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PubMed2006

Putting the natural killer cell in its place.

Natural killer (NK) cells were originally described as 'null' lymphocytes, but we have increasing evidence of their role in recognizing pathogen, and our knowledge of NK cell receptors continues to expand exponentially. Human NK cells have many receptors for human leucocyte antigen (HLA) class I. These killer immunoglobulin-like receptors (KIRs) and CD94/NKG2 receptors can signal in both positive and negative ways to regulate NK cell functions. The inhibitory receptors are the best characterized, but even in these cases much of their functional biology remains elusive. In this review, some recent advances in terms of the three-immunoglobulin (3Ig)-domain KIRs are discussed. Natural cytotoxicity receptors (NCRs) are among the activatory receptors found on NK cells. While pathogen ligands for these receptors have been described, endogenous ligands remain elusive. NCRs and NKG2D, a receptor for stress-induced antigens, appear to play complementary functional roles in terms of NK cell activation. More recently described on NK cells are the Toll-like receptors. In particular, these receptors of the innate immune system allow NK cells to directly sense pathogen, and their ligation on accessory cells indirectly activates NK cells through cytokine production. It is becoming clear that none of these receptor systems functions in isolation and that it is the sum of the signals (which will reflect the pathogenic situation), in addition to the cytokine milieu, that will direct NK cell activation. The resulting cytotoxicity, cytokine production and direct cell-cell regulatory interactions with other cells of the immune system, for example dendritic cells, ultimately determine the role of the NK cell in the context of an overall immune response.

Cytotoxicity, Immunologic↗
PubMed1985

Defective leukocyte interferon response in children with recurrent infections accompanied by arthralgia.

Children with recurrent and/or unusually severe infections were investigated for possible defects in the interferon (IFN)-natural killer (NK) cell system. Two series, each of 13 children, were examined, one in 1982 and one in 1983. Healthy children, seven in 1982 and eight in 1983, served as controls. Peripheral blood mononuclear leukocytes were examined for IFN production induced by the IFN-alpha inducers Sendai virus and Escherichia coli and by the IFN-gamma inducers Concanavalin A and Lens culinaris lectin. None of these inducers discriminated patients from controls. However, the bacteria Staphylococcus aureus Cowan I (SACol), inducers of atypical IFN in null lymphocytes, yielded significantly lower IFN production in infection-prone children than in controls, particularly in children with recurrent infections accompanied by arthralgia. No differences in basal NK activity or in the in vitro enhancement of such activity by IFN-alpha were found between patients and controls.

Bacterial Infections↗
PubMed1979

Characterization of bovine leukocytes involved in antibody-dependent cell cytotoxicity.

By the use of cell surface markers combined with physical separation techniques, bovine mononuclear leukocytes active as K cells in antibody-dependent cell cytotoxicity were characterized. The most active cells were glass wool adherent and were presumed to be macrophages. In the glass wool nonadherent population, heterogeneity was detected with respect to the complement (C) receptor but all cells expressed the Fc receptor. The C receptor-positive population adhered to nylon wool but was not a B cell and was assumed to be monocyte. The C receptor-negative population, the true lymphoid K cell, was nonadherent to nylon and was suggested to be an Fc receptor-positive null lymphocyte. The results were compared to those obtained with other species.

Animals↗
PubMed1990

Effect of chemotherapy on cell counts in peripheral blood & bronchoalveolar lavage of patients with pulmonary tuberculosis.

Cell counts in peripheral blood and bronchoalveolar lavage fluid were estimated in 38 patients with active tuberculosis; 12 patients with tuberculosis who had successfully completed more than 9 months of chemotherapy with isoniazid, rifampicin, and ethambutol; 10 Mantoux negative bronchitic subjects; and 6 control subjects. There were 50 males and 16 females aged 16-50 yr. Age, haemoglobin, total and differential serum proteins, were comparable in the various groups. Patients with active tuberculosis had higher ESR and significantly raised absolute (2.24 +/- 0.13 x 10(3); P less than 0.05), B (0.56 +/- 0.03 x 10(3); P less than 0.01) and Null lymphocyte counts (0.56 +/- 0.05 x 10(3); P less than 0.01) in blood. After chemotherapy there was no significant change in lymphocyte counts (2.43 +/- 0.21; P greater than 0.05). In bronchoalveolar lavage (BAL) total cell counts were increased five fold in patients with active disease (40.8 +/- 5.79 x 10(4)/ml) and although these showed considerable reduction after therapy they were higher (18.33 +/- 4.73 x 10(4)/ml) than those in controls (8.3 +/- 1.2 x 10(4)/ml; P greater than 0.05). In bronchitic subjects, total cell counts and macrophage counts in BAL fluid were elevated (P less than 0.01; less than 0.05 respectively) but lymphocyte counts were comparable to controls (3.4 +/- 1.35 x 10(4)/ml vs 1.09 +/- 0.19 x 10(4)/ml; P greater than 0.05). Lymphocytosis in the bronchoalveolar lavage fluid of patients with pulmonary tuberculosis persisted even after adequate treatment.

Adolescent↗
PubMed1990

Prostaglandin E2, monocyte adherence and interleukin-1 in the regulation of human natural killer cell activity by monocytes.

Monocytes have previously been shown both to augment and suppress human natural killer (NK) cell activity depending upon the conditions. An interleukin-1/interleukin-2 (IL-1/IL-2)-dependent mechanism has been shown to be involved in the augmentative effect. In the current study, the role of the method of monocyte isolation was evaluated. Monocytes isolated by Percoll gradient centrifugation were ineffective for modulating NK activity, but monocytes isolated by adherence from most donors exhibited increased augmentation with increased interval of adherence (up to 1 h). However, monocytes isolated by adherence from certain donors reproducibly exhibited increased suppression with increased interval of adherence. The observation of augmentation was correlated with an increase in the balance between IL-1 production and prostaglandin E (PGE) production by the monocytes. The roles of PGE2 and IL-1 were therefore examined by mixing these cytokines with enriched null lymphocyte preparations in the absence or presence of monocytes in the NK assay system. The participation of PGE2 was further examined using monocytes treated with indomethacin (10(-6) M), and the participation of monocyte-membrane-bound IL-1 was evaluated using monocytes fixed with 1% paraformaldehyde. The results revealed that PGE2 production is involved in the suppression of human NK activity by human monocytes, and the functional balance between IL-1 and PGE2 determines whether suppression or augmentation is observed. The data of this and previous studies are consistent with the suggestion that membrane-associated IL-1 is the important IL-1 moiety for the augmentation of human NK activity by monocytes.

Adult↗
PubMed1979

[Dependence of the functional activity of immunocompetent mouse spleen cells on their hemopoietic microenvironment].

Accumulation of erythropoietic, granulopoietic cell elements, a change in the ration and absolute count of the T, B cells, and "null" lymphocytes, as well as a sharp inhibition of primary immune response were found in the spleen of CBA mice treated with antierythrocyte sera. The inductive phase of immunogenesis proved to be sensitive to the action of antierythrocyte sera. The data obtained apparently demonstrated the existence of a functional relationship between the immunocompetent spleen cells and their non-lymphoid hemopoietic microenvironment.

Animals↗
PubMed1984

Inhibition of phagocytosis by monoclonal antibodies to human myeloid differentiation antigens.

The influence of eight antimyeloid monoclonal antibodies on human leukocyte phagocytosis was investigated using flow cytometry. A granulocyte-specific monoclonal antibody, VIM-D5, inhibited the phagocytosis of both zymosan particles and Staphylococcus aureus in a dose-dependent fashion. In the presence of 5 micrograms/ml, the numbers of phagocyte-associated zymosan particles and bacteria were reduced by about 35% and 40%, respectively. Another monoclonal antibody, VIM-12, reacting with granulocytes, monocytes, and null lymphocytes, inhibited both granulocyte and monocyte phagocytosis of S. aureus. The inhibition was dose dependent, and in the presence of 10 micrograms/ml, the number of phagocyte-associated bacteria was reduced by about 40%. VIM-12 did not influence the phagocytosis of zymosan particles. Both VIM-D5 and VIM-12 inhibited the internalization phase of phagocytosis, whereas the attachment to the phagocyte surface was unaltered. The combined effect of VIM-D5 and VIM-12 was additive, amounting to about 70% reduction of phagocytosis of bacteria. The remaining six antimyeloid antibodies had no effect on leukocyte phagocytosis. The combined use of antimyeloid monoclonal antibodies and flow cytometry appears to be a promising tool for the study of phagocyte functions.

Antibodies, Monoclonal↗
PubMed1980

Cell-cell interactions in in vitro erythropoiesis.

Cell-cell interactions between T and null lymphocytes induce erythropoietin-stimulated differentiation of peripheral blood-derived erythroid progenitors. Monocytes do not inhibit the engagement of this differentiation. By the use of murine hybridoma antibodies, which are uniquely reactive with mature T lymphocytes, the dependence of immature peripheral blood BFU-E differentiation on mature T lymphocytes, or a T cell-conditioned medium is confirmed. Studies with the same antibody show that the more mature and numerous BFU-E found in marrow have no requirement for mature T cells or T cell-conditioned medium. These findings do not preclude the presence in bone marrow of immature T or even non-T cells which may serve as inducers of erythropoietin-dependent erythroid differentiation of mature marrow BFU-E.

Cell Communication↗
PubMedDate not supplied

Immunologic and functional features of the leukemic cell of hairy cell leukemia: evidence for a Null hypothesis.

We report results of the immunologic evaluation of three unusual patients with hairy cell leukemia (HCL) whose HC were surface immunoglobulin (slg) negative. Mononuclear cell preparations containing 82%, 51%, and 42% hairy cells (HC), respectively, were obtained from three males with the typical syndrome and characteristic tartrate-resistant acid phosphatase-staining HC. Monocyte features were lacking in that HC did not stain for alpha-napthylacetate esterase, lacked receptors for C3, failed to produce chemiluminescence, and produced decreased 51Cr release in antibody-dependent cellular cytotoxicity against human red cell targets. Receptors for sheep erythrocytes, a T-cell marker, were decreased. Evidence against a B-cell origin of HC was provided by low numbers of slg staining and C3 receptor-bearing cells. Our results favor the hypothesis that HC in these three patients represent neoplastic proliferation of Null lymphocytes. Such an origin may explain the heterogeneity of markers previously described on HC of patients with HCL.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1995

Early-onset multifocal inflammation in the transforming growth factor beta 1-null mouse is lymphocyte mediated.

Transforming growth factor beta 1 (TGF beta 1)-null mice die fro complications due to an early-onset multifocal inflammatory disorder. We show here that cardiac cells are hyperproliferative and that intercellular adhesion molecule 1 (ICAM-1) is elevated. To determine which phenotypes are primarily caused by a deficiency in TGF beta 1 from those that are secondary to inflammation, we applied immunosuppressive therapy and genetic combination with the severe combined immunodeficiency (SCID) mutation to inhibit the inflammatory response. Treatment with antibodies to the leukocyte function-associated antigen 1 doubled longevity, reduced inflammation, and delayed heart cell proliferation. TGF beta 1-null SCID mice displayed no inflammation or cardiac cell proliferation, survived to adulthood, and exhibited normal major histocompatibility complex II (MHC II) and ICAM-1 levels. TGF beta 1-null pups born to a TGF beta 1-null SCID mother presented no gross congenital heart defects, indicating that TGF beta 1 alone does not play an essential role in heart development. These results indicate that lymphocytes are essential for the inflammatory response, cardiac cell proliferation, and elevated MHC II and ICAM-1 expression, revealing a vital role for TGF beta 1 in regulating lymphocyte proliferation and activation, which contribute to the maintenance of self tolerance.

Animals↗
PubMed2004

Stat6(null phenotype) human lymphocytes exhibit increased apoptosis.

BACKGROUND: Inflammatory bowel disease (IBD) is associated with altered apoptosis and increased levels of Th1 cytokines (IL-12, TNF-alpha, and IFN-gamma). These proinflammatory events may result from dysfunctional IL-4/Stat6 signal transduction that normally promotes Th2 lymphocyte differentiation and consequential down-regulation of the immune response. The goal of the present study was to measure apoptosis, levels of relevant cytokines, and the effects of cytokine manipulation on apoptosis in cell lines derived from IBD patients that express dysfunctional Stat6 (Stat6(null phenotype)) and wild-type Stat6 (Stat6(high phenotype)). MATERIALS AND METHODS: Lymphocytes with Stat6(null phenotype) (n = 5) or wild-type (n = 5) status were cultured with and without the addition of exogenous cytokines or neutralizing antibodies (IL-12, TNF-alpha, and IFN-gamma). Apoptosis was determined by flow cytometry using Annexin V-PE dual staining. Cytokine levels were determined by ELISA. RESULTS: Stat6(null phenotype) cells exhibited increased apoptosis compared with wild-type cell lines (13.3% +/- 2.9 versus 4.5% +/- 0.4, P < 0.0001). Four of five Stat6(null phenotype) cell lines expressed 5- to 10-fold elevations in IL-12 and IFN-gamma. Addition of exogenous cytokines or neutralizing antibodies had no effect on apoptosis. CONCLUSIONS: Apoptotic cell death is elevated in Stat6(null phenotype) cell lines suggesting a role for Stat6 in apoptosis regulation, a previously unrecognized observation. Increased levels of IL-12 and IFN-gamma were found in the Stat6(null phenotype) cell lines; however, the apoptosis observed is not the consequence of increased IL-12, IFN-gamma, or TNF-alpha. Stat6(null phenotype) cell lines exhibit variably increased levels of these Th1 cytokines, consistent with their human source, and may be a valid source for investigations into IBD pathophysiology.

Antibodies↗
PubMed2000

Reduced gut intraepithelial lymphocytes in VLA1 null mice.

Very late antigen 1 (VLA1) is an integrin collagen receptor that is expressed by lymphocytes in several disease states. VLA1 blockade has been shown to ameliorate gut disease in experimental graft-versus-host disease. Here we show that in the VLA1 null mouse, which is generally healthy, there is a 50% reduction in gut intraepithelial lymphocytes (IELs) despite an otherwise normal lymphocyte distribution in peripheral blood and lymphoid organs. The gammadelta to alphabeta ratios of IELs are unchanged. We also find that IL2-stimulated splenocytes from VLA1 null animals show a deficiency in adhesion to fibrillar and basement membrane collagen as well as reduced proliferation in response to collagen substratum. These results suggest that some, but not all, intraepithelial lymphocytes require VLA1 to survive or proliferate within the gut epithelium or possibly to traverse the basement membrane.

Animals↗
PubMed1983

An apparent lack of HLA restriction in the stimulation of granulocyte-macrophage colony formation from normal human null cells by helper T lymphocytes.

Haemopoietic progenitor cells capable of producing granulocyte-macrophage (GM) colonies have been demonstrated in the 'null' lymphocyte population of normal peripheral blood. The helper and suppressor roles of different T cell subpopulations have been implicated in the regulation of granulopoiesis in disease as well as in normal individuals. However, it is not certain whether such interactions between T cells and progenitor cells are HLA-restricted. We undertook further investigation of the effect of T cell subpopulations (TG and TnonG) on GM colony formation in vitro. In particular, we studied the possibility of HLA restriction in this process. Our results demonstrate that the enhancement of GM colony growth by T lymphocytes is not restricted by HLA compatibility between T cells and null cells, that such stimulation is radio-sensitive and that it is provided by the TnonG cell subpopulation.

Adult↗
PubMed1996

Lymphocyte subsets and adhesion molecules in cutaneous inflammation induced by inflammatory agonists: correlation between E-selectin and gamma delta TcR+ lymphocytes.

Kinetic and phenotypic heterogeneity in leukocyte subsets and adhesion-molecule expression is characteristic of many inflammatory conditions. We have studied the effect of various cytokines and inflammatory agonists on the type of leukocyte present and the adhesion molecules expressed in acute lesions (up to 3 days old) in porcine skin by immunohistology. Four major histocompatability complex-homozygous inbred pigs received replicate intradermal injections of IL-1 alpha, TNF-alpha, PMA, or PHA. Injections were timed so that lesions were obtained at 2, 4, 9, and 24 hours. Another two animals were studied at time points up to 72 hours. Leukocyte subsets and endothelial adhesion molecules were visualized on cryosections by use of monoclonal antibodies and alkaline phosphatase immunohistologic techniques. Substantial heterogeneity in leukocyte phenotypes was observed with all agonists, with lymphocyte subsets showing the greatest variation. Thus, CD2+ and gamma delta TcR+ (Null) T lymphocytes were present in all lesions, but to a varying extent such that few T cells were seen after PMA injection, approximately equal proportions of each after TNF-alpha, but substantially more gamma delta TcR+ (Null) lymphocytes were noted after PHA administration. Endothelial adhesion molecules were also variously affected, with E-selectin (CD62E) being transiently up-regulated by IL-1 alpha but CD62E showed early and sustained expression after TNF-alpha and PHA administration. The E-selectin ligand was demonstrated on infiltrating gamma delta TcR+ lymphocytes by use of a recombinant porcine E-selectin. The L-selectin ligand, identified by the mAb MECA-79, was only observed in late acute sites (< 24 hours) of TNF-alpha and PHA. Endothelial expression of class II major histocompatability complex was also variously up-regulated by all agonists. The results underline the heterogeneity of leukocyte phenotypes and endothelial adhesion molecule expression in acute cutaneous lesions dependent upon the nature of the inflammatory agonist and indicate an association between endothelial E-selectin and the presence of a gamma delta TcR+ (Null) T lymphocyte subset.

Animals↗
PubMedDate not supplied

Enhanced sensitivity to oxidant-induced micronucleus frequency in elderly individuals is not associated with glutathione S-transferase M1 (GSTM1) null genotype in lymphocytes.

BACKGROUND: A large number of studies have demonstrated that various kinds of DNA damage accumulate during aging and that oxidative stress possibly contributes to this process. Glutathione S-transferase M1 (GSTM1) can prevent their possible effects on DNA via detoxification of reactive substances that induced oxidative stress. OBJECTIVE: To investigate the relationship between GSTM1 polymorphism and DNA sensitivity to oxidative stress with age, we used micronucleus (MN) frequency as a marker of DNA damage in lymphocytes from young and elderly subjects. METHODS: This study was performed in 30 young (age range 20-36 years) and 30 elderly (age range 66-87 years) healthy individuals who were chosen on the basis of their GSTM1 genotype (15 GSTM1 null and 15 GSTM1 positive for each group). Lymphocytes were cultured after Ficoll isolation and treated for 48 h with a 30-muM dose of cumene hydroperoxide (CumOOH), a dose that does not decrease cell viability. RESULTS: There was no significant difference in the MN frequency observed in control cultures from young and elderly individuals. However, the MN frequency in CumOOH-treated cultures was significantly higher in the elderly group than the young group (p < 0.001). No association was found between the GSTM1 phenotype and CumOOH-induced MN frequency. CONCLUSIONS: The results suggest that lymphocytes of elderly individuals are more susceptible to in vitro MN induction by CumOOH. However, this difference in susceptibility is not explained by the lack of GSTM1.

Adult↗
PubMed1983

The prognostic value of T-lymphocyte levels in malignant melanoma. A five-year follow-up.

Serial immunologic tests (active E-rosettes = T-Ea; total E-rosettes = T-Et; total lymphocytes and null cells) were performed every 3 months for 5 years on 113 melanoma patients. A significant reduction in absolute T-Ea, T-Et, null cells, and total lymphocytes was noted in the patients who died, by comparison with those who are still alive. The latter presented a significant reduction in absolute T-Et only, plus a significant increase in null cells when compared with normals. The 38 patients without metastases, at the end of the study, presented a reduction in T-Et and an increase in null cells compared with the normals, while the 75 patients with metastases presented a reduction in T-Et, null cells and total lymphocytes when compared with the patients without metastases and a reduction in T-Ea, T-Et, and total lymphocytes when compared with the normals. Null cells show a linear decrease in patients who died and a linear increase in those who survived. A total of 80.2% of patients with a fall in T-Et displayed metastases usually within 2 to 10 months (mean, 6.8). Patients with normal T-Ea, T-Et, and total lymphocyte values showed a significant prolonged survival when compared to those with lower values. In addition, survival seemed to be always a function of immunologic test values, irrespective of the tumor site.

Adult↗
PubMed1985

Preliminary clinical trial of autologous bone marrow transplantation after in vitro monoclonal antibody and complement treatments in null cell-type acute lymphocytic leukemia.

Autologous bone marrow transplantation (BMT) in null cell-type acute lymphocytic leukemia (Null-ALL) was carried out after depletion of leukemia cells from transplanted bone marrow. Patients' autologous bone marrow cells were harvested during remission and treated in vitro with complement and three monoclonal antibodies (NL-1, NL-22 and HL-47) reactive to Null-ALL cells, and then cryopreserved. Three patients were transplanted with the antibody-treated bone marrow cells during the first remission period after preconditioning with intensive chemotherapy and total body irradiation, while transplantations in two other patients, who were in poor clinical condition, were done during the fourth remission period and the third relapse, respectively. Good preservation of hematopoietic stem cells after antibody treatment and cryopreservation of bone marrow cells was demonstrated in all five cases studied. Clinically, prompt recovery of white blood cells and platelets was observed in the three patients who received BMT during the first remission period; two of them have continued remission (2 and 15 months), while the other relapsed after 7 months of remission. these results suggested that autologous BMT with these three antibodies may be an effective mode of therapy for Null-ALL patients.

Antibodies, Monoclonal↗