Document 0978
 DOCN  M9650978
 TI    Kinetics of ex-vivo cytokine production by splenocytes during murine
       acquired immunodeficiency syndrome (MAIDS).
 DT    9505
 AU    Akarid K; Pocidalo MA; Desforges B; Sinet M; INSERM U 13, Hopital
       Bichat-Claude Bernard, Paris, France.
 SO    Eur Cytokine Netw. 1995 May-Jun;6(3):181-5. Unique Identifier : AIDSLINE
       MED/96159499
 AB    The role of T helper 1 (Th1) and T helper 2 (Th2) responses in the
       murine acquired immunodeficiency syndrome (MAIDS) is unclear. It has
       been suggested that differential activation of T cell subsets,
       particularly a shift to Th2 cytokine production, may be associated with
       disease progression. To clarify the regulation of the cytokine network
       in the course of MAIDS, we examined the kinetics of cytokine production
       by isolated splenocytes. C57/BL6 mice were infected with the LP-BM5
       mixture. The spleen cell proliferative response, together with IL-2,
       IFN-gamma, IL-10 and IL-4 production by unstimulated and ConA or
       anti-CD3 MoAb-stimulated spleen cells, were determined at various times
       after inoculation (weeks 1, 3, 6 and 9). Spleen cells isolated from
       murine leukemia virus complex (LP-BM5) infected mice spontaneously
       produced significant amounts of IL-2 and IFN-gamma one and three weeks
       post-infection, compared to uninfected controls. The capacity of
       isolated T cells to produce the Th1 cytokines IL-2 and IFN-gamma in
       response to stimulation with ConA and anti-CD3 MoAb decreased after 3
       weeks of infection. The fall in IL-2 production ran parallel to the fall
       in the T cell proliferative response to ConA. IL-10 production in
       response to ConA and anti-CD3 MoAb increased after three weeks
       post-inoculation, and followed the reverse kinetic pattern to IFN-gamma
       and IL-2. In contrast, no significant spontaneous IL-4 production and no
       increase in IL-4 production in response to ConA or anti-CD3 MoAb
       occurred during the course of MAIDS, relative to uninfected controls.
       These results suggest that LP-BM5 infection leads to a fall in Th1
       cytokine production rather than a clear switch to Th2 cytokine
       production.
 DE    Animal  Cells, Cultured  Concanavalin A/PHARMACOLOGY
       Cytokines/*BIOSYNTHESIS/GENETICS  Female  Gene Expression
       Regulation/DRUG EFFECTS  Interferon Type II/BIOSYNTHESIS/GENETICS
       Interleukin-10/BIOSYNTHESIS/GENETICS
       Interleukin-2/BIOSYNTHESIS/GENETICS  Interleukin-4/BIOSYNTHESIS/GENETICS
       Kinetics  Lymphocyte Transformation  Mice  Mice, Inbred C57BL
       Mitogens/PHARMACOLOGY  Murine Acquired Immunodeficiency
       Syndrome/*PATHOLOGY  Muromonab-CD3/PHARMACOLOGY
       Spleen/*METABOLISM/PATHOLOGY  Th1 Cells/*METABOLISM  Th2
       Cells/*METABOLISM  JOURNAL ARTICLE

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