       Document 0900
 DOCN  M9440900
 TI    Selective anergy of V beta 8+ T cells in human immunodeficiency
       virus-infected individuals.
 DT    9404
 AU    Dadaglio G; Garcia S; Montagnier L; Gougeon ML; Departement SIDA et
       Retrovirus, Institut Pasteur, Paris,; France.
 SO    J Exp Med. 1994 Feb 1;179(2):413-24. Unique Identifier : AIDSLINE
       MED/94125022
 AB    We have analyzed the V beta usage by CD4+ and CD8+ T cells from human
       immunodeficiency virus (HIV)-infected individuals in response to an in
       vitro stimulation with the superantigenic erythrogenic toxin A (ETA) of
       Streptococcus pyogenes. ETA amplifies specifically CD4+ and CD8+ T cells
       from control donors expressing the V beta 8 and the V beta 12 elements.
       When peripheral T cells from asymptomatic HIV-infected individuals were
       stimulated with ETA, there was a complete lack of activation of the V
       beta 8+ T cell subset, whereas the V beta 12+ T cell subset responded
       normally to the superantigen. This V beta-specific anergy, which was
       also observed in response to staphylococcal enterotoxin E (SEE),
       affected both CD4+ and CD8+ T cells and represented an intrinsic
       functional defect rather than a specific lack of response to bacterial
       superantigens since it was also observed after a stimulation with V beta
       8 monoclonal antibodies. The V beta 8 anergic T cells did not express
       interleukin 2 receptors (IL-2Rs) and failed to proliferate in response
       to exogenous IL-2 or IL-4, suggesting that this anergy was not a
       reversible process, at least by the use of these cytokines. The
       unresponsiveness of the V beta 8 T cell subset is frequent since it was
       found in 56% of the patients studied, and comparison of the clinical
       status of responder vs. anergic patients indicated that the only known
       common factor between them was HIV infection. In addition, it is
       noteworthy that the anergy of the V beta 8 subset may be a very early
       phenomenon since it was found in a patient at Centers for Disease
       Control stage I of the disease. These data provide evidence that a
       dominant superantigen may be involved in the course of HIV infection and
       that the contribution of HIV has to be considered.
 DE    Adult  Antibodies, Monoclonal/IMMUNOLOGY  Antigens, Bacterial/IMMUNOLOGY
       Antigens, CD4  Antigens, CD8  *Clonal Anergy  Exotoxins/IMMUNOLOGY
       Female  Human  HIV Infections/*IMMUNOLOGY  Male  Receptors,
       Interleukin-2/BIOSYNTHESIS  Streptococcus pyogenes/IMMUNOLOGY
       Superantigens/IMMUNOLOGY  Support, Non-U.S. Gov't  T-Lymphocytes,
       Suppressor-Effector/*IMMUNOLOGY  T4 Lymphocytes/*IMMUNOLOGY  JOURNAL
       ARTICLE

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

