home
***
CD-ROM
|
disk
|
FTP
|
other
***
search
/
Shareware Overload Trio 2
/
Shareware Overload Trio Volume 2 (Chestnut CD-ROM).ISO
/
dir26
/
med9410p.zip
/
M94A3191.TXT
< prev
next >
Wrap
Text File
|
1994-10-25
|
3KB
|
49 lines
Document 3191
DOCN M94A3191
TI Involvement of IFN-gamma in the progression of the murine acquired
immunodeficiency syndrome.
DT 9412
AU Uehara S; Hitoshi Y; Numata F; Takatsu K; Dep. Immunol., Sci., Univ.
Tokyo, Japan.
SO Int Conf AIDS. 1994 Aug 7-12;10(1):132 (abstract no. PA0148). Unique
Identifier : AIDSLINE ICA10/94369384
AB OBJECTIVE: The murine acquired immunodeficiency syndrome (MAIDS) caused
by defective LP-BM5 murine leukemia viruses (MuLV) is a disease that
shows progressive splenomegary, severe immunodeficiency and
hypergammaglobulinemia. The onset of MAIDS requires the presence of CD4+
T cells and B cells, and the development of MAIDS is assumed to require
cytokine-mediated cellular interactions. However the role of cytokine in
the pathogenesis of MAIDS is undefined. We therefore investigated the in
vivo effects of anti-cytokine mAbs on the MAIDS development. METHODS: 1)
At various periods of time after LP-BM5 MuLV infection we examined serum
Ig isotypes using ELISA and cytokine mRNA expression in spleens by
RT-PCR method. 2) We injected LP-BM5 MuLV into mice treated with mAb
against cytokines. Spleen weight, proliferative responses of splenocytes
and serum Ig level were assayed 5 weeks after the infection. RESULTS:
Among measured Ig isotypes the level of IgG2a, of which secretion is
stimulated by IFN-gamma, was prominently elevated. The expression of
IFN-gamma and IL-10 mRNAs in spleen were markedly enhanced along with
the infection, whereas IL-2,-4,-5,-6, TNF-alpha,-beta mRNA levels were
almost unchanged. Anti-IFN-gamma mAb inoculation prevented the
progression of MAIDS-related symptoms such as splenomegary, impaired T
and B cell responses to mitogens and enhanced Ig levels. DISCUSSION AND
CONCLUSIONS: Our data suggest that IFN-gamma induced by LP-BM5 MuLV
infection promotes the MAIDS development. Recently Kanagawa et al.
reported that IL-4 and TH2 type response may determine the fatal outcome
of MAIDS. But our results suggest that TH1 type cytokine is also
responsible for the initiation of the disease. We will discuss the role
of IFN-gamma in the development of MAIDS.
DE Animal Antibodies/PHARMACOLOGY B-Lymphocytes/IMMUNOLOGY
Cytokines/*BIOSYNTHESIS Enzyme-Linked Immunosorbent Assay Gene
Expression IgG/BIOSYNTHESIS/BLOOD/CLASSIFICATION Immunoglobulin
Isotypes/BLOOD Interferon Type II/ANTAGONISTS &
INHIB/BIOSYNTHESIS/*PHYSIOLOGY *Leukemia Viruses, Murine Mice Murine
Acquired Immunodeficiency Syndrome/*IMMUNOLOGY/ PHYSIOPATHOLOGY
Polymerase Chain Reaction/METHODS RNA, Messenger/ANALYSIS/BIOSYNTHESIS
Spleen/IMMUNOLOGY Time Factors T4 Lymphocytes/IMMUNOLOGY MEETING
ABSTRACT
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).