       Document 0706
 DOCN  M9630706
 TI    Major histocompatibility complex class I-restricted CD8+ T cells and
       class II-restricted CD4+ T cells, respectively, mediate and regulate
       contact sensitivity to dinitrofluorobenzene.
 DT    9603
 AU    Bour H; Peyron E; Gaucherand M; Garrigue JL; Desvignes C; Kaiserlian D;
       Revillard JP; Nicolas JF; INSERM U.80, Universite Claude Bernard Lyon I,
       Faculte A.; Carrel, France.
 SO    Eur J Immunol. 1995 Nov;25(11):3006-10. Unique Identifier : AIDSLINE
       MED/96085168
 AB    Contact sensitivity (CS) is a form of delayed-type hypersensitivity to
       haptens applied epicutaneously and is thought to be mediated, like
       classical delayed-type hypersensitivity responses, by CD4+ T helper-1
       cells. The aim of this study was to identify the effector T cells
       involved in CS. We studied CS to the strongly sensitizing hapten
       dinitrofluorobenzene (DNFB) in mice rendered deficient by homologous
       recombination in either major histocompatibility complex (MHC) class I,
       MHC class II, or both, and which exhibited deficiencies in,
       respectively, CD8+, CD4+, or both, T cells. MHC class I single-deficient
       and MHC class I/class II double-deficient mice, both of which have a
       drastic reduction in the number of CD8+ T cells, were unable to mount a
       CS response to DNFB. In contrast, both MHC class II-deficient mice and
       normal mice treated with an anti-CD4 monoclonal antibody (mAb) developed
       exaggerated and persistent responses relative to heterozygous control
       littermates. Furthermore, anti-CD8 mAb depletion of class II-deficient
       mice totally abolished their ability to mount an inflammatory response
       to DNFB. Removal of residual CD4+ T cells in class II-deficient mice by
       anti-CD4 mAb treatment did not diminish the intensity of CS. These data
       clearly demonstrate that class I-restricted CD8+ T cells are sufficient
       for the induction of CS to DNFB, and further support the idea that MHC
       class II-restricted CD4+ T cells down-regulate this inflammatory
       response.
 DE    Animal  CD4-Positive T-Lymphocytes/*IMMUNOLOGY  CD8-Positive
       T-Lymphocytes/*IMMUNOLOGY  Dermatitis, Allergic Contact/*IMMUNOLOGY
       Dinitrofluorobenzene/*IMMUNOLOGY  Down-Regulation (Physiology)/GENETICS
       Female  Haptens/*IMMUNOLOGY  Histocompatibility Antigens Class
       I/GENETICS  Histocompatibility Antigens Class II/GENETICS  Major
       Histocompatibility Complex/*GENETICS  Male  Mice  Mice, Inbred C57BL
       Mice, Mutant Strains  Support, Non-U.S. Gov't  JOURNAL ARTICLE

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

