Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CD57 Antigens”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Phenotypic properties and cytotoxic functions of human CD8+ cells expressing the CD57 antigen.

The CD8+CD57+ granular lymphocyte subset is significantly expanded in a number of clinical disorders. Because several studies have suggested that CD8+CD57+ cells might be in vivo primed, antigen-specific cytotoxic T lymphocytes, we have analyzed the phenotypic and functional properties of CD8+CD57+ cells. Using three-color flow cytometry, virtually all freshly isolated CD3+CD8+CD57+ cells were found to have phenotypic properties characteristic of 'naive' T lymphocytes; these cells coexpressed the CD45RA antigen, lacked expression of the CD45RO antigen, and expressed reduced levels of CD58 adhesion molecules. When purified CD45RA+ T cells were stimulated with alloantigens, approximately 50% of CD8+CD57- cells lost CD45RA antigen expression. In contrast, CD8+CD57+ cells (which were > 90% CD3+) remained CD45RA+. Although CD8+CD57+ cells could mediate lectin-dependent cytotoxicity, both before and after the mixed lymphocyte reaction cultures, CD8+CD57+ cells had no antigen-specific cytotoxic activity against allogeneic target cells; only the subset of CD8+CD57- cells which converted to the CD45RA- phenotype had specific cytotoxic activity. Interestingly, although CD8+CD57+ cells did not lyse allogeneic cells, 50-90% of these cells acquired HLA-DR antigen expression during the mixed lymphocyte reaction. This did not appear to be a passive effect produced solely by lymphokines, because soluble factors released by alloactivated T cells induced only modest HLA-DR expression on purified CD8+CD57+ cells. Thus, whereas CD8+CD57+ cells may become activated when in the milieu of an immunologically specific response, our data suggest that these cells do not develop into or appear to represent antigen-specific cytotoxic T cells.

Antigens↗

Immunolocalization of p53, glutathione S-tranferase pi and CD57 antigens in oral leukoplakia.

OBJECTIVE: The purpose of the present study was to evaluate the relationship between histological epithelial dysplasia, the immunolocalization of p53 and glutathione S-transferase pi on the immunolocalization of the CD57 antigen. MATERIALS AND METHODS: Seventy biopsies were included in the study and the streptavidin-biotin-peroxidase method was used to detect the antigens. RESULTS: The results demonstrated a significant relationship between p53, GST-pi positive staining with moderate/severe epithelial dysplasia. There was no relationship between p53 and GST-pi. The mean number of CD57+ lymphoid cells was higher in the lesions with increased epithelial dysplasia and positive for GST-pi. No difference was found regarding CD57 immunolocalization in leukoplakias positive and negative for p53. CONCLUSIONS: As the presence of CD57+ lymphoid cells are indicative of immunosuppression, our study suggests that the severity of epithelial dysplasia and positive immunolabelling for GST-pi are associated with local immune response alterations in oral leukoplakias. Our data also give support to the idea that GST-pi and p53 are not time-point related during oral cancer development.

Biomarkers, Tumor↗

Proliferation of IL-2 activated lymphocytes preferably occurs in aggregates by cells expressing the CD57 antigen.

Aggregates of lymphocytes were investigated in long-term cultures of IL-2 stimulated peripheral blood mononuclear cells. Cells in clusters formed broad contact areas where coated pits and vesicles were often detectable. Proliferating cells were preferably found in aggregates indicating that the cell clusters represent proliferation centres in which cell division may be promoted by accessory signal transduction mediated by the close cell-to-cell contact. In bulk cultures CD57+ cells yielded increased proliferation capacity compared to CD57- cells. In addition, CD57+ cells were preferably localized in aggregates where they occupied the same position at the periphery of the clusters than the proliferating cells, suggesting that both cell types may be identical. It is discussed that the CD57 antigen represents a differentiation marker which is upregulated when CD57- cells start to proliferate assisted in cell aggregates.

Antigens, CD↗

Modulation of T-cell adhesion markers, and the CD45R and CD57 antigens in human alcoholics.

Direct and indirect evidence indicates that T cells are altered in alcoholics. The most commonly reported changes under direct examination have been consistent with an increased level of activation as reflected by shifts in the ratio of common leukocyte antigen isoforms expressed at the cell surface, by increases in the expression of class II antigen, or by alterations in the expression of various adhesion molecules. Functional evidence for T-cell abnormality includes loss of delayed hypersensitivity and a number of findings attributed to dysregulation of B cells by alcoholic T cells; these include the widely reported distrubances of immunoglobulin production in vivo and a range of abnormal responses when T and B cells are combined in vitro. Detailed flow cytometric examination of T cells from alcoholics with or without active liver disease reveals a significant loss of L-selectin CD8+ T cells, but not usually of CD4+ T cells. There is an inverse increase in the expression of CD11b on the CD8+ cells that have decreased L-selectin+ percentages. Both CD8+ and CD4+ T cells in alcoholics display a significant loss of the CD45RA isoform and a gain of cells exhibiting the CD45RO isoform. Other surface alterations include increased expression of CD57, a marker most commonly associated on T cells with conditions of chronic increased antigenic exposure. It is argued that these and other T-cell alterations in alcoholics are cytokine-driven in part and result in T-cell differentiation states that are functionally inappropriate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Clinic and immunophenotypic studies on midline malignant histiocytosis].

OBJECTIVE: To understand the clinic opatholgic changes of midline malignant histiocytosis (MMH), and to explain the source of atypical lymphoid cells (ALC) of MMH, so as to search after the relation between MMH and malignant lymphoma. METHOD: Histopathologic section of 39 cases of MMH were taken HE staining and the histopathologic changes were obsered under microscope. The immunohistochemical staining was also used to examine the immunophenotype of ALC. RESULT: 1. Pathologic changes of MMH: coaglation necrosis and mixed inflammatory cells infiltration, with epithelial infiltration which distributed around the center of blood vessel were their characteristics. 2. Immunohistochemical staining result: 28 in 39 cases of MMH (71.8%) expressed the immunophenvtype of T-cell; among them 13 (33.3%) were finded both positive reaction to CD3 and CD57 antigens with ALCs at the same time. CONCLUSION: According to immunophenotypic studies, most ALCs came from proliferation and infiltration of atypical T cell. ALCs of MMH expressed not only T-cell markers (CD3), but also NK-associated antigen (CD57). MMH was a mucosa related peripheral T/NK cell lymphoma originally.

Adult↗

Phenotype of Hodgkin and Sternberg-Reed cells and expression of CD57 (LEU7) antigen.

Possible associations between the immunophenotype of Hodgkin (H) and Sternberg-Reed (S-R) cells, the expression of CD57 (Leu 7) antigen, and the presence of Epstein-Barr virus (EBV) were investigated in lymph node specimens from 50 cases of Hodgkin's disease (HD), including 26 cases of mixed cellularity and 24 cases of nodular sclerosis. Tissues were fixed in 10% neutral formalin, or/and B5 solution. H and S-R cells were CD30+, CD15+ (85% of the cases) and LCA (CD45). A proportion of neoplastic cells positive for either T-cell markers (CD3) or B-cell markers (CD20) was observed in 10% and 34% of the cases, respectively. Membrane positivity for CD57 antigen was found in H and S-R cells in 10 cases (8 cases of mixed cellularity, and 2 cases of nodular sclerosis). Such immunopositivity was only observed in B5-fixed sections. No staining for CD57 antigen was identified in H and S-R cells of any case with CD20 positive neoplastic cells. H and S-R cells of both CD57-positive and CD57-negative cases were further studied by immunohistochemistry for LMP1, by in-situ hybridization for EBER and by polymerase chain reaction (PCR) for EBV-DNA. No association was identified between the expression of CD57 antigen and the presence of EBV sequences, transcripts or proteins. Our findings do not support a B-cell origin for H and S-R cells in CD57-positive cases of Hodgkin's disease and suggest that these neoplastic cells may be related to natural killer (NK) or T-cells expressing CD57 antigen.

Antigens, CD↗

Selective alterations in natural killer cell subsets in patients with atopic dermatitis.

We examined the immunophenotypic characteristics of natural killer (NK) cell subsets in patients with severe atopic dermatitis (AD), rhinitis allergica (RA) and in healthy controls. Expression of CD16, CD56 and CD57 antigens on peripheral blood lymphocytes was evaluated by simultaneous double immunocytofluorometry. Our results showed significantly lower percentages of cells with CD16, CD56 and CD57 surface antigens in patients with AD. Furthermore subdivision of the AD group into two subgroups, AD1 and AD0 (with and without antigen-specific IgE antibodies against potent inhalative allergens, i.e. mite, grass, rye, birch, cat) revealed that patients of subgroup AD1 showed a more prominent decrease compared to that of subgroup AD0. Moreover, we found a significant negative correlation between the percentage of CD56 + CD16 + NK cells and total IgE levels in serum, which were significantly higher in patients of subgroup AD1 than in AD0. NK cell activity was deficient in patients with AD but there was no difference between both subgroups. These data indicate that considerable heterogeneity in immunologic regulation may exist in patients with AD with regard to their NK cell subsets.

Adult↗

Large granular lymphocytes (LGLS) activity in women with spontaneous abortions during the 1st trimester of gestation.

BACKGROUND: Despite increasing knowledge about the cell subsets that exist in the decidua in normal early pregnancy, little is known about the decidual cell subsets in women with spontaneous pregnancy failure. Decidual large granular lymphocytes (LGLs) are the most abundant lymphoid cell type found in 1st trimester maternal decidua. The function of LGLs remains controversial although freshly isolated LGLs have been shown to exert a weak natural killer cell (NK) activity. METHODS: Decidual leukocytes were investigated in 15 cases of spontaneous abortion and 15 cases of voluntary miscarriage, at 8th, 10th and 12th gestational week using a panel of monoclonal antibodies against Granzyme B (GRAN-B), CD2, CD38, CD56, and CD57 antigens and the immunoperoxidase technique. LGLs were demonstrated with the phloxine-tartazine stain. RESULTS: There was a statistically significant increase in the number of CD56 and CD57 positive cells (33.3%) to the advantage of spontaneous abortions (p<0.0001). No statistically significant difference was found in the number of GRAN-B, CD2 and CD38 positive cells in normal early pregnancy and in spontaneous abortion (overall gestational age p=0.22, 8th gestational week p=0.18, 10th and 12th gestational week, p=0.091). CONCLUSIONS: Our findings confirm previous studies referring that LGLs may have a cytotoxic activity similar to the NK activity and suggest an adverse pregnancy outcome.

Abortion, Spontaneous↗

Ultrastructure of CD57+ cells isolated from human tonsils or blood.

The presence of CD4+, CD57+ T cells in the germinal centers has been reported by several authors. The CD57 antigen is also expressed by natural killer (NK) cells. We purified CD57+ cells from human tonsils and blood by microdissection, rosetting with sheep red blood cells and magnetic cell sorting (MACS) and examined the ultrastructural morphology of these cells. Clear differences were found in cell aspect: blood NK contained large granules which were not found in the tonsillar CD57+ cells. These latter appeared medium-sized and not fully activated. After immunolabeling, the tonsillar CD57+ cells were mainly found in the light zone of the germinal centers.

Antibodies, Monoclonal↗

CD57+ cells in radicular cyst.

AIM: As CD57 antigen is an important modulator of the immune system, the purpose of the present study was to compare the expression of this antigen on radicular cysts (RC) with hyperplastic or atrophic epithelium. METHODOLOGY: Twenty cases of RC were retrieved and classified as atrophic or hyperplastic. A biotin-streptavidin amplified system was used for identification of the CD57 receptor. RESULTS: The results demonstrated a greater percentage of CD57+ cells in RC with atrophic epithelium compared to hyperplastic epithelium. CONCLUSION: As the expression of CD57 is indicative of immunosuppression, it may constitute a negative immunomodulator of RC's epithelium growth. Further studies are necessary to understand the importance of this cell to the biological activity or inactivity of RC's epithelium development.

CD57 Antigens↗

Phenotypic, functional and molecular analysis of CD3- LGL expansions indicates a relationship to two different CD3- normal counterparts.

In this study we have analysed the CD3 and TCR transcript expression in three CD3- large granular lymphocyte (LGL) expansions. These LGL populations show a heterogenous attern of expression for CD2, CD8, CD16, CD56 and CD57 antigens. LGL1 is CD2+CD8-CD16+CD56+CD57+, while LGL2 is CD2-CD8+CD16-CD56-CD57-; LGL3 is similar to LGL1, except for CD8 antigen expression. Functional analysis has revealed a different behaviour of these LGL expansions in a cytotoxicity assay against the NK-sensitive K562 cell line. LGL1 and 3 display a significant NK-like activity, while LGL2 is inefficient against K562 target cells. TCR and CD3 transcript characterization of LGL expansions 1 and 3 showed that they expressed multiple TCR delta transcripts, a non-functional TCR beta transcript, CD3-zeta and -epsilon mRNA, but they lacked CD3 delta transcript and they lacked or expressed at very low levels of CD3 gamma transcript. On the other hand, LGL2 expressed TCR delta, CD3-gamma, -epsilon and -zeta transcripts, while it lacked CD3 delta mRNA. On the basis of these data, LGL1 and 3 seem to be closely related to peripheral blood mature natural killer (NK) cells, whereas LGL2 displays a pattern of TCR and CD3 expression similar to that found in CD1-2-3-4-8-16-thymocytes.

Adult↗

Human germinal center CD4+CD57+ T cells act differently on B cells than do classical T-helper cells.

We have isolated two subtypes of helper T cells from human tonsils: CD4+CD57+ cells, mostly located in the germinal center (GC), and CD4+CD57- cells, distributed through the interfollicular areas but also present in the GC. In a functional study, we have compared the capacities of these T-cell subtypes to stimulate B cells in cocultures. In order to block T-cell proliferation while maintaining their activation level, we pretreated isolated T cells with mitomycin C prior to culture in the presence of B cells and added polyclonal activators such as PHA and Con A, combined or not with IL-2. Contrary to CD4+ CD57- cells, CD4+CD57+ cells did not markedly enhance B-cell proliferation. Even when sIgD.B cells typical of germinal center cells were tested, the CD4+CD57+ cells had no significant effect. This is in accordance with the location of these cells: They mainly occupy the light zones of the GC where few B cells divide. Even when added to preactivated, actively proliferating cells, CD4+CD57 cells failed to modulate B-cell multiplication. On the supernatants of B-cell-T-cell cocultures, we examined by the ELISA technique the effect of T cells on Ig synthesis. Contrary to CD57+ T cells, whose effect was strong, CD57- T cells weakly stimulated Ig synthesis. More IgM than IgG was generally found. Because CD57 antigen is a typical marker of natural killer cells, we tested the cytolytic activity of tonsillar CD4+CD57+ cells on K562 target cells. Unlike NK cells, neither CD4+CD57+ nor CD4+CD57- cells exhibit any cytotoxicity. Thus, germinal center CD4+CD57+ cells are not cytolytic and do not strongly stimulate either B-cell proliferation or Ig secretion. CD4+CD57- cells, however, enhance B-cell proliferation and differentiation, thus acting like the classical helper cells of the T-dependent areas.

B-Lymphocytes↗

CD8+/CD57 cells and apoptosis suppress T-cell functions in multiple myeloma.

The aim of this study was to evaluate the role of CD8+/CD57+ lymphocytes in the immune dysregulation of multiple myeloma (MM). Cytofluorimetry of peripheral blood lymphocytes (PBL) purified from 39 MM patients showed an inverse relationship between the percentage of CD8+/CD57+ cells and CD4/CD8 ratio. Analysis of their activation antigens revealed that they were prevalently HLA-DR+ and Fas+. Removal of CD8+/CD57+ cells from MM PBL significantly improved cell proliferation and pokeweed mitogen (PWM)-induced polyclonal Ig production in vitro, whereas the addition of supernatants from patients' CD8+/CD57+ cell cultures to normal PBL suppressed both the PWM-driven Ig synthesis and the proliferative rate of stimulated PBL, supporting the contention that CD8+/CD57+ cells release in vitro an inhibitory factor that is directly involved in T-cell regulatory function. However, since the proliferative recovery of PWM- and phytohaemagglutinin (PHA)-stimulated MM PBL in the absence of CD8+/CD57+ lymphocytes was only partial, a dysregulated activation-induced apoptosis was anticipated. In fact, patients' PBL displayed an increased susceptibility to apoptosis and this was significantly enhanced after PWM and, even more, after PHA stimulation. Analysis of CD57 antigen expression on apoptotic or viable cells demonstrated a substantial defect of apoptosis in the CD8+/CD57+ population. Our results indicate that both the immunosuppressive effect of CD8+/CD57+ cells and the enhanced susceptibility to apoptosis of PBL could be involved in the pathogenesis of the immunodeficiency observed in this disease.

Apoptosis↗

Increased percentage of CD3+, CD57+ lymphocytes in patients with rheumatoid arthritis. Correlation with duration of disease.

OBJECTIVE: To determine whether a small CD3+ lymphocyte population expressing 110-kd CD57 antigens (HNK1) is expanded in patients with rheumatoid arthritis (RA), as it is in patients who have undergone bone marrow transplantation and patients with the acquired immunodeficiency syndrome, and to investigate whether it is involved in the pathogenesis of RA. METHODS: The phenotype of CD3+, CD57+ lymphocytes was analyzed by flow cytometry, and correlations between the percentage of these cells in the blood and various clinical and biologic parameters were investigated. RESULTS: The percentage of CD3+, CD57+ lymphocytes was increased in RA patients compared with controls. These lymphocytes expressed T cell receptor alpha/beta. Eighty percent expressed the CD8 accessory molecule, and 20% expressed the CD4 accessory molecule. The leukocyte common antigen CD45RA isoform was expressed by these CD3+, CD57+ lymphocytes in blood. The HLA-DR antigen was expressed in synovial fluid but not in blood. Finally, the percentage of these lymphocytes in the blood correlated with the duration of RA. CONCLUSION: The expansion of the CD3+, CD57+ lymphocyte population and their activation in the synovial fluid of RA patients suggest that these cells are involved in the inflammatory process.

Adult↗

Cytotoxic perforin+ and TIA-1+ infiltrates are associated with cell adhesion molecule expression in dilated cardiomyopathy.

OBJECTIVE: To phenotypically characterize cytotoxic T-lymphocytes (CTLs: Perforin+ and TIA-1+ phenotypes) and to study the interactions with cell adhesion molecules (CAMs) in dilated cardiomyopathy (DCM). BACKGROUND: DCM is linked to intramyocardial inflammation, being characterized by T-lymphocytic infiltration and CAMs abundance. However, the pathogenic significance of increased CD3+ lymphocytes remains obscure as these do not correlate with CTLs (perforin+ and TIA1+ phenotypes). CAMs participate in the phenotypic repertoire and effector pathways of CTLs. METHODS: CAMs-expression (ICAM-1, VCAM-1, LFA-3, CD29, CD62E and CD62P and beta(2)-integrins), CD3+ (T-lymphocytes), CD57+ (NK-cells) and adhesion related (CD18+, CD11a+, CD11b+, CDw49d+) phenotyped infiltrates were investigated in endomyocardial biopsies (EMBs) from 89 DCM patients (33 female; LVEF<40%) using immunohistochemisty. The enteroviral genome was identified by nested RT-PCR. RESULTS: CAMs abundance was confirmed in 55 DCM patients (62%) and 29 EMBs (33%) were graded CTLs+ (>1.5 TIA-1+ and/or >2.0 perforin+ infiltrates/hpf). CTLs correlated with all endothelial CAMs-markers studied (P<0.01), the adhesion related phenotypes of infiltrates (LFA-1, VLA-4, CD18) and CD57+ NK-cells (P<0.02). There was no correlation of CTLs with CD3+ T-lymphocytes, CD11b+ macrophages, enteroviral infection (present in n=16/18%), clinical history and LVEF (P>0.05). Phenomena suggestive of CTLs mediated myocytolysis were observed in 10 patients (11%). CONCLUSIONS: CTLs-infiltrates are associated with endothelial CAMs-abundance and co-express adhesion related (beta2-integrins, VLA-4) and NK-cellular antigens (CD57) in DCM. Endothelial CAMs expression also reflects cytotoxic activation of intramyocardial infiltrates, which is not reflected by immunologically nai;ve CD3 T-lymphocytes.

Aged↗

CD57+ T lymphocytes are derived from CD57- precursors by differentiation occurring in late immune responses.

CD3+ T cells expressing the 110-kDa CD57 antigen are found in survivors of renal, cardiac and bone marrow transplants, in patients with acquired immune deficiency syndrome and in patients with rheumatoid arthritis. They are also present in normal individuals and expand upon ageing. They do not grow in culture and their role in the immune response is poorly understood. The expression of the various isoforms of the leukocyte common antigen (CD45) identifies a spectrum of differentiation in CD4+ and CD8+ T cells ranging from naive (CD45RA+CD45RBbrightCD45RO-) through early primed cells (CD45RA-RBbrightROdull) to highly differentiated memory cells which are CD45RA-RBdullRObright. CD45 isoforms expressed by CD57+ T cells showed distinct differences between CD4+ and CD8+ populations, but in each case indicated an advanced state of differentiation. The expression of T cell receptor V beta families was highly variable between individuals, but both CD57+ and CD57- cells show a full range of the specificities tested. V beta expression was more closely related within either the CD4+ or the CD8+ subsets, irrespective of CD57 expression, than between these subsets, suggesting a relationship between CD57+ and CD57- cells within the same T cell pool. This possibility was supported by experiments showing that CD3+CD57+ lymphocytes were similar to CD3+CD57- T cells in terms of the production of basic T cell cytokines [interleukin (IL)-2, IL-4, and interferon-gamma]. Furthermore, in vitro stimulation of CD3+CD57- T cells in secondary mixed leukocyte reaction or by co-culture with IL-2 and IL-4 induced the appearance of CD3+CD57+ cells with phenotypic and functional similarities to in vivo CD3+CD57+ cells. These data strongly suggest that the expression of CD57 is a differentiation event which occurs on CD57- T cells late in the immune response.

Antigens, CD↗

Evidence for in vivo clonal proliferation of unique population of blood CD4-/CD8- T cells bearing T-cell receptor alpha and beta chains in two normal men.

Rare T lymphocytes bearing CD3 surface antigen and T-cell receptor (TCR) alpha and beta chains, but lacking both CD4 and CD8 antigens, viz, TCR alpha beta+CD4-8- cells, appear at a frequency of 0.1% to 2% in peripheral blood TCR alpha beta+ cells of normal donors. Here we report two unusual cases, found among 100 healthy individuals studied, who showed an abnormally elevated frequency of these T cells, ie, 5% to 10% and 14% to 19%. Southern blot analyses of the TCR alpha beta+CD4-8- clones all showed the identical rearrangement patterns for each individual, demonstrating that these are derivatives of a single T cell. The same rearrangement patterns were also observed for the freshly isolated lymphocytes of TCR alpha beta+CD4-CD8- fraction, which excludes the possible bias in the processes of in vitro cloning. These TCR alpha beta+CD4-8- T cells were found to express other mature T-cell markers such as CD2, CD3, and CD5 antigens, as well as natural killer (NK) cell markers (CD11b, CD16, CD56, and CD57 antigens) for both individuals. Further, although lectin-dependent or redirected antibody-dependent cell-mediated cytotoxicities were observed for both freshly sorted lymphocytes of TCR alpha beta+CD4-8- fraction and in vitro established clones, NK-like activity was not detected.

Antigens, CD↗