Isolation, molecular properties and allotype of mouse C1q.

Seino, Jin; Fukuoka, Yoshihiro; Okuda, Tomoko; Tachibana, Takehiko

doi:10.1620/tjem.142.351

Cited by 1 publication

(1 citation statement)

References 22 publications

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“…IgG, IgM and C3 were detected by a direct method using FITCconjugated goat anti-mouse IgG (Zymed Inc., San Francisco, CA), goat anti-mouse IgM and rabbit anti-mouse C3 antibodies (Zymed), respectively. The staining of C1q and C4 in glomeruli was performed using rabbit anti-mouse C1q and C4 antibodies [24,25], respectively, followed by biotinylated goat anti-rabbit IgG antibodies (Vector Labs Inc., Burlingame, CA) and FITC-labelled avidin (Vector). To detect Mac-2 antigens [26], kidney samples were ®xed overnight at 48C with a periodate-lysine-paraformaldehyde solution [27] prior to freezing.…”

Section: Histopathological Examinationmentioning

confidence: 99%

Experimental lupus nephritis in severe combined immunodeficient (SCID) mice: remodelling of the glomerular lesions by bystander IgM antibodies

Ito

Terasaki

Kondo

et al. 2000

Clinical and Experimental Immunology

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MRL/Mp-lpr/lpr (MRL/lpr) mice develop glomerular lesions with regular variations in their histopathological manifestations, similar to those in lupus nephritis. These lesions are mainly either cell-proliferative or wire loop-like and are associated with glomerular deposits of immunoglobulins, most frequently IgG and IgM. We previously established a nephritogenic IgG3-producing hybridoma clone, B1, from an MRL/lpr mouse, which induces only a 'wire loop-like' type of glomerular lesion when injected into SCID mice. Injection of SCID mice with an anti-trinitrophenyl IgM antibody-producing hybridoma clone, Sp6, following injection of the B1 clone, however, resulted in the development of a 'cell-proliferative' type of glomerular lesion, associated with an accumulation of both antibodies in glomeruli. This accumulation occurred even though Sp6 IgM antibodies did not react with B1 IgG3 antibodies and vice versa. A mutant clone of Sp6, T/13microE/3.1, which produces antibodies deficient in C1q binding, produced a similar effect as that of the Sp6 clone, i.e. 'cell-proliferative' lesions. Again the B1 antibodies did not react with T/13microE/3. 1-IgM antibodies and vice versa. We therefore conclude that bystander IgM antibodies contribute to the remodelling of glomerular lesions in situ, following glomerular injury by the nephritogenic antibodies.

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Section: Histopathological Examinationmentioning

confidence: 99%