Page 117 - The Vasculitides, Volume 1: General Considerations and Systemic Vasculitis

Experimental Autoimmune Vasculitis 93

References

[1] Kain, R., Exner, M., Brandes, R., et al. Molecular mimicry in pauci-immune focal
necrotizing glomerulonephritis. Nat. Med. 2008; 14:1088-1096.

[2] Suzuki, K., Nagao, T., Nakayama, T. Proposal of anti-moesin as a novel biomarker for
ANCA-associated vasculitis. Clin. Exp. Nephrol. 2013; 17:638-641.

[3] Xiao, H., Schreiber, A., Heeringa, P., et al. Alternative complement pathway in the
pathogenesis of disease mediated by anti-neutrophil cytoplasmic autoantibodies. Am. J.
Pathol. 2007; 170:52-64.

[4] Neumann, I., Birck, R., Newman, M., et al. SCG/Kinjoh mice: a model of ANCA-
associated crescentic glomerulonephritis with immune deposits. Kidney Int. 2003; 64:
140-148.

[5] Xiao, H., Heeringa, P., Hu, P., et al. Antineutrophil cytoplasmic autoantibodies specific
for myeloperoxidase cause glomerulonephritis and vasculitis in mice. J. Clin. Invest.
2002; 110:955-963.

[6] Xiao, H., Heeringa, P., Liu, Z., et al. The role of neutrophils in the induction of
glomerulonephritis by anti-myeloperoxidase antibodies. Am. J. Pathol. 2005; 167:39-
45.

[7] Huugen, D., Xiao, H., van Esch, A., et al. Aggravation of anti-myeloperoxidase
antibody-induced glomerulonephritis by bacterial lipopolysaccharide: role of tumor
necrosis factor-alpha. Am. J. Pathol. 2005; 167:47-58.

[8] Xiao, H. The role of genetic background in an animal model of ANCA associated
vasculitis. Presse Med. 2013; 42:517-520.

[9] Jennette, J. C., Xiao, H., Falk, R. J., et al. Experimental models of vasculitis and
glomerulonephritis induced by antineutrophil cytoplasmic autoantibodies. Contrib.
Nephrol. 2011; 169:211-220.

[10] Xiao, H., Dairaghi, D. J., Powers, J. P., et al. C5a Receptor (CD88) Blockade Protects
against MPO-ANCA GN. J. Am. Soc. Nephrol. 2013 Oct. 31. [Epub. ahead of print].

[11] http://clinicaltrials.gov/show/NCT01363388.
[12] Schreiber, A., Xiao, H., Falk, R. J., et al. Bone marrow-derived cells are sufficient and

necessary targets to mediate glomerulonephritis and vasculitis induced by anti-
myeloperoxidase antibodies. J. Am. Soc. Nephrol. 2006; 17:3355-3364.
[13] Ruth, A. J., Kitching, A. R., Kwan, R. Y., et al. Anti-neutrophil cytoplasmic antibodies
and effector CD4+ cells play nonredundant roles in anti-myeloperoxidase crescentic
glomerulonephritis. J. Am. Soc. Nephrol. 2006; 17:1940-1949.
[14] Gan, P. Y., Steinmetz, O. M., Tan, D. S., et al. Th17 cells promote autoimmune anti-
myeloperoxidase glomerulonephritis. J. Am. Soc. Nephrol. 2010; 21:925-931.
[15] Nogueira, E., Hamour, S., Sawant, D., et al. Serum IL-17 and IL-23 levels and
autoantigen-specific Th17 cells are elevated in patients with ANCA-associated
vasculitis. Nephrol. Dial. Transplant. 2010; 25:2209-2217.
[16] Summers, S. A., Steinmetz, O. M., Gan, P. Y., et al. Toll-like receptor 2 induces Th17
myeloperoxidase autoimmunity while Toll-like receptor 9 drives Th1 autoimmunity in
murine vasculitis. Arthritis Rheum. 2011; 63:1124-1135.
[17] Chavele, K. M., Shukla, D., Keteepe-Arachi, T., et al. Regulation of myeloperoxidase-
specific T cell responses during disease remission in antineutrophil cytoplasmic

Complimentary Contributor Copy