関: antiglobulin

WordNet

not in favor of (an action or proposal etc.)
a person who is opposed (to an action or policy or practice etc.); "the antis smelled victory after a long battle"
social insect living in organized colonies; characteristically the males and fertile queen have wings during breeding season; wingless sterile females are the workers (同)emmet, pismire
any of a large variety of proteins normally present in the body or produced in response to an antigen which it neutralizes, thus producing an immune response

PrepTutorEJDIC

《話》(特定の慣習・政策・行動などに)反対する人
『アリ』
=ain't
抗体,免疫体,抗毒素
(次にくる語の発音が母音で始まるときに用いる) / (子音[h]で始まり第1音節に強勢のない語の場合はanを用いることがある.ただし,この場合は[h]を発音しない)

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1. 血液疾患における免疫グロブリンの静脈内投与 intravenous immune globulin in hematologic disorders
2. 免疫グロブリンの構造 structure of immunoglobulins
3. 慢性リンパ性白血病の病態生理および遺伝学的特徴 pathophysiology and genetic features of chronic lymphocytic leukemia
4. 硬化性粘液水腫 scleromyxedema
5. HIV感染の血液学的症状：血小板減少症と凝固異常 hematologic manifestations of hiv infection thrombocytopenia and coagulation abnormalities

English Journal

Immunological and histological evaluation of clinical samples from psoriasis patients treated with anti-CD6 itolizumab.

Aira LE1, López-Requena A2, Fuentes D3, Sánchez L1, Pérez T4, Urquiza A5, Bautista H6, Falcón L7, Hernández P1, Mazorra Z1.Author information 1Center of Molecular Immunology; Havana, Cuba.2Center of Molecular Immunology; Havana, Cuba; Biotech Pharmaceutical Co. Ltd.; Beijing, China.3National Center for Laboratory Animal Breeding; Havana, Cuba.4Hermanos Ameijeiras Hospital; Havana, Cuba.5Medical Surgical Research Center; Havana, Cuba.6Manuel Fajardo Hospital; Havana, Cuba.7Carlos Juan Finlay Hospital; Havana, Cuba.AbstractPsoriasis is a chronic inflammatory disease with a prevalence of approximately 2-3% in the general population. The majority of diagnosed patients have plaque psoriasis, and about 20% have moderate-to-severe disease. Itolizumab, a new monoclonal antibody specific for the CD6 molecule mainly expressed on T lymphocytes, has demonstrated to inhibit in vitro ligand-induced proliferation and pro-inflammatory cytokine production. We assessed the immunological and histopathological effect of the antibody using clinical samples taken from 26 patients with moderate-to-severe psoriasis included in a clinical trial. The precursor frequency of lymphocytes activated with anti-CD2/CD3/CD28 beads, as well as the number of interferon (IFN)-γ-secreting T cells after stimulation, were measured at different time points of the study. Serum cytokine levels and anti-idiotypic antibody response to itolizumab were also evaluated. Additionally, lymphocyte infiltration and epidermis hyperplasia were studied in five patients. A significant reduction in T cell proliferation capacity and number of IFN-γ-producing T cells was found in treated patients. Serum levels of interleukin-6, tumor necrosis factor and IFN-γ showed an overall trend toward reduction. No anti-idiotypic antibody response was detected. A significant reduction in the epidermis hyperplasia was observed in analyzed patients. These results support the relevance of the CD6 molecule as a therapeutic target for the treatment of this disease.
mAbs.MAbs.2014 May 1;6(3):782-92. doi: 10.4161/mabs.28376. Epub 2014 Mar 4.
Psoriasis is a chronic inflammatory disease with a prevalence of approximately 2-3% in the general population. The majority of diagnosed patients have plaque psoriasis, and about 20% have moderate-to-severe disease. Itolizumab, a new monoclonal antibody specific for the CD6 molecule mainly expressed
PMID 24594862

Intravenous human immunoglobulin treatment of serum from HLA-sensitized patients in kidney transplantation.

Picascia A1, Grimaldi V, Paolillo R, Vasco M, Casamassimi A, De Luca FP, Cavalca F, Schiano C, Napoli C.Author information 1U.O.C. Division of Immunohematology, Transfusion Medicine and Transplant Immunology [SIMT], Regional Reference Laboratory of Transplant Immunology [LIT], Azienda Ospedaliera Universitaria (AOU) and.AbstractAbstract Objective: Intravenous immunoglobulin (IVIG) products are known to have beneficial immunomodulatory effects on several inflammatory and autoimmune disorders. These effects could be attributed to a different inhibitory action on complement factors, but other mechanisms could be implicated, e.g., immunocomplexes development and/or anti-idiotypic antibodies. Positive results on the reduction of anti-Human Leukocyte Antigens (HLA) antibodies in highly sensitized patients have also been found. The present study focuses on the effect of IVIG on the reduction of Panel Reactive Antibody level and crossmatch positivity in sensitized patients awaiting kidney transplantation. Methods: The study was performed adapting an in vitro assay on sensitized patients' sera in waiting list for kidney transplantation. Sera of twelve highly sensitized patients were evaluated for the cytotoxicity inhibition after 10% IVIG treatment. Results: A reduction of anti- HLA antibody levels was observed in 75% (9/12) of treated patients in vitro, while 25% (3/12) resulted unresponsiveness. Particularly, our data showed a significantly higher Panel Reactive Antibody reduction for T lymphocytes (p < 0.010) than B lymphocytes (p < 0.032). Conclusions: In this study, we have used an in vitro assay to investigate susceptibility to desensitization with IVIG treatment of sensitized patient sera. These findings reveal that the variable effect of IVIG on reducing Panel Reactive Antibody in our immunized patients could be attributed to a different inhibitory action on complement, likely due to the type and the titre of anti-HLA antibodies.
Renal failure.Ren Fail.2014 May;36(4):585-8. doi: 10.3109/0886022X.2014.880326. Epub 2014 Jan 23.
Abstract Objective: Intravenous immunoglobulin (IVIG) products are known to have beneficial immunomodulatory effects on several inflammatory and autoimmune disorders. These effects could be attributed to a different inhibitory action on complement factors, but other mechanisms could be implicated, e
PMID 24456257

B cell-mediated pathogenesis of ANCA-mediated vasculitis.

Jennette JC1, Falk RJ.Author information 1Department of Pathology and Laboratory Medicine, and Department of Medicine, School of Medicine, University of North Carolina at Chapel Hill, 308 Brinkhous-Bullitt Building, CB#7525, Chapel Hill, NC, 27599-7525, USA, jcj@med.unc.edu.AbstractB cells and their progeny that produce and release anti-neutrophil cytoplasmic autoantibodies (ANCA) are the primary cause for an aggressive form of necrotizing small vessel vasculitis. Cytoplasmic ANCA antigens are released at the surface and in the microenvironment of cytokine-primed neutrophils. Binding of ANCA to ANCA antigens activates neutrophils by both Fc receptor engagement and direct Fab'2 binding to antigen on the cell surface. ANCA-activated neutrophils release factors that induce alternative complement pathway activation, which establishes a potent inflammatory amplification loop that causes severe necrotizing vascular inflammation. The origin of the ANCA autoimmune response is unknown but appears to involve genetically determined HLA specificities that allow the autoimmune response to develop. One putative immunogenic mechanism begins with an immune response to a peptide that is complementary to the autoantigen and evolves through an anti-idiotypic network to produce autoantibodies to the autoantigen. Another putative immunogenic mechanism begins with an immune response to a microbe-derived molecular mimic of the autoantigen resulting in antibodies that cross-react with the autoantigen. Release of neutrophil extracellular traps, apoptosis, and increased granule protein expression of ANCA antigens may facilitate the initiation of an ANCA autoimmune response, augment established pathogenic ANCA production, or both. The ANCA B cell autoimmune response is facilitated by quantitatively and qualitatively impaired T cell and B cell suppression and by release from activated neutrophils of B cell-activating factors that enhance B cell proliferation and retard B cell apoptosis.
Seminars in immunopathology.Semin Immunopathol.2014 Apr 29. [Epub ahead of print]
B cells and their progeny that produce and release anti-neutrophil cytoplasmic autoantibodies (ANCA) are the primary cause for an aggressive form of necrotizing small vessel vasculitis. Cytoplasmic ANCA antigens are released at the surface and in the microenvironment of cytokine-primed neutrophils.
PMID 24777746

Japanese Journal

Antigen itself antibody : an alternative one-step immunoassay for measuring the anti-idiotypic antibody titer

Kabir M. Enamul,Krishnaswamy Senthilkumar,Selvakumar Dakshnamurthy [他]
Microbiology and immunology 58(9), 523-529, 2014-09
NAID 40020207328

Different buffer effects in selecting HM-1 killer toxin single-chain fragment variable anti-idiotypic antibodies

Krishnaswamy Senthilkumar,Kabir M. Enamul,Miyamoto Masahiko [他],FURUICHI Yasuhiro,KOMIYAMA Tadazumi
The journal of biochemistry 147(5), 723-733, 2010-05-01
NAID 10027875919

Vaccination with autoreactive CD4+Th1 clones in lupus-prone MRL/Mp-Faslpr/lpr mice

Fujii Takao,Okada Masato,Fujita Yoshimasa,Sato Takeshi,Tanaka Masao,Usui Takashi,Umehara Hisanori,Mimori Tsuneyo
Journal of Autoimmunity 33(2), 125-134, 2009-09
… CD4+αβ Th1 clones, dna51 (Vβ8.3) and rnp2 (Vβ14), which stimulated anti-dsDNA or U1 ribonucleoprotein (U1RNP) antibody (Ab) production respectively, were isolated from splenocytes of MRL/lpr mice. … Anti-idiotypic humoral and T cell responses against the transferred autoreactive Th1 clones were determined in parallel. …
NAID 120001596907