Dysregulation of autoimmunity caused by silica exposure and alteration of Fas-mediated apoptosis in T lymphocytes derived from silicosis patients.

T. Otsuki, H. Hayashi, Y. Nishimura, F. Hyodo, M. Maeda, N. Kumagai, Y. Miura, M. Kusaka, K. Uragami

    Research output: Contribution to journalReview article

    29 Citations (Scopus)

    Abstract

    Silicosis patients suffer from pulmonary fibrosis caused by silica inhalation, as well as autoimmune diseases known as the adjuvant effects of silica. Caplan syndrome complicated with rheumatoid arthritis (RA) is well known epidemiologically, and the incidence of complicated systemic sclerosis (SSc), systemic lupus erythematosus (SLE) and antineutrophilic cytoplasmic antibody (ANCA)-related nephritis have been reported frequently in silicosis patients. To explore the detailed mechanisms of silica-induced dysregulation of autoimmunity, we had focused on Fas/CD95 and Fas-mediated apoptosis because Fas is one of the most important molecules regarding apoptosis of lymphocytes and its alteration makes some T cells survive longer. Additionally, if the long-survived T cells include the self-recognizing T-cell clones, it is easily thought that autoimmune diseases will appear in this situation. Furthermore, regulatory T cells (Treg) showing CD4+25+ and forkhead box P3 (FoxP3)-positive have been a central player in regulating activation of self- and foreign-antigen recognizing T cells, and it has been reported that activation of Treg causes its higher expression of Fas/CD95. Thus, in this review, we introduce the alteration of Fas and related molecules as found in silicosis and also present the Treg function of the CD4+25+ fraction in peripheral blood mononuclear cells derived from silicosis patients.

    Original languageEnglish
    Pages (from-to)11S-16S
    JournalInternational journal of immunopathology and pharmacology
    Volume24
    Issue number1 Suppl
    Publication statusPublished - Jan 1 2011

    Fingerprint

    Silicosis
    Autoimmunity
    Silicon Dioxide
    Apoptosis
    T-Lymphocytes
    Autoimmune Diseases
    Caplan Syndrome
    Nephritis
    Pulmonary Fibrosis
    Systemic Scleroderma
    Autoantigens
    Regulatory T-Lymphocytes
    Systemic Lupus Erythematosus
    Inhalation
    Blood Cells
    Rheumatoid Arthritis
    Clone Cells
    Lymphocytes
    Antibodies
    Incidence

    All Science Journal Classification (ASJC) codes

    • Immunology and Allergy
    • Immunology
    • Pharmacology

    Cite this

    Dysregulation of autoimmunity caused by silica exposure and alteration of Fas-mediated apoptosis in T lymphocytes derived from silicosis patients. / Otsuki, T.; Hayashi, H.; Nishimura, Y.; Hyodo, F.; Maeda, M.; Kumagai, N.; Miura, Y.; Kusaka, M.; Uragami, K.

    In: International journal of immunopathology and pharmacology, Vol. 24, No. 1 Suppl, 01.01.2011, p. 11S-16S.

    Research output: Contribution to journalReview article

    Otsuki, T, Hayashi, H, Nishimura, Y, Hyodo, F, Maeda, M, Kumagai, N, Miura, Y, Kusaka, M & Uragami, K 2011, 'Dysregulation of autoimmunity caused by silica exposure and alteration of Fas-mediated apoptosis in T lymphocytes derived from silicosis patients.', International journal of immunopathology and pharmacology, vol. 24, no. 1 Suppl, pp. 11S-16S.
    Otsuki, T. ; Hayashi, H. ; Nishimura, Y. ; Hyodo, F. ; Maeda, M. ; Kumagai, N. ; Miura, Y. ; Kusaka, M. ; Uragami, K. / Dysregulation of autoimmunity caused by silica exposure and alteration of Fas-mediated apoptosis in T lymphocytes derived from silicosis patients. In: International journal of immunopathology and pharmacology. 2011 ; Vol. 24, No. 1 Suppl. pp. 11S-16S.
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    AU - Maeda, M.

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