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At least 1,243 records · Page 69Linked to original sources
PubMed1988

Expression of CR2 (C3d receptor) on the cell membranes of adult T cell leukemia.

MT-2 cells, which produce human T-cell lymphotropic virus type I (HTLV-I), are known to have a complement receptor. We have established that the complement receptor is CR2 which binds C3d on immune complexes but not CR1. CR2 was also detected on ATL-3I cells but no complement receptor was detected on ATL-1K cells which lack ATL antigen (ATLA). Since CR2 is not detectable on normal T lymphocytes, the presence of CR2 on some ATL cells might suggest that ATL cells were derived from a particular minor lineage of T cells, or HTLV-I has a capacity to induce CR2, which has been demonstrated to be an a-type growth factor for B lymphocytes and to be a receptor for Epstein-Barr virus.

Antigens, Differentiation, B-Lymphocyte↗
PubMed2006

Murine Fc receptors for IgG are redundant in facilitating presentation of immune complex derived antigen to CD8+ T cells in vivo.

Antigen(Ag)-immunoglobulin (Ig)G complexes (IC) are more efficiently processed and presented than soluble Ag. IC can bind to various cell types via different types of Fc-Receptors or, upon binding to complement factors, by complement receptors. Murine professional antigen-presenting cells (APC) express four types of FcgammaReceptors (FcgammaR) via which they are able to capture IC; three activating receptors (FcgammaRI, III and IV) and one inhibitory receptor (FcgammaRII). It has been demonstrated that FcgammaR play a pivotal role in facilitating the presentation of Ag derived from IC. Nonetheless, relative little information is available on the relative contribution of the activating or inhibitory FcgammaR or complement to the presentation of immune-complexed Ag to CD8+ T cells. To study the contribution of the different FcgammaR and complement receptors in IC-facilitated Ag-presentation, we analyzed the ovalbumin(OVA)-specific CD8+ T cell proliferation in FcgammaR- and complement component 3 (C3)-deficient mice after subcutaneous injection of OVA-IC. Here we show that the efficient Ag-presentation was FcgammaR-, but not C3-mediated, as it was inhibited in FcgammaRI/II/III-deficient mice but unaffected in the C3-depleted mice. Moreover, FcgammaRIV does not play a role under these conditions. However, no difference was found between wild-type and FcgammaRI/III-deficient or wild-type and FcgammaRII-deficient mice. These results indicate that Ag-presentation via the activating FcgammaR is not enhanced in the absence of FcgammaRII, and point to redundancy of the FcgammaR, including FcgammaRII, in the uptake and presentation of s.c. injected soluble IC to CD8+ T cells.

Animals↗
PubMed2005

Phenotypic perturbation of B cells in the Wiskott-Aldrich syndrome.

Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency/platelet disease due to mutations of WASP, a cytoskeletal regulatory protein of blood cells. Patients exhibit a range of immune defects generally attributed to defective T-cell function, including poor response to immunization, skewed immunoglobulin isotypes, eczema, recurrent infections, autoimmune disease and increased frequency of malignancies. Here we show a deficit of total B-cells in WAS patients of various ages and identify phenotypic perturbations involving complement receptors and CD27. Whereas B-cells of normal healthy donors are overwhelmingly CD21/CD35-positive, B-cells expressing these receptors are significantly reduced in number in WAS patients, and their paucity may cause suboptimal antigen capture and presentation. The frequencies of IgD(-) and IgG(+) patient B-cells were not different from healthy donors (although absolute numbers were decreased), indicating that isotype switching is occurring. In contrast, the frequency of cells positive for CD27, the marker of post germinal centre B-cells, was significantly decreased even among isotype-switched cells, and B-cells resembling germinal centre progenitors (CD10(+)CD27(-)CD38(bright)) were more frequent in adult patients, suggesting impaired germinal centre maturation/differentiation. The documentation of these phenotypic perturbations and deficit of total cells suggest that defects intrinsic to B-cells contribute to the impaired humoral immunity that characterizes this disease.

Adult↗
PubMed1988

C3 receptors on macrophages.

The complement receptors on macrophage are responsible for their binding and ingestion of opsonized targets. The two established receptors are CR1, which recognizes C3b, and CR3, which recognizes iC3b, the natural product of C3b from cleavage by the complement control protein factor I and its cofactors. CR1 belongs to a group of proteins that contain a structural element characterized by its size of 60-65 amino acids, and four conservatively positioned cysteines, which engage in a self-contained 1-3, 2-4 disulphide arrangement. This structural unit is called SCR (short consensus repeat) and is found in the complement proteins C1r, C1s, C2, factor B, factor H, C4BP, DAF, MCP and CR2, each of which interacts with some cleavage products of C3 and/or C4. CR1 has 30 SCR units accounting for its entire extracellular structure. It has a transmembrane segment and a small cytoplasmic domain. CR3 is a heterodimer containing an alpha and beta subunit held together by non-covalent forces. The beta subunit is also found in the two leukocyte antigens, LFA-1 and p150,95, which have alpha subunits distinct from that of CR3. The beta subunit contains 56 cysteine residues, 42 of which lie in a span of 256 residues immediately adjacent to the transmembrane segment. It shares extensive sequence homology with subunits of membrane protein complexes that bind fibronectin and vitronectin, implicating that they all belong to an extended set of surface adhesion molecules not restricted to the immune system. p150,95 is also expressed on macrophages and it has iC3b binding activity. It also shares some functional properties with CR3 as an adhesion surface molecule.

Chemical Phenomena↗
PubMed2003

Altered regulation of Fc gamma RII on aged follicular dendritic cells correlates with immunoreceptor tyrosine-based inhibition motif signaling in B cells and reduced germinal center formation.

Aging is associated with reduced trapping of Ag in the form of in immune complexes (ICs) by follicular dendritic cells (FDCs). We postulated that this defect was due to altered regulation of IC trapping receptors. The level of FDC-M1, complement receptors 1 and 2, FcgammaRII, and FDC-M2 on FDCs was immunohistochemically quantitated in draining lymph nodes of actively immunized mice for 10 days after Ag challenge. Initially, FDC FcgammaRII levels were similar but by day 3 a drastic reduction in FDC-FcgammaRII expression was apparent in old mice. FDC-M2 labeling, reflecting IC trapping, was also reduced and correlated with a dramatic reduction in germinal center (GC) B cells as indicated by reduced GC size and number. Nevertheless, labeling of FDC reticula with FDC-M1 and anti-complement receptors 1 and 2 was preserved, indicating that FDCs were present. FDCs in active GCs normally express high levels of FcRs that are thought to bind Fc portions of Abs in ICs and minimize their binding to FcRs on B cells. Thus, cross-linking of B cell receptor and FcR via IC is minimized, thereby reducing signaling via the immunoreceptor tyrosine-based inhibition motif. Old FDCs taken at day 3, when they lack FcgammaRII, were incapable of preventing immunoreceptor tyrosine-based inhibition motif signaling in wild-type B cells but old FDCs stimulated B cells from FcgammaRIIB(-/-) mice to produce near normal levels of specific Ab. The present data support the concept that FcR are regulated abnormally on old FDCs. This abnormality correlates with a reduced IC retention and with a reduced capacity of FDCs to present ICs in a way that will activate GC B cells.

Aging↗
PubMed1992

Assessment and prognosis of rheumatoid arthritis.

Efforts continue to identify and consistently utilize those clinical, laboratory, imaging, and other features of rheumatoid arthritis that best reflect the disease process and its impact on individual patients. We seek descriptions that are accurate, reproducible, simple, sensitive, and predictive. Such assessments will lead to development of prognoses for individual patients and to more rational patient management. The past year has witnessed reemphasis of health status indexes (instruments) and other simple approaches to clinical assessment of patients, eg, use of standardized grip strength, button test, walk time, and modified articular indexes. Computed tomography and magnetic resonance imaging provided clinically important and otherwise unappreciated (but expensive) information about joint integrity and inflammatory disease with sensitivity and resolution considerably beyond conventional techniques. Laboratory assessment of patients included consideration or reconsideration of the utility of measurements of C-reactive protein, rheumatoid factors, immune complexes, complement receptors and complement activation products, antiperinuclear factors, trace elements, interleukins and interleukin receptors, soluble cell surface receptors, lymphoid cell phenotypes, and synovial immunohistology; all are important in the pathogenesis of rheumatoid arthritis and all have contributed variably to predicting patient outcomes. None were shown to be more clinically informative than erythrocyte sedimentation rate or C-reactive protein. The variables that have been associated with unfavorable prognosis for rheumatoid arthritis are also discussed. We hope that continued study will lead to identification and adoption of simple assessments that will prove to be powerful predictors of good or poor patient outcomes and stratification of patient risk. This uniform measure of disease assessment will improve judgments of potential benefits of therapeutic interventions.

Arthritis, Rheumatoid↗
PubMed1993

Expression of CD35 (CR1) and CD11b (CR3) on circulating neutrophils and eosinophils from allergic asthmatic children.

Complement receptors on neutrophils and eosinophils play a role in activation and adhesion. During asthmatic reactions these receptors have been found elevated on circulating granulocytes. In the present study we compared the expression of CD35 (complement receptor type 1) and CD11b (complement receptor type 3) on neutrophils and eosinophils from asthmatic and non-asthmatic children. This was done in whole blood samples using depolarized light scattering for the discrimination of neutrophils and eosinophils. The non-stimulated expression as well as the upregulated expression of receptors by the chemotactic peptide N-formylmethionyl-leucyl-phenyl-alanine (fMLP) were studied. The results showed that without prior stimulation only the expression of CD35 on neutrophils was significantly elevated in children with asthma (P<0.05). After up-regulation with fMLP, the CD11b expression on neutrophils (P<0.005, fMLP: 0.002 microM) and eosinophils (P<0.05, fMLP: 0.02 microM) was significantly higher in asthmatic children than in the controls. These results indicate that the inducible expression of CD11b on neutrophils and eosinophils from allergic asthmatic children is primed in vivo.

Asthma↗
PubMed1976

Subpopulations of human lymphoblastoid cell lines. Correlation with the expression of surface receptors and content of Epstein-Barr virus genome.

Forty lymphoblast cell lines derived from normal subjects, patients with infectious mononucleosis, leukemia, and Burkitt's lymphoma have been studied for surface receptors including surface Ig, complement receptors by the EAC rosette and fluorescent (Raji cell) techniques, and Fc (aggregate) receptor by direct and indirect immunofluorescence. Because of the B-cell tropism of the Epstein-Barr virus (EBV), an effort was made to correlate the expresion of various surface properties of lymphoblastoid cell lines with the content of EBV viral DNA as determined by complementary RNA-DNA (cNRA-DNA) hybridization on membrane filters or by DNA-DNA renaturation kinetic analysis. The only correlation established was with the Fc receptor determined by direct immunofluorescence. No correlation of EBV genome equivalents per cell with complement receptor or surface Ig was noted, suggesting that the expression of these receptors is not influenced by EBV viral DNA content. Subgroups of lymphoblastoid cell lines were on the basis of variable expression of surface receptors, designated B1, B2, B3, B4, and T. The distribution of lymphoblastoid cell lines into these subgroups were in the ratio of 14:4:1:4:1. The B1, B2, and B4 cell lines (except Molt 4F) were found to contain EBV. The B3 subgroup, for wich cell line 698 was the sole example, expressed surface immunoglobulins but no other B-cell characteristics, and H.S.B., a T-cell line, lacked detectable EBV.

Burkitt Lymphoma↗
PubMed1999

Epstein-Barr virus infection of human astrocyte cell lines.

Epstein-Barr virus (EBV) is implicated in different central nervous system syndromes. The major cellular receptor for EBV, complement receptor type 2 (CR2) (CD21), is expressed by different astrocyte cell lines and human fetal astrocytes, suggesting their susceptibility to EBV infection. We demonstrated the infection of two astrocyte cell lines, T98 and CB193, at low levels. As infection was mediated by CR2, we used two stable CR2 transfectant astrocyte cell lines (T98CR2 and CB193CR2) to achieve a more efficient infection. We have monitored EBV gene expression for 2 months and observed the transient infection of T98 and T98CR2 cells and persistent infection of CB193 and CB193CR2 cells. The detection of BZLF1, BALF2, and BcLF1 mRNA expression suggests that the lytic cycle is initiated at early time points postinfection. At later time points the pattern of mRNA expressed (EBER1, EBNA1, EBNA2, and LMP1) differs from latency type III in the absence of LMP2A transcription and in the expression of BALF2 and BcLF1 but not BZLF1. A reactivation of the lytic cycle was achieved in CB193CR2 cells by the addition of phorbol esters. These studies identify astrocyte cell lines as targets for EBV infection and suggest that this infection might play a role in the pathology of EBV in the brain.

Astrocytes↗
PubMed1998

Soluble form of complement C3b/C4b receptor (CR1) results from a proteolytic cleavage in the C-terminal region of CR1 transmembrane domain.

The complement C3b/C4b receptor (CR1) is an integral protein, anchored in the plasma membrane through a hydrophobic domain of 25 amino acids, but is also found in the plasma in soluble form (sCR1). A recombinant, soluble form of CR1 has been demonstrated to reduce complement-dependent tissue injury in animal models of ischaemia/reperfusion. In view of the important pathophysiological relevance of sCR1, we have investigated the mechanisms governing CR1 release by using various mutated and chimaeric receptors transiently expressed in COS cells. Pulse-chase experiments revealed that (1) sCR1 is produced by a proteolytic process, (2) the cleavage site lies within the C-terminus of CR1 transmembrane domain, (3) the proteolytic process involves a fully glycosylated CR1 form and (4) this process takes place in late secretory vesicles or at the plasma membrane.

Amino Acid Sequence↗
PubMed1979

Kinetics of B-lymphocytes stimulation by pokeweed Pa-1 mitogen and bacterial lipopolysaccharide.

The presence of two subpopulations in mouse B lymphocytes responding to pokeweed Pa-1 mitogen or bacterial lipopolysaccharide (LPS) in terms of DNA synthesis was demonstrated. The analysis of surface markers of these two subpopulations revealed that one of the subpopulations carried the complement receptor (CR+) and the other lacked the complement receptor (CR-). The kinetics of stimulation by Pa-1 and LPS differed between these two subpopulations. CR+ -B cells exhibited the first peak of DNA synthesis 27 h after the addition of the mitogen, whereas CR- -B cells showed the first maximal response after 39 h. When the responses of CR+ -B cells 27 h and of CR- -B cells 39 h after various pulsed exposures to the mitogen were compared with those after continuous exposures to the mitogen, two successive 3 h exposures (0-3 and 12-15 h for CR+ -B cells; 0-3 and 21-24 h for CR- -B cells) yielded the same level of response as continuous exposure for 27 h (CR+ -B cells) or 39 h (CR- -B cells). These results indicate that both B-cell subpopulations require two signals for maximal stimulation.

Animals↗
PubMed1978

Characteristics of complement receptor-bearing cells in the spleens of tumor-bearing mice.

In the course of mammary tumor development, a population of nylon nonadherent cells with CR appears in the spleens of tumor-bearing mice although none are ever detected in normal mice. These cells apparently arise in response to immunologic stimulation. In a series of studies we have further characterized subsets of T cells (CR+ and CR-) with regard to their responses to mitogens in the lymphocyte transformation assay. Nylon column nonadherent cells from the spleens of tumor-bearing mice were rosetted in a complement receptor assay using EAC rosetting, and CR+ cells were separated from CR- by centrifugation in a discontinuous Ficoll gradient. CR+ T cells responded strongly to PHA and Con A and in addition responded to LPS, an activity not usually associated with conventional T cells. In contrast, CR- T cells from tumor-burdened mice responded to PHA but failed to respond to Con A or LPS.

Animals↗
PubMed1978

Characterization of surface receptors on bovine leukocytes.

Three bovine leukocyte populations--peripheral blood lymphocytes (PBL), mammary gland polymorphonuclear neutrophils (PMN) and macrophages (Mo)--were characterized with respect to five surface markers: surface immunoglobulin (SIg), sheep erythrocyte receptor, complement (C) receptor and Fc receptors for both IgG and IgM. The majority of PMN and Mo possessed C and Fc receptors for IgG, but lacked SIg and the erythrocyte receptor. The PMN, but not Mo, also expressed a Fc receptor for IgM. The PBL were heterogeneous with respect to their surface characteristics and evidence was presented for the following subtypes: (a) cells with the E receptor alone; (b) cells with E receptor plus the Fc(IgG) receptor; (c) cells with SIg plus the C receptor but minus the Fc(IgG) receptor; (d) lymphocytes with SIg plus the C receptor and the Fc(IgG) receptor, and (e) cells lacking E receptors and SIg but bearing Fc(IgG). It was assumed, but not proven, that some of these latter cells must also bear the C receptor. The significance of the various cell types in antiviral defense is briefly discussed.

Animals↗
PubMed1996

Dehydroepiandrosterone modulation of lipopolysaccharide-stimulated monocyte cytotoxicity.

Dehydroepiandrosterone (DHEA), the predominant androgen secreted by the adrenal cortex, can be converted to both potent androgens and estrogens. In addition to its role as a precursor for other steroid hormones, DHEA has been proposed to play an important role in immunity. This study has investigated DHEA modulation of LPS-induced monocyte cytotoxicity. Cytotoxicity markers assessed include tumor cell killing, IL-1 secretion, reactive oxygen intermediate release, nitric oxide synthetase activity as measured by the release of reactive nitrogen intermediates, complement receptor-1 cell surface protein, and TNF-alpha protein presence. Monocytes stimulated with LPS concentrations of 1.0 micrograms/ml displayed the above cytotoxic markers, whereas monocytes stimulated with DHEA alone or with LPS at a lower concentration of 0.2 ng/ml did not. However, when used simultaneously, DHEA and LPS 0.2 ng/ml displayed a synergistic effect on monocyte cytotoxicity against cancerous cell lines, IL-1 secretion, reactive nitrogen intermediate release, complement receptor-1 cell-surface protein, and TNF-alpha protein to levels comparable with levels obtained using LPS 1.0 microgram/ml. Finally, Scatchard plot analysis demonstrated the presence of a DHEA receptor in monocytes, suggesting that DHEA effects on LPS-stimulated monocytes are mediated through a receptor-dependent process.

Adjuvants, Immunologic↗
PubMed1996

Enhancement of macrophage phagocytosis upon iC3b deposition on apoptotic cells.

Apoptotic cells activate homologous complement and are opsonized with iC3b. We assessed the effect of iC3b opsonization upon phagocytosis of apoptotic Jurkat cells by macrophages, which were differentiated from THP-1 cells by treatment with retinoic acid. Macrophage phagocytosis of apoptotic Jurkat cells was enhanced upon incubation of the apoptotic cells with normal human serum. The enhanced macrophage phagocytosis of normal serum-treated apoptotic cells was decreased by anti-human C3 F(ab')2 and anti-CR3 and anti-CR4 mAbs to the level of phagocytosis of those treated with complement-blocked serum. These results suggest that interaction between iC3b on apoptotic cells and complement receptor type 3 (CR3) and/or complement receptor type 4 (CR4) on macrophages could play an important role for the clearance of apoptotic cells by macrophages in vivo.

Apoptosis↗
PubMed1982

Ultrastructural localization of human complement C3b receptors in the human kidney as determined by immunoperoxidase staining with the monoclonal antibody C3RTo5.

The precise localization of human complement C3b receptors in human kidneys was investigated by means of indirect immunoperoxidase staining of frozen kidney sections with the monoclonal antibody C3RT05, which is specific for human C3b receptors. Transmission electron microscopy indicated that C3b receptors are located on the entire cell membrane of the visceral epithelial cells of the glomeruli.

Antibodies, Monoclonal↗