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Results for “CSF immune cells”

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At least 19 recordsLinked to original sources

PubMed2026

DNA methylation landscape of cerebrospinal fluid cells in multiple sclerosis: an epigenome-wide association study.

BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system in which DNA methylation may link genetic and environmental risk factors. METHODS: We profiled genome-wide DNA methylation in cerebrospinal fluid (CSF) cells from people with MS (pwMS) and matched controls. Differentially methylated positions (DMPs) and regions (DMRs) were integrated with transcriptomic data, T-cell chromatin annotations, and pathway analyses. Protocadherin gamma (PCDHγ) expression was assessed in primary CD4+ T-cell subsets and confirmed by flow cytometry. FINDINGS: We identified 2710 DMPs and 4330 DMRs associating with genes that were enriched in immune signalling, adhesion and migration processes, and were accompanied by corresponding RNA changes. MS-associated methylation changes enriched in the cohesin chromatin-regulation pathway localised to T-cell regulatory regions, and this pathway included multiple protocadherin (PCDH) genes, which displayed consistent methylation and expression changes in CSF cells of pwMS compared to controls. PCDHγ cluster gene expression was detected in CD4+ T-cell subsets, and flow cytometry confirmed PCDHγ protein expression in peripheral blood T cells. Moreover, co-expression analysis suggests a role of PCDH genes in aryl hydrocarbon receptor (AHR) signalling. Protein-level validation showed fewer PCDHγ-positive CD4+ T cells in pwMS and activation-induced PCDHγ upregulation after T-cell stimulation. INTERPRETATION: DNA methylation changes in CSF resident cells reflect dysregulated T cell activation and migration in pwMS and suggest involvement of protocadherin molecules in MS pathogenesis. FUNDING: European Research Council, Swedish Research Council, Swedish Brain Foundation, Swedish MS Foundation, Knut and Alice Wallenberg Foundation, European Union and others.

Humans↗

PubMed1992

M-CSF (monocyte colony stimulating factor) and M-CSF receptor expression by breast tumour cells: M-CSF mediated recruitment of tumour infiltrating monocytes?

Infiltrating immune cells in 30 primary human epithelial breast tumours were studied using specific anti-CD3 (T cells), anti-CD68 (macrophages), anti-CD57 (NK cells), and an anti-pan-B cell antibody (L26). The majority of tumour infiltrating inflammatory cells are T cells (40-50%) and monocytes/macrophages (15-35%). The macrophage specific chemo-attractant and growth factor CSF-1 is detected by immunohistochemical techniques (IHC) at the level of invasive breast cancer cells in 46/50 tumours but not at the level of in-situ (pre-invasive) cancer. A mosaic staining pattern was usually observed, with a very high expression in areas of obvious stromal invasion (90% cells positive) and absent or trace staining in intraductal carcinoma. Macrophages and plasma cells are equally intensely positive. In-situ hybridisation experiments confirm the production of CSF-1 (mRNA) by tumour cells and show the same pattern of expression. Expression of the CSF-1 receptor protein (fms) was also observed by IHC in 41/48 invasive tumours, albeit at weaker intensities than in tumour infiltrating monocytes/macrophages. A concomitant expression of both CSF-1 and fms in in-situ carcinoma was never seen (n = 14). It is therefore proposed that the associated expression of CSF-1 and its receptor may be linked to the invasive potential of breast cancer, the monocytic infiltrate being an indication of the quantitative importance of CSF-1 production by the tumour.

Antibodies, Monoclonal↗

PubMed1992

[Clinical and experimental study of qing wen oral liquid in the treatment of viral infectious fever].

110 cases of viral fever patients receiving Qing Wen oral liquid were observed. The total effective rate was 94.5% in comparing to 86.5% in the control group, P < 0.01. The shortening of time concerning both the beginning on the declining of fever and normalization of body temperature were obvious in comparison with the control. The remedy was also effective in improving symptoms and signs, alleviating renal failure, improving microcirculation and providing bi-directional regulation to the immune system, thus the progression of the disease was controlled. Animal experiments showed that Qing Wen oral liquid could protect the rabbits with hemorrhagic fever, delay the incubation period and the peak of fever, lower the febrile index and PGE content, improve the hemorheology and enhance the cell-mediated immunity in CSF.

Adult↗

PubMed1992

[Current aspects of neurosyphilis: therapy-resistant cases with high-dosage penicillin?].

The occurrence of atypical and abortive cases of neurosyphilis in the last two decades has tended to make this rather infrequent, treatable condition difficult to diagnose; therefore it is advisable to perform large-scale serologic tests among neurologic and psychiatric patients. The diagnosis is confirmed by the detection of treponema antibodies in the central nervous system (TPHA index, ITpA index). When serologic test results are positive, secondary diagnostic criteria are provided by pathologic CSF findings (elevated cell count, humoral immune reaction). The course of the disease and the CSF parameters are favourably influenced by appropriate therapy. Over the last two decades, there has been an increase in the number of reports of cases refractory to the low-dose penicillin treatment recommended by the WHO and the CDC until two years ago. There have also been reports of treponema resistance in association with this therapeutic strategy and furthermore of failure to detect CSF concentrations of penicillin capable of eradicating the spirochetes. Counter measures have been taken worldwide in the last few years in the form of high-dose penicillin therapy (approx. 20 million IU/day for 2 to 3 weeks), in the hope that this would eliminate the resistance. We observed two patients treated with 18 and 24 million IU penicillin for 10 and 14 days respectively. The pathogens remained resistant, and the disease continued to progress. In one of these cases, immunologic processes might have been predominantly responsible for the resistance to the treatment, while in the other resistant pathogens can be assumed to be responsible. Repeated courses of treatment with higher doses of penicillin and/or with ceftriaxone finally succeeded.(ABSTRACT TRUNCATED AT 250 WORDS)

Ceftriaxone↗

PubMed1991

Peptide antisera to human colony-stimulating factor 1 receptor detect ligand-induced conformational changes and a binding site for phosphatidylinositol 3-kinase.

A peptide antiserum (anti-A) directed to the intracellular, juxtamembrane region (residues 552 to 574) of the human colony-stimulating factor 1 receptor (CSF-1R) precipitated only ligand-activated, native receptors from solution but bound to unstimulated forms after their denaturation. Two peptide antisera (anti-KI1 and -KI2), directed to residues 679 to 700 and 701 to 721, respectively, in the CSF-1R kinase insert (KI) domain and including mapped sites of ligand-induced phosphorylation at Tyr-699 and Tyr-708, bound at least 80% of the receptor molecules expressed in either CSF-1-stimulated or unstimulated cells. Immune complexes formed with anti-KI1, anti-A, or a peptide antiserum to the CSF-1R carboxyl terminus (anti-C-ter) coprecipitated CSF-1R complexed to a phosphatidylinositol 3-kinase (PtdIns 3-K) from CSF-1-stimulated cells, whereas anti-KI2 serum did not. In an in vitro assay, binding of CSF-1R to PtdIns 3-K required receptor tyrosine phosphorylation but not CSF-1R-mediated phosphorylation of the lipid kinase, and the association was specifically blocked by anti-KI2 or antibodies to phosphotyrosine. Neither anti-KI1, anti-A, nor anti-C-ter serum inhibited binding. We conclude that (i) only a minority of ligand-activated receptors form a stable complex with PtdIns 3-K in vivo, (ii) efficient binding of the lipid kinase requires receptor tyrosine phosphorylation within the CSF-1R KI domain, and (iii) a region within the KI domain defined by residues 701 to 721 at least partially overlaps the PtdIns 3-K binding site.

Amino Acid Sequence↗

PubMed1991

Studies on monoclonal antibody against recombinant human granulocyte colony-stimulating factor.

Three hybridoma cell lines producing monoclonal antibodies (McAb) against recombinant human granulocyte colony-stimulating factor (rhG-CSF) have been established by fusing mouse myeloma cell line SP2/0 cells with spleen cells from a BALB/c mouse immunized with rhG-CSF. Ascites was obtained from BALB/c mice by injecting the hybridoma cells intraperitoneally. Three McAbs were purified by the caprylic acid-ammonium sulfate method. For each, the IgG subclass, valence and activity, molecular weight, specificity and affinity were determined. The applications of McAbs against rhG-CSF in the clinic and laboratory are discussed.

Animals↗

PubMed1975

Preparation and neutralization characteristics of an anti-CSF antibody.

Nine of ten rabbits immunized with a partially purified L-cell CSF had demonstrable titers of anti-CSF activity. In vitro the antibody was markedly inhibitory to both post-endotoxin mouse sera and several mouse tissue extracts. CSF containing conditioned media prepared from a number of sources showed variable inhibition suggesting that murine CSF's may be characterized by marked antigenic differences. Human sources of CSF were also inhibited thus indicating a degree of cross-reactivity between murine and human factors. These studies may provide the initial steps toward definition of the role of CSF in vivo.

Animals↗

PubMed1991

[Studies on monoclonal antibody against recombinant human granulocyte colony-stimulating factor].

Three hybridomas producing monoclonal antibodies (McAb) against recombinant human granulocyte colony-stimulating factor (rhG-CSF) have been established by fusing mouse myeloma SP 2/0 cells with spleen cells from a BALB/c mouse immunized with rhG-CSF. Ascites was produced from BALB/c mice by injecting substrain 2D4-B4 hybridoma cells intraperitoneally. The antibody was purified either by the caprylic acid-ammonium sulfate method or by euglobulin precipitation. The caprylic acid-ammonium sulfate method was superior to euglobulin precipitation in terms of purification and recovery of IgG. The 2D4-B4 McAb was determined to belong to the IgG3 subclass with a molecular weight of about 172,400 It was proved by Western Blot to react specifically with rhG-CSF. The stability and affinity of the McAb were analyzed as well. The potential clinical and experimental applications of this McAb are discussed.

Animals↗

PubMed1990

Establishment of specific monoclonal antibodies against recombinant human granulocyte colony-stimulating factor (hG-CSF) and their application for immunoperoxidase staining of paraffin-embedded sections.

Detection of granulocyte colony-stimulating factor (G-CSF), one of the substances responsible for proliferation and differentiation of granulocytes, has been performed up to the present by use of the granulocyte colony-formation assay, because of the lack of a specific anti-G-CSF antibody. This has prevented the advancement of biological investigations of cell dynamics linked to G-CSF, e.g., cell localization of G-CSF and its pathophysiological changes. In the present work, two monoclonal antibodies (MAb), 1E7 and 4A6, against recombinant human G-CSF (rhG-CSF) were developed by cell hybridization between NS-1 myeloma cells and splenocytes from a mouse immunized with rhG-CSF. 1E7 and 4A6 were shown to be reactive with hG-CSF but not with other CSF (hGM-CSF, hIL-3, and mouse GM-CSF) by Western blot analysis. An immunoperoxidase staining method using these MAb was then established. This method was applicable to frozen sections, paraffin-embedded sections, and cells fixed with 4% paraformaldehyde. Positive staining for G-CSF was observed in tumor cells secreting G-CSF and also in Chinese hamster ovary (CHO) cells transfected with hG-CSF cDNA. However, no staining was seen in tumor cells secreting no G-CSF, untransfected CHO cells, lung fibroblasts, or bone marrow stromal cells after short periods of culture. These results confirmed the immunospecificity of MAb 1E7 and 4A6 and the validity of their application to immunohistochemistry using paraffin-embedded sections.

Animals↗

PubMed1977

Cell-mediated cytotoxicity against measles virus in SSPE. I. Enhancement by antibody.

In patients with subacute sclerosing panencephalitis (SSPE) virus persistency has been explained by a blocking factor of specific cell-mediated immunity in SSPE serum and cerebrospinal fluid (CSF). In the present study the effect of SSPE serum and CSF on cell-mediated cytotoxicity against 51Cr-labeled allogenic measles virus-infected target cells was tested. Pretreatment of SSPE peripheral lymphoid cells by serum or CSF neither blocked nor increased measles-specific cytotoxicity when cells were subsequently tested in FCS containing tissue culture medium. However, killing activity was always enhanced after pretreatment of target cells or direct addition of serum or CSF to the cytotoxic assay. Enhancement was also observed with non-SSPE-derived measles antibodies. The effect was dependent on measles antibody concentrations. These results suggest that antibody-dependent killing by K cells is intact in patients with SSPE. It is possible that virus-infected brain cells are protected from an immune attack in vivo by antibody-induced antigenic modulation.

Antibodies, Viral↗

PubMed1991

Spontaneous release of granulocyte colony-stimulating factor (G-CSF) by alveolar macrophages in the course of bacterial pneumonia and sarcoidosis: endotoxin-dependent and endotoxin-independent G-CSF release by cells recovered by bronchoalveolar lavage.

Because granulocyte colony-stimulating factor (G-CSF) is known to induce granulopoiesis and activate mature neutrophils, this factor could be important in determining the number and functional activity of neutrophils at sites of lung disease. The purpose of this study was to evaluate the ability of lung immune and inflammatory cells to produce G-CSF, and to seek evidence for the spontaneous production of this factor by cells recovered by lavage from controls and patients with lung diseases in which neutrophils may play a pathogenetic role. Lavage cells from controls produced little G-CSF spontaneously. Alveolar macrophages (AM), but not lymphocytes, produced large amounts following endotoxin stimulation. Lavage cells from patients with respiratory failure associated with bacterial pneumonia, but not those with respiratory failure from noninfectious causes, spontaneously released G-CSF (32 +/- 24 and less than 1 U/10(6) AM, respectively). Lavage cells from five of 15 patients with sarcoidosis and one of five patients with diffuse pulmonary fibrosis also spontaneously released G-CSF, which could not be explained by endotoxin exposure. The release of G-CSF by endotoxin-dependent and -independent mechanisms could play a role in the recruitment and activation of neutrophils in bacterial pneumonia and participate in the pathogenesis of some interstitial lung diseases.

Adult↗

PubMed1977

Autoradiographic demonstration of proliferating cells in cerebrospinal fluid.

The proliferative activity of cells, isolated from 82 human CSF specimens, was examined by 3H-thymidine autoradiography. High labelling indices (LI) were found in acute viral meningitis (up to 8 per cent) and radiculitis (up to 6 per cent). CSF cell proliferation was also shown in the subacute stages of viral diseases and in other inflammatory processes (LI ranging from 0.5 per cent to 3 per cent). Most of the cells labelled from these CSF specimens were large lymphocytes, "lymphoid cells" and plasmacytes. Their presence in CSF is presumed to indicate an immune reaction. By the demonstration of a proliferative activity of these cells, aseptic inflammatory processes can be differentiated from "unspecific" pleocytosis. Because of a correlation between the LI of CSF cells and the stages of some inflammations, this method is suggested for an assessment of pregression or remission of chronic processes, e.g. "chronic meningitis" and multiple sclerosis. It can also be used in experimental research: the same type of mononuclear cells was labelled after having been cultured for 23 hours prior to the incubation with 3H-thymidine. Proliferating tumor cells as well as proliferating non-neoplastic mononuclear cells were demonstrated in CSF from various neoplastic diseases. In the clinical diagnosis of these processes, the method is of limited value. It proved very useful, however, for an assessment of the therapeutic effects of intrathecal cytostatic therapy. CSF specimens from non-inflammatory and non-neoplastic diseases regularly contained very few proliferating cells (LI: less than 0.1).

Autoradiography↗

PubMed1992

In vivo metabolic response of hepatic nonparenchymal cells and leukocytes to granulocyte-macrophage colony-stimulating factor.

This study investigates the in vivo glucose utilization of various immune-competent cells after an intra-arterial injection of a nonlethal dose (30 micrograms/kg body weight) of murine recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF). Injection of GM-CSF resulted in a rapid but transient reduction in the number of circulating neutrophils. After 20 min the number of neutrophils returned to normal values, and by 4 h it was about 80% greater than in time-matched saline-injected controls. One hour after the treatment, neutrophils were accumulated in the livers of GM-CSF-injected animals but not in control livers. In vivo glucose utilization by circulating neutrophils and mononuclear cells and various liver cell types was investigated by combining the 2-deoxyglucose tracer technique with cell isolation procedures. GM-CSF increased the in vivo glucose utilization of circulating and infiltrating neutrophils by more than 200%. Glucose utilization by circulating mononuclear cells was also doubled. After GM-CSF injection, glucose utilization by Kupffer cells was increased by 130% and by hepatic endothelial cells was increased by 60%. Indomethacin pretreatment blunted the hyperglycemia caused by GM-CSF injection; however, it did not inhibit the increased glucose utilization by immune-competent cells. This suggests that the effect of GM-CSF on glucose utilization by these cells is not mediated by prostanoids and is at least partially independent of the mass action of elevated glucose concentration. These findings indicate that GM-CSF may be an important member of the cytokine cascade that mediates the acute in vivo metabolic response of immune-competent cells in sepsis or endotoxemia.

Animals↗

PubMed1991

Autoreactive T and B cells responding to myelin proteolipid protein in multiple sclerosis and controls.

The pathogenesis of multiple sclerosis (MS) could involve an autoimmune response to proteolipid protein (PLP). Immunization of experimental animals with this major myelin protein can lead to experimental allergic encephalomyelitis. To identify a possible role of PLP as target antigen in MS, we evaluated T cell immunity to PLP in blood and cerebrospinal fluid (CSF) from patients with MS and controls by counting cells which in response to PLP in short-term cultures secreted interferon-gamma. The PLP-specific B cell response was analyzed by counting cells secreting anti-PLP antibodies. PLP-reactive T cells were detected in blood of most MS patients (mean value 1 per 20,408 mononuclear cells), and at 41-fold higher numbers in CSF (mean 1 per 500 CSF cells). Anti-PLP IgG antibody-secreting cells were detected in blood from most MS patients (mean 1 per 30,303 cells), but such cells were 49-fold more frequent in CSF (mean 1 per 625 cells). PLP-reactive T and B cells were also detected in blood and CSF from control patients, but at much lower numbers. A strong and persistent autoimmune response to PLP as well as to other myelin proteins, enriched in CSF, is proposed to be pathogenetically important in MS.

Adolescent↗

PubMed2026

Reprogramming of TLR-Ferroptosis Signaling and Immunometabolic Pathways Overcomes Myeloid Suppression to Improve Checkpoint Blockade in Prostate Cancer.

UNLABELLED: The limited efficacy of immunotherapies in advanced prostate cancer stems from a tumor microenvironment (TME) in which myeloid-driven immune suppression, stromal remodeling, and metabolic barriers converge to limit antitumor immunity. In this study, we characterized the immunometabolic properties of an ultrasmall prostate-specific membrane antigen-targeting silica particle therapy as a first-in-class strategy to reprogram the Toll-like receptor (TLR)-ferroptosis axis in MYC-driven prostate cancer. As single agents, these particles suppressed lipid and steroid biosynthesis, disrupted lipid peroxidation control, and impaired nutrient flux, sensitizing tumors to ferroptosis. Coordinated redox remodeling, stromal reprogramming, and innate immune activation reversed myeloid suppression and promoted CD8+ T-cell infiltration. When combined with CSF-1R inhibition and immune checkpoint blockade, the particles suppressed tumor growth, extended survival beyond 100 days, and achieved up to 50% complete remission in MYC-overexpressing models. These findings position TLR-ferroptosis axis remodeling as a mechanistic blueprint for rational, particle-driven immunotherapies with broad translational potential in prostate cancer and other immunologically refractory malignancies. SIGNIFICANCE: Clinically validated, PSMA-targeted ultrasmall core-shell silica particles reprogram immunometabolic pathways via a TLR-ferroptosis axis, enabling tumor microenvironment remodeling and potentiating checkpoint blockade in prostate cancer, with translational implications for treatment-resistant disease.

Male↗

PubMed1975

Capacity of sensitized thymus-derived lymphocytes to induce fatal lymphocytic choriomeningitis is restricted by the H-2 gene complex.

Adoptive immunization of syngeneic, immunosuppressed recipients infected with lymphocytic choriomeningitis (LCM) virus causes fatal neurologic disease within 2 to 4 days of cell transfer, providing that donors are sampled when the in vitro 51-Cr release assay shows maximal specific activity of sensitized thymus-derived lymphocytes (T cells). Prior treatment of immune spleen cells with AKR anti-omicron ascitic fluid and complement causes total abrogation of this in vivo activity. Fatal neurologic disease is induced only when donor and recipient share at least one set of H-2 antigenic specificities. Parent yields F1 and F1 yields parent combinations are as effective as syngeneic systems, but mice given allogeneic immune cells survive as long as controlsmdifferences at the M-locus in H-2 compatible mice do not inhibit effector activity. Homing of transferred lymphocytes to spleen is similar in syngeneic or allogeneic recipients, but only syngeneic immune cells cross the blood-cerebrospinal fluid (CSF) barrier and cause choriomeningitis. Fatal LCM, is, therefore, apparently induced by a specifically sensitized omicron-bearing cell population, activity of which is restricted by the H-2 gene complex.

Animals↗

PubMed1992

Humoral and cellular immunologic study of cerebrospinal fluid in a patient with Behçet encephalitis.

To study the immunopathogenesis of neuro-Behçet syndrome, we performed serial cerebrospinal fluid (CSF) examinations in a patient with Behçet's syndrome and involvement of the central nervous system. Before and after immunosuppressive treatment, we measured the CSF indexes of immunoglobulins (Ig), and the third (C3) and the fourth (C4) component of complement, and quantified immune complexes and lymphocyte subsets in CSF and peripheral blood. During active encephalitis, humoral abnormalities were intrathecal production of IgM and, to a lesser degree, IgG and IgA, presence of immune complexes in CSF but not in peripheral blood, intrathecal C3 production, and elevated CSF C3 and C4 concentrations; lymphocyte subset analysis showed an increased CSF CD8+ T-cell percentage, in combination with slightly increased PB CD3+ and CD8+ T-cell subsets. After effective immunosuppressive treatment, humoral and cellular CSF values were normal. We conclude that intrathecally produced immunoglobulins, immune complexes, and C3 as well as CD8+ T cells are likely to participate in the development of Behçet encephalitis.

Adult↗

PubMed1991

[The effects and pharmacokinetics of rhG-CSF on the treatment of neutropenia in patients with renal failure].

rhG-CSF (recombinant human granulocyte colony stimulating factor) promotes production and release of neutrophil from bone marrow, and it enhances neutrophil function. In this study, the pharmacokinetics, effects on neutrophil and immune functions and efficacy and safety of rhG-CSF were studied in patients with end-stage renal failure (CRF). To 9 patients with CRF; 2 patients on conservative therapy and 7 patients under regular hemodialysis, 50 micrograms/m2 rhG-CSF were administered intravenously under the schedule of single or 2 week consecutive injection. In single injection study, serial changes in plasma rhG-CSF concentration and peripheral blood cell count were examined following the administration. In consecutive injection study, plasma rhG-CSF concentration, anti-rhG-CSF antibody, peripheral blood cell counts, blood chemistry and coagulation factors, and neutrophil and immune functions were examined. As the results, 1) Half life of rhG-CSF, 2.87 +/- 0.65 hr, was about 2 times longer than that in healthy subjects, and it was not affected by hemodialysis treatment. 2) Marked increase in leukocyte and neutrophil counts and mild increase in lymphocyte count were observed during single and consecutive administration of rhG-CSF. There was no significant change in other leukocyte differentiations, RBC, or platelet count. 3) Neutrophil alkaline phosphatase score increased significantly during single and consecutive administration, and other neutrophil function also improved in several patients with impaired neutrophil function. 4) Slight bone pain and increase in serum alkaline phosphatase were observed in about a half of patients during consecutive injection study. Neither antibody nor accumulation of rhG-CSF was noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗