17 results on '"Soichi Haraguchi"'
Search Results
2. IRAK-4- and MyD88-Dependent Pathways Are Essential for the Removal of Developing Autoreactive B Cells in Humans
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Eric Meffre, Ben Zion Garty, Capucine Picard, Horst von Bernuth, Yen Shing Ng, Sergei Rudchenko, Emmanuelle Jouanguy, Graham Davies, Dinakantha S. Kumararatne, Noorbibi K. Day, Yildiz Camcioglu, Roja Motaghedi, Iva Srdanovic, John I. Gallin, Isabelle Isnardi, Soichi Haraguchi, Jean-Laurent Casanova, Anne Puel, Shen-Ying Zhang, and Rainer Doffinger
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Male ,Naive B cell ,Immunology ,Clonal Deletion ,Autoimmunity ,Lymphocyte Activation ,medicine.disease_cause ,Article ,Young Adult ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Humans ,Immunology and Allergy ,Child ,MOLIMMUNO ,B cell ,Autoantibodies ,Oligonucleotide Array Sequence Analysis ,030304 developmental biology ,B-Lymphocytes ,0303 health sciences ,biology ,Gene Expression Profiling ,Toll-Like Receptors ,Autoantibody ,Infant ,Membrane Transport Proteins ,TLR9 ,Cell Differentiation ,hemic and immune systems ,TLR7 ,biochemical phenomena, metabolism, and nutrition ,Recombinant Proteins ,Immunity, Innate ,3. Good health ,Interleukin-1 Receptor-Associated Kinases ,Self Tolerance ,medicine.anatomical_structure ,Infectious Diseases ,Antibodies, Antinuclear ,Myeloid Differentiation Factor 88 ,biology.protein ,Female ,Antibody ,030215 immunology - Abstract
Most autoreactive B cells are normally counterselected during early B cell development. To determine whether Toll-like receptors (TLRs) regulate the removal of autoreactive B lymphocytes, we tested the reactivity of recombinant antibodies from single B cells isolated from patients deficient for IRAK-4, and MyD88, whose cells do not respond to TLRs except TLR3 and from UNC-93B-deficient patients whose cells are irresponsive to TLR3, TLR7, TLR8 and TLR9. All patients suffered from defective central and peripheral B cell tolerance checkpoints resulting in the accumulation of large numbers of autoreactive mature naïve B cells in their blood. Hence, TLR7, TLR8, and TLR9 may normally prevent the recruitment of developing autoreactive B cells in healthy donors. Paradoxically, IRAK-4-, MyD88- and UNC-93B-deficient patients do not display autoreactive antibodies in their serum nor develop autoimmune diseases revealing that IRAK-4/MyD88/UNC-93B pathways blockade is likely to thwart the development of autoimmunity in humans.
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- 2008
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3. Inherited mannose-binding lectin deficiency as evidenced by genetic and immunologic analyses: association with severe recurrent infections
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Patricia A. Martin, Danica L. Lerner, Lisa Johnson, Noorbibi K. Day, Aaron Lerner, Soichi Haraguchi, and Robert A. Good
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Adult ,Male ,Pulmonary and Respiratory Medicine ,Immunology ,Enzyme-Linked Immunosorbent Assay ,chemical and pharmacologic phenomena ,Infections ,Mannose-Binding Lectin ,Recurrence ,Genotype ,medicine ,Humans ,Immunology and Allergy ,Family ,Genetic Predisposition to Disease ,Allele ,Immunodeficiency ,Mannan-binding lectin ,Innate immune system ,Reverse Transcriptase Polymerase Chain Reaction ,business.industry ,bacterial infections and mycoses ,MBL deficiency ,medicine.disease ,Pedigree ,Complement system ,Antibody opsonization ,Female ,business - Abstract
Background Mannose-binding lectin (MBL), an acute-phase serum protein of hepatic origin, plays an essential protective role in host innate immunity in targeting microbial pathogens for destruction via opsonization, enhancement of phagocytosis and complement activation. MBL deficiency, characterized by low serum MBL, has been attributed to genetic mutations in both structural and promoter regions of the gene coding for the protein. Concomitant MBL deficiency in patients with chronic immunologic disease has been associated with increased susceptibility to complicating infections that may hasten disease progression. Objective Few cases of inherited MBL deficiency in adults and possible associations with recurrent infection have been reported. To address this issue, we investigated the MBL profile of four generations within a single adult family whose members have experienced a variety of persistent infections. Methods MBL serum levels and MBL genotypes of each participating family member were ascertained by enzyme-linked immunoadsorbent assay and reverse transcriptase-polymerase chain reaction, respectively. MBL complement activation, as measured by C4b deposition against mannan-coated wells, was assayed using an enzyme-linked immunoadsorbent assay. Routine immunologic and cellular tests were carried out to evaluate the immunologic status of each family member. Results Six of the 7 family members screened carried one or more of the variant MBL alleles in their genotype and had correspondingly low serum MBL and reduced ability to affect C4b opsonization. Medical histories of the participating family members revealed an array of mild to severe recurrent infections despite no apparent immunodeficiency. Conclusions Our studies show that MBL deficiency is an inherited characteristic and may be a crucial factor in maintaining immunologic health.
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- 2003
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4. Different mechanisms are utilized by HIV-1 Nef and staphylococcal enterotoxin A to control and regulate interleukin-10 production
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Robert A. Good, Noorbibi K. Day, Nutthapong Tangsinmankong, and Soichi Haraguchi
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Mrna expression ,Immunology ,Human immunodeficiency virus (HIV) ,Enzyme-Linked Immunosorbent Assay ,Biology ,Staphylococcal enterotoxin A ,medicine.disease_cause ,Gene Products, nef ,Tacrolimus ,Microbiology ,Enterotoxins ,Immunologic diseases ,Protein biosynthesis ,Superantigen ,medicine ,Humans ,Immunology and Allergy ,RNA, Messenger ,nef Gene Products, Human Immunodeficiency Virus ,Cells, Cultured ,Sirolimus ,Reverse Transcriptase Polymerase Chain Reaction ,Interleukin-10 ,Interleukin 10 ,Cyclosporine ,HIV-1 ,Leukocytes, Mononuclear ,Immunosuppressive Agents - Abstract
Interleukin-10 (IL-10) plays an important immunopathogenic role in immunologic diseases, especially in HIV infection and atopic dermatitis. The control and regulatory mechanisms of IL-10 production have not been described in these diseases. Recently, we demonstrated that HIV-1 Nef induces IL-10 production in monocytes and that staphylococcal enterotoxin A (SEA) induces IL-10 production in T-lymphocytes. Here we show that Nef-induced IL-10 production and mRNA expression are strongly blocked by rapamycin, but are not blocked by cyclosporin (CsA) or FK506. Conversely, we show that CsA and FK506 completely inhibit SEA-induced IL-10 protein production and mRNA expression. The results of this study demonstrate that IL-10 production by Nef and SEA is controlled and regulated by different mechanisms.
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- 2002
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5. Immunologic Reconstitution Following Bone Marrow Transplantation for X-Linked Hyper IgM Syndrome
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Robert P. Nelson, Remi Hitchcock, Martin R. Klemperer, John E. Duplantier, Noorbibi K. Day, Hans D. Ochs, Kuniaki Seyama, Robert A. Good, and Soichi Haraguchi
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Male ,Cellular immunity ,Hyper IgM syndrome ,X Chromosome ,Genetic Linkage ,CD40 Ligand ,Immunology ,chemical and pharmacologic phenomena ,Immunoglobulin E ,Antigen ,immune system diseases ,medicine ,Humans ,Immunology and Allergy ,Dysgammaglobulinemia ,B cell ,Immunodeficiency ,Bone Marrow Transplantation ,biology ,Infant ,hemic and immune systems ,medicine.disease ,medicine.anatomical_structure ,Child, Preschool ,Mutation ,biology.protein ,Bone marrow - Abstract
X-linked hyper IgM syndrome (XHIM), caused by mutations of the CD40 ligand (CD40L) gene, is characterized by recurrent bacterial and opportunistic infections, an increased incidence of autoimmunity and malignancies, and immunodeficiency due to abnormal T/B cell interaction. Because of poor long-term prognosis, bone marrow transplantation (BMT) has been proposed as an alternative treatment. An 8-month-old boy with XHIM and a splice site mutation of CD40L underwent BMT using a fully matched sibling donor. Markers of engraftment and immunologic reconstitution were measured serially. After BMT, activated T cells expressed functional CD40L, and genomic DNA obtained from circulating white cells contained predominantly wild-type CD40L sequences. Serum immunoglobulin levels including IgE and antibody responses to recall antigens normalized, and immunization with the T-cell-dependent neoantigen, bacteriophagephi;X174, demonstrated amplification of the response and isotope switching. BMT provides a permanent cure for XHIM if a fully matched sibling donor is available and the procedure is performed before complications have occurred.
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- 2001
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6. Thymic output markers indicate immune dysfunction in DiGeorge syndrome
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Richard F. Lavi, John W. Sleasman, Nutthapong Tangsinmankong, Noorbibi K. Day, Wasu Kamchaisatian, Soichi Haraguchi, and Diana P. Martin
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CD4-Positive T-Lymphocytes ,Male ,Thymic Factor, Circulating ,Adolescent ,Immunology ,MEDLINE ,Thymus Gland ,CD8-Positive T-Lymphocytes ,Lymphocyte Activation ,Immune Dysfunction ,Bioinformatics ,Text mining ,DiGeorge syndrome ,DiGeorge Syndrome ,Humans ,Immunology and Allergy ,Medicine ,Child ,Extramural ,business.industry ,Infant ,medicine.disease ,Child, Preschool ,Female ,business ,Biomarkers - Published
- 2006
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7. HIV-1 recombinant gp41 induces IL-10 expression and production in peripheral blood monocytes but not in T-lymphocytes
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Angelos Koutsonikolis, Noorbibi K. Day, Emerita N. Brigino, Robert A. Good, Soichi Haraguchi, and Una E. Owens
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T-Lymphocytes ,Immunology ,Cell ,Gene Expression ,Chemical Fractionation ,HIV Envelope Protein gp120 ,Gp41 ,Peripheral blood mononuclear cell ,Monocytes ,law.invention ,law ,Gene expression ,medicine ,Humans ,Immunology and Allergy ,RNA, Messenger ,Northern blot ,Messenger RNA ,Dose-Response Relationship, Drug ,Chemistry ,Molecular biology ,HIV Envelope Protein gp41 ,Recombinant Proteins ,Interleukin-10 ,Interleukin 10 ,medicine.anatomical_structure ,HIV-1 ,Recombinant DNA - Abstract
The effects of recombinant gp41 (rgp41) protein of the human immunodeficiency virus type 1 (HIV-1) on interleukin 10 (IL-10) expression and production using human peripheral blood mononuclear cells was investigated. Expression of IL-10 mRNA was demonstrated within 3 h of cell exposure to endotoxin-free rgp41 by RT-PCR and Northern blot analyses in a time- and dose-dependent manner. IL-10 protein was detected in the supernatants of peripheral blood mononuclear cells following stimulation with rgp41 also in a dose dependent manner. Fractionation of peripheral blood mononuclear cells showed that purified monocytes but not purified T-lymphocytes induced expression of IL-10 mRNA by rgp41. Recombinant HIV-1 gp120 exhibits similar influences on the induction of IL-10. These results indicate that both of these components of envelope proteins may play an important role in HIV related immunomodulation by influencing regulatory functions of monocytes and macrophages.
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- 1997
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8. Interleukin receptor–associated kinase (IRAK-4) deficiency associated with bacterial infections and failure to sustain antibody responses
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Capucine Picard, Hans D. Ochs, Soichi Haraguchi, Robert A. Good, Nutthapong Tangsinmankong, Jean-Laurent Casanova, Noorbibi K. Day, and Rajivi P. Rucker
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Blotting, Western ,Receptors, Cell Surface ,Consanguinity ,Antigen ,Immunopathology ,Humans ,Medicine ,Child ,Interleukin 6 ,Membrane Glycoproteins ,Interleukin-1 receptor–associated kinase 4 deficiency ,biology ,Interleukin-6 ,business.industry ,Toll-Like Receptors ,Immunologic Deficiency Syndromes ,Interleukin ,Bacterial Infections ,Blotting, Northern ,medicine.disease ,Antibodies, Bacterial ,Phosphotransferases (Alcohol Group Acceptor) ,Interleukin-1 Receptor-Associated Kinases ,Pediatrics, Perinatology and Child Health ,Immunology ,Pneumococcal pneumonia ,biology.protein ,Interleukin receptor ,Female ,Antibody ,business ,Signal Transduction - Abstract
We previously described a girl with recurrent episodes of pneumococcal pneumonia with septicemia and other infections,(1) found to have interleukin-1 receptor-associated kinase 4 deficiency (IRAK-4) deficiency.(2) In this report, we show that our patient is unable to sustain antibody responses either to polysaccharide or protein antigens or to a neoantigen-bacteriophage.
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- 2004
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9. Immunosuppressive retroviral peptides: cAMP and cytokine patterns
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Robert A. Good, Soichi Haraguchi, and Noorbibi K. Day
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chemistry.chemical_classification ,Sequence Homology, Amino Acid ,medicine.medical_treatment ,Molecular Sequence Data ,Immunology ,Retroviridae Proteins ,Peptide ,Biology ,Immune Dysfunction ,Interleukin 10 ,Cytokine ,chemistry ,Downregulation and upregulation ,Immunity ,Cyclic AMP ,medicine ,Animals ,Cytokines ,Humans ,Amino Acid Sequence ,Tumor necrosis factor α ,Immunosuppressive Agents ,Intracellular - Abstract
The mechanism(s) by which retroviral proteins exert immunosuppressive influences has remained enigmatic. Here, Soichi Haraguchi, Robert Good and Noorbibi Day propose that induction of intracellular cAMP by a synthetic, immunosuppressive, retroviral envelope peptide causes a shift in the cytokine balance, leading to suppression of cell-mediated immunity by upregulation of interleukin 10 (IL-10) and downregulation of IL-2, IL-12 and tumor necrosis factor α production. This may be a crucial step towards generation of immune dysfunction.
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- 1995
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10. Prolactin acts on the extreme 5′ portion of MMTV LTR involving a mammary cell-specific enhancer
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Soichi Haraguchi, Noorbibi K. Day, and Robert A. Good
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viruses ,Response element ,Breast Neoplasms ,Biochemistry ,Chloramphenicol acetyltransferase ,Endocrinology ,Tumor Cells, Cultured ,Humans ,Breast ,Enhancer ,Molecular Biology ,Repetitive Sequences, Nucleic Acid ,Regulation of gene expression ,Reporter gene ,biology ,Mouse mammary tumor virus ,Transfection ,biology.organism_classification ,Long terminal repeat ,Prolactin ,Cell biology ,Enhancer Elements, Genetic ,Gene Expression Regulation ,Mammary Tumor Virus, Mouse ,Cancer research ,hormones, hormone substitutes, and hormone antagonists - Abstract
We have previously shown that a human mammotropic polypeptide hormone, prolactin (PRL) can act synergistically with steroid hormones to regulate gene expression directed by the long terminal repeat of mouse mammary tumor virus (MMTV LTR) in a human ductal carcinoma cell line T47D cells using a chloramphenicol acetyltransferase reporter gene system and gene transfection methods. In the present study, using various recombinant plasmids we analyzed functional elements in the MMTV LTR that is essential for the PRL responses. We show that the PRL-responsive elements are located in the extreme 5' end of the MMTV LTR, a region previously described by others to be a mammary cell-specific enhancer.
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- 1993
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11. Suppression of human interferon-γ production by a 17 amino acid peptide homologous to the transmembrane envelope protein of retroviruses: Evidence for a primary role played by monocytes
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Soichi Haraguchi, Wing T. Liu, Robert A. Good, George J. Cianciolo, and Noorbibi K. Day
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T-Lymphocytes ,medicine.medical_treatment ,Molecular Sequence Data ,Immunology ,Peptide ,Cell Communication ,Enterotoxin ,Cycloheximide ,Biology ,Peripheral blood mononuclear cell ,Monocytes ,Interferon-gamma ,chemistry.chemical_compound ,Viral Envelope Proteins ,medicine ,Humans ,Interferon gamma ,Amino Acid Sequence ,Cells, Cultured ,chemistry.chemical_classification ,Monocyte ,Molecular biology ,Transmembrane protein ,Retroviridae ,medicine.anatomical_structure ,Cytokine ,chemistry ,Biochemistry ,Peptides ,medicine.drug - Abstract
CKS-17, a synthetic amino acid peptide homologous to a highly conserved region of retroviral transmembrane protein exerts a suppressive action on staphylococcal enterotoxin A (SEA)-induced the production of IFN-γ by human peripheral blood mononuclear cells (PBMC) (Ogasawara et al., J. Immunol. 141 , 615, 1988). This action has been shown in the present study to be preceded by dramatic clustering of PBMC. Clusters appear within 3 hr of exposure of PBMC to CKS-17; they are dose dependent, inhibited by cycloheximide, and require a temperature of 37 °C. The cells in the clusters are predominantly monocytes. Although it has been previously shown that CKS-17 inhibits monocyte-mediated killing by inactivating IL-1 (Kleinerman et al., J. Immunol. 139 , 2329, 1987) and production of IL-2 by murine thymoma cells treated with IL-1 (Gottlieb et al., J. Immunol. 142 , 4321, 1989), in the present study we show that IL-1 does not prevent clustering of PBMC by CKS-17. Using CKS-17 and highly purified monocytes or lymphocytes, profound alterations occur only with monocytes, as revealed by light or electron microscopy. SEA- or staphylococcal enterotoxin B-induced production of IFN-γ is inhibited when highly purified monocytes pretreated with CKS-17 are cocultured with highly purified T lymphocytes. Thus, CKS-17 induces dramatic clustering of cells apparently by inducing alterations of monocytes but not lymphocytes, suggesting that CKS-17 may interfere with the capacity of monocytes to facilitate production of IFN-γ by T lymphocytes.
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- 1992
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12. Emergence of HIV-1 variants containing codon insertions and deletions in the β3-β4 hairpin loop domain of reverse transcriptase
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Alexandra Rey, Angela Andreopoulos, Remi Hitchcock, Lisa Johnson, Robert A. Good, Michelle James-Yarish, Diana Skapura, Noorbibi K. Day, Elmer Dinglasan, Soichi Haraguchi, Vasavi Kaliki, and Aruna Chinta
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Mutation ,Genotype ,Immunology ,Human immunodeficiency virus (HIV) ,Genetic Variation ,Biology ,medicine.disease_cause ,Virology ,HIV Reverse Transcriptase ,Reverse transcriptase ,Protein Structure, Tertiary ,Loop (topology) ,Mutagenesis, Insertional ,Domain (ring theory) ,HIV-1 ,medicine ,Humans ,Immunology and Allergy ,Codon ,Sequence Deletion - Published
- 2000
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13. 648 Molecular mechanisms for IL-12 deficiency in a patient with recurrent infections
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S Uthaisangsok, Michelle James-Yarish, Soichi Haraguchi, A Takahashi, R Hitchcock, Noorbibi K. Day, and Robert A. Good
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Recurrent infections ,business.industry ,Immunology ,Interleukin 12 ,Immunology and Allergy ,Medicine ,business - Published
- 2000
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14. IRAK-4 Deficiency: Age Associated Improvement of Symptoms and Responses to Vaccines
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N. Tang, Soichi Haraguchi, Jean-Laurent Casanova, L.E. Isakson, HansD. Ochs, and Noorbibi K. Day
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Immunology ,Immunology and Allergy - Published
- 2009
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15. HIV-1 nef decreases CXCR4 expression on CD4+ T-lymphocytes*1
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Noorbibi K. Day, Wasu Kamchaisatian, P. Emmanuel, John W. Sleasman, Nutthapong Tangsinmankong, Robert A. Good, and Soichi Haraguchi
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Regulation of gene expression ,medicine.medical_specialty ,Immunology ,Significant difference ,Human immunodeficiency virus (HIV) ,virus diseases ,Stimulation ,Biology ,medicine.disease_cause ,CXCR4 ,In vitro stimulation ,On cells ,Endocrinology ,Internal medicine ,medicine ,Immunology and Allergy ,Incubation - Abstract
Rationale HIV-1 co-receptors, CXCR4 and CCR5, are essential for HIV entry and its life cycle. Expression of CXCR4 on T-lymphocytes is lower during HIV-infection and is normalized by antiretroviral therapy. We propose that HIV-1 Nef, an important HIV-1 regulatory protein, may play an important role in HIV-1 co-receptor expression on T lymphocytes during HIV infection. Methods CXCR4 and CCR5 expression on CD4 + T-lymphocytes was measured using quantitative flow cytometric assay in 23 HIV-infected children and 10 healthy subjects after 24-hour in vitro stimulation with various HIV-1 regulatory proteins (Nef 100 ng/ml, Tat 1 ng/ml, Gag 500 ng/ml, and gp120IIIB 250 ng/ml). Results Without HIV-1 regulatory protein stimulation, mean CXCR4 expression on CD4 + T-lymphocytes was significantly higher in healthy subjects compared to HIV-infected children (36.79% vs 24.60%; p=0.005). Following 24-hour incubation with Nef, mean CXCR4 expression on T-lymphocytes of healthy subjects was significantly decreased when compared to the expression on cells without stimulation (30.38% vs. 36.79%; p=0.012). There was no longer significant difference in mean CXCR4 expression on T-lymphocyte between HIV-infected children and healthy subjects after Nef stimulation (24.81% vs. 30.4%; p=NS). There was no significant change in mean CXCR4 expression on T-lymphocytes after stimulation with other HIV-1 proteins in HIV-infected children or healthy subjects. No significant change in the CCR5 expression on CD4 + T-lymphocytes was seen after stimulation with various HIV-1 proteins. Conclusions HIV-1 Nef protein decreases CXCR4 expression on CD4 + T-lymphocytes in healthy subjects. This may be an important mechanism for CXCR4 down-regulation during HIV-1 infection.
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- 2004
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16. A family study of mannose-binding lectin deficiency presented as severe recurrent infections evidenced by genetic and immunological analysis
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Diana P. Martin, Lacey Johnson, Robert A. Good, Noorbibi K. Day, and Soichi Haraguchi
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Recurrent infections ,Immunology ,Immunology and Allergy ,Biology ,Mannan-binding lectin - Published
- 2003
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17. 887 HIV-1 Nef protein induces interleukin-10 production in peripheral blood mononuclear cells and H9 cell line
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Noorbibi K. Day, U E Owens, Emerita N. Brigino, A. Koutsonikolis, Soichi Haraguchi, and Robert A. Good
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Interleukin 10 ,Nef Protein ,Chemistry ,Cell culture ,Immunology ,Human immunodeficiency virus (HIV) ,medicine ,Immunology and Allergy ,medicine.disease_cause ,Molecular biology ,Peripheral blood mononuclear cell - Published
- 1996
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