       Document 0048
 DOCN  M95B0048
 TI    Interleukin 12 suppresses autoantibody production by reversing helper
       T-cell phenotype in hepatitis B e antigen transgenic mice.
 DT    9511
 AU    Milich DR; Wolf SF; Hughes JL; Jones JE; Department of Molecular
       Biology, Scripps Research Institute, La; Jolla, CA 92037, USA.
 SO    Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6847-51. Unique Identifier
       : AIDSLINE MED/95350166
 AB    Helper T (Th) cells are classified as Th1 or Th2 cells by virtue of
       cytokine secretion and function as mediators of cellular or humoral
       immunity, respectively. Cytokines also regulate the differentiation of
       Th cells. For example, interleukin (IL)-12 promotes Th1 and suppresses
       Th2 cell development, suggesting that IL-12 may be useful
       therapeutically in Th2-mediated autoimmune and allergic disorders.
       Therefore, the effect of systemic IL-12 treatment on in vivo
       autoantibody synthesis in hepatitis B e antigen (HBeAg)-expressing
       transgenic mice, which is dependent on self-reactive Th2 cells, was
       examined. Low-dose IL-12 significantly inhibited autoantibody production
       by shifting the Th2-mediated response toward Th1 predominance.
       Additionally, previous studies suggest that a predominance of
       HBeAg-specific Th2-type cells may contribute to chronicity in hepatitis
       B virus infection. Therefore, IL-12 may also prove beneficial in
       modulating the HBeAg-specific Th response to favor viral clearance in
       chronic hepatitis B virus infection.
 DE    Animal  Antibodies, Viral/BIOSYNTHESIS  Autoantibodies/*BIOSYNTHESIS
       Autoimmune Diseases/THERAPY  Cells, Cultured
       Cytokines/BLOOD/PHARMACOLOGY  Hepatitis B e
       Antigens/GENETICS/*IMMUNOLOGY  IgG/BLOOD  Immunoglobulin Isotypes/BLOOD
       *Immunosuppression  Immunotherapy, Adoptive
       Interleukin-12/GENETICS/*PHARMACOLOGY  Mice  Mice, Transgenic  Phenotype
       Recombinant Proteins/PHARMACOLOGY  T-Lymphocytes,
       Helper-Inducer/*IMMUNOLOGY  Th1 Cells/IMMUNOLOGY  Th2 Cells/IMMUNOLOGY
       JOURNAL ARTICLE

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

