       Document 0472
 DOCN  M9610472
 TI    Cellular mechanisms in the immune response to malaria in Plasmodium
       vinckei-infected mice.
 DT    9601
 AU    Perlmann H; Kumar S; Vinetz JM; Kullberg M; Miller LH; Perlmann P;
       Department of Immunology, Stockholm University, Sweden.
 SO    Infect Immun. 1995 Oct;63(10):3987-93. Unique Identifier : AIDSLINE
       MED/96009756
 AB    Infection of mice with the malaria parasite Plasmodium vinckei vinckei
       is 100% lethal. However, after two infections followed by drug cure,
       BALB/c mice develop a solid immunity which is antibody independent but
       mediated by CD4+ T cells. To elucidate the mechanisms of this immunity,
       spleen cells from immune mice were challenged in vitro with lysates of
       P. vinckei-infected or uninfected erythrocytes. The parasite antigen
       induced proliferation of T cells from immune mice but not from nonimmune
       mice. When gamma interferon production by cells from immune mice was
       assayed at the single-cell level, 1 to 3 cells per 1,000 cells were
       found to release this cytokine when exposed to antigen. In contrast, the
       numbers of interleukin 4 (IL-4)-producing cells from both immune and
       control mice were < or = 4 per 10(6) cells, regardless of antigen
       exposure. Investigation in a bioassay showed that P. vinckei antigen
       induced the release of IL-4 from spleen cells of immune mice but not
       from those of control mice. Nevertheless, that IL-4 is of minor
       significance in this system is also suggested by the absence of
       elevation of immunoglobulin E levels in blood samples from these mice,
       in contrast to what is seen with P. chabaudi infection, in which
       IL-4-producing Th2 cells are of major importance for immunity during
       later phases of infection. Taken together, the present results indicate
       that immunity to P. vinckei is a Th1 response, with gamma interferon
       being an important protective factor. Whether or not the Th1 response,
       through overproduction of tumor necrosis factor alpha, is also
       responsible for pathology and death in this infection remains to be
       clarified.
 DE    Animal  Antibodies, Protozoan/BIOSYNTHESIS  DNA/BIOSYNTHESIS  Female
       Immunoglobulin Isotypes/BIOSYNTHESIS  Interferon Type II/BIOSYNTHESIS
       Interleukin-4/BIOSYNTHESIS  Malaria/*IMMUNOLOGY  Mice  Mice, Inbred BALB
       C  Plasmodium/*IMMUNOLOGY  Support, Non-U.S. Gov't  Support, U.S. Gov't,
       P.H.S.  Th1 Cells/IMMUNOLOGY  JOURNAL ARTICLE

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

