Autoantibodies and Autoimmunity
475
S4
F1.P
F1.Hg
F3.P
F3.Hg
C.Na
F4.P
F4.Hg
F6.P
F6.Hg
G1.P
G1.Hg
A.Na
B.Na
G5.Hg
F2.Hg
A.Na
B.Hg
SJL
SJL
SJL
B10.S
34
43.0
25.7
18.4
(a)
(b)
(c)
Fig. 5
Antifbrillarin autoantibodies in H-2
s
murine strains (SJL and
B10.S) aFter treatment with mercuric chloride. Autoantibodies were
detected by immunoblotting using mouse liver nucleoli resolved by
sodium dodecyl sulFate/polyacrylamide gel electrophoresis
(SDS-PAGE). (a) Prototype human antifbrillarin serum (S4), serum
From a NaCl-treated SJL mouse (C.Na), and serum From mice ±1 and
±3 beFore (P) and aFter (Hg) mercuric chloride treatment.
(b) Immunoblotting using sera From three additional SJL mice beFore
and aFter mercuric chloride treatment. (c) Immunoblotting using
sera From two SJL mice treated with NaCl (A.Na; B.Na); two SJL mice
treated with mercuric chloride (G5.Hg; ±2,Hg); and two B10.S mice,
one treated with NaCl (A.Na) and the other treated with mercuric
chloride (B.Hg). (Reproduced From Hultman et al.,
Clin. Exp.
Immunol.
78 (1989), 470–477 with permission From the publishers.)
DBA/2 lymphocytes into a cross between
the DBA/2 and C57B16 mice produces
a chronic GVHD, which results in an
autoimmune response similar to human
SLE including the presence of autoantibod-
ies against chromatin and DNA. Injection
of lymphocytes from the A/J strain into
Balb/c X A/J hybrids also produces a
chronic GVHD in which autoantibodies to
snRNP particles including the U3 snoRNP
are found. The relationship of different
autoantibody speciFcities to the use of
different strains of inbred mice in the
GVHD model again highlights the influ-
ence of genotype on autoimmunity and
autoantibodies.
The third type of model does not require
any manipulation of the animal at all; the
disease develops spontaneously. The best
described of these are the murine strains
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