of MHC class II on CD11b(+) cells. IC inoculation of anti-CD40 also increased the total number of CD45(+) cells and the number of CD11b(+) cells, but increases in CD80 and MHC class II expression on CD11b(+) cells were insignificant. After anti-CD40 treatment, CD45(hi)11c(+) cells increased in number and altered their expression of CD11b. CONCLUSIONS: Retinal MG were readily identified as the most numerous population. A small population of cells with perivascular cell (PVC)-like properties was found. They were CD45(hi)11c(+), some had elevated MHC class II, and they were affected by anti-CD40 treatment in vivo. No conventional DCs were found, although there was a distinct DEC-205(+) population. Overall, the effects of IFN-gamma and anti-CD40 treatment were attenuated in the retina in vivo and also on CD45(+) cells in culture, compared with the control.

Animals↗
PubMed2001

Investigation of human spleen dendritic cell phenotype and distribution reveals evidence of in vivo activation in a subset of organ donors.

Although the mouse spleen dendritic cell (DC) is perhaps the most intensively studied DC type, little has been published concerning its human equivalent. In this report, rare event flow cytometry and in situ immunofluorescence were used to study the surface phenotype and distribution of HLA-DR(+) CD3(-)14(-)16(-)19(-) human spleen DC. Spleens from organ donors with different clinical histories were used. Most (81% +/- 9%; n = 14) spleen DCs expressed high levels of the integrin CD11c. CD11c(+) DCs were distributed in 3 distinct regions-the peri-arteriolar T-cell zones, the B-cell zones, and the marginal zone, where they formed a ring of cells surrounding the white pulp, just inside a ring of CD14(+) red pulp macrophages, apparently more regularly organized than the previously described marginating DC population in the mouse spleen. The T-cell zones contained CD86(+) DCs, among which a subpopulation expressed CD83. These mature/activated CD86(+) DCs represented a minority (12% +/- 8%) of total spleen DCs in most organ donors: most spleen DCs are immature. In 3 of 18 (17%) donors, however, most (54%-81%) of spleen DCs were CD86(+), suggesting that in vivo DC activation had occurred. In one donor, a radical shift in DC distribution from the marginal zone to the T-cell zones was also observed. This activation of spleen DCs in vivo was reminiscent of the effects of experimental microbial product injection in mice, and it seemed to correlate with bacterial infection or multiple trauma. (Blood. 2001;97:3470-3477)

Adult↗
PubMed2000

CpG-DNA-mediated transient lymphadenopathy is associated with a state of Th1 predisposition to antigen-driven responses.

Infections can influence concurrent and subsequent Th1 vs Th2 immune responses to Ags. Through pattern recognition of foreign unmethylated CpG dinucleotides, the vertebrate innate immune system can sense infectious danger and typically replies with a Th1-polarized adaptive immune response. We examined whether CpG-DNA exposure would influence subsequent responses to infection and soluble Ags. CpG-DNA injection led to local lymphadenopathy characterized by maintenance of cellular composition with some biasing toward elevated dendritic cell composition. Sustained local production of IL-12 and IFN-gamma from dendritic cells and T cells was shown. Prior injection by up to 2 wk with CpG-DNA protected BALB/c mice from Th2 driven lethal leishmaniasis. CpG-DNA injection by up to 5 wk before soluble Ag challenge resulted in the generation of Ag-specific CTL, Th1 recall responses to Ag, and Th1-polarized Ag-specific Abs. Thus, CpG-DNA instigated a local predisposition for intense CTL responses and Th1-polarized immune responses to subsequent infections or Ag challenge. The induction by the innate immune system of a locally contained hypersensitivity could represent a capacitating immune reaction yielding rapid conditioned responses to secondary infections.

Adoptive Transfer↗
PubMed1989

Demonstration of the increase in serine esterase-positive T cells in hairy-cell leukemia patients undergoing alpha-interferon therapy.

An increased number of serine esterase non-B lymphocytes including CD4+ helper/cytotoxic cells were observed in hairy-cell leukemia patients during (56 +/- 18) and immediately post (52 +/- 16) alpha-interferon therapy compared with pretreatment status (17 +/- 5) and normal donors (29 +/- 3). This increase in lymphocytes bearing one of the putative cytotoxicity-linked proteins was paralleled by a higher cytotoxicity towards K562 cells in the NK and LDCC assays during therapy and similarly, but to a much reduced level, against the hairy-cell derived JOK-1 target cells. Phenotypically, a higher percentage of non-B cells also expressing DR or CD11 antigens were seen in the HCL patients during IFN therapy. In lymphocyte target binding assays, a high affinity of effector to target conjugate formation was observed when either of the hairy cell lines JOK-1 or Hair-M was chosen as targets for IFN-therapy effector cells. Although predominantly CD4+ cells exhibited the in vitro affinity for effector/target conjugation with autologous HCs, the polarisation of serine esterase activity towards the E/T membrane contact area was shown by both CD4+ and CD8+ cells during a short incubation period and before target cell death.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1993

Proliferation of human T lymphocytes induced with superantigens is not dependent on costimulation by the CD28 counter-receptor B7.

Staphylococcal enterotoxins, also known as superantigens (SAg), bind class II MHC molecules on APC and upon direct cell-to-cell contact stimulate proliferation of T cells expressing appropriate V beta gene products. The T cell surface molecule CD28 binds its costimulatory counter-receptor, B7 expressed on APC, and augments IL-2 production and T cell growth. Although the role of B7 costimulation during Ag-specific responses of T cells is established, its involvement during the activation of T cells with SAg has not been examined. Using a soluble Ig C gamma 1 chimera of CTLA-4, a second receptor for B7 and a homologue of CD28, this study examines the role of B7 expressed on APC during the induction of proliferation of CD4+ T cells upon stimulation with SAg (SAg/staphylococcal enterotoxins). CTLA-4lg, which has a higher avidity for B7 than CD28, had no effect on the synthesis of IL-2 as well as proliferative responses of CD4+ T cells induced by SAg presented on allogeneic EBV-transformed B cells, and IFN-gamma-activated endothelial cells. In contrast, T cell proliferation induced by alloAg presentation by the same APC was significantly inhibited by CTLA-4lg. mAb directed at the CD11a/CD18 molecule inhibited both SAg-induced and alloAg-induced proliferation of T cells. AlloAg-primed CD4+ T cells, which expressed both class II MHC and intercellular adhesion molecule-1 but not B7, presented SAg to and induced proliferation of both resting and SAg-primed T cells. These responses were inhibited by mAb directed at CD11a/CD18 but not by CTLA-4 Rg. These results suggest that SAg-induced responses differ from those induced by alloAg in that they are not obligatorily dependent on the costimulation by B7. In contrast, adhesive interaction between CD11a/CD18 on T cells and its counter-receptor on SAg-presenting cells is necessary and probably sufficient to support SAg-induced proliferation of T cells.

Animals↗