       Document 0917
 DOCN  M95A0917
 TI    The interleukin network in the immunopathogenesis of oral diseases [see
       comments]
 DT    9510
 AU    Sosroseno W; Herminajeng E; Goeno S; Department of Dental Public Health,
       Faculty of Dentistry, Gadjah; Mada University, Yogyakarta, Indonesia.
 SO    Asian Pac J Allergy Immunol. 1994 Dec;12(2):161-8. Unique Identifier :
       AIDSLINE MED/95336554
 CM    Comment in: Asian Pac J Allergy Immunol 1994 Dec;12(2):85-6
 AB    Interleukins produced by both lymphoid and non-lymphoid cells play a
       crucial role in the immune response. This paper discusses the possible
       interleukin network in the immunopathogenesis of some oral diseases. In
       chronic inflammatory periodontal diseases and periapical inflammation,
       interleukins such as IL-1 and IL-6 may be responsible in tissue
       destruction. High levels of IL-12 but not IL-4 and IL-10 may reduce the
       course of candidal infection. The progression of HIV infection has been
       associated with the regulation of distinct cytokines; thus, the
       pathogenesis of Kaposi's sarcoma may be regulated by IL-6. In
       autoimmune-associated oral diseases such as lichen planus, the role of
       Langerhans cells in presenting autoantigens may parallel with increased
       levels of IL-6. It seems, therefore, that the course of these diseases
       is regulated by these polypeptides which may in turn modulate the
       disease severity. However, whether altered levels of interleukins in
       certain oral disorders can be used as a diagnostic marker requires
       further investigation.
 DE    Acquired Immunodeficiency Syndrome/*COMPLICATIONS  Animal  Autoimmune
       Diseases/*ETIOLOGY  Candidiasis, Oral/ETIOLOGY  Esophageal
       Diseases/ETIOLOGY  Human  Interleukins/*IMMUNOLOGY  Mice  Mice,
       Transgenic  Mouth Diseases/*ETIOLOGY  Mouth Neoplasms/ETIOLOGY
       Periapical Periodontitis/ETIOLOGY  Periodontitis/ETIOLOGY  JOURNAL
       ARTICLE  REVIEW  REVIEW, ACADEMIC

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

