Research Topics
Our group is interested in immune inhibitory pathways and their role in preventing autoimmunity.
Fig. 1. We have generated a new model for systemic autoimmune disease in mice deficient in FcγRIIB, an IgG-binding receptor that inhibits antibody production and inflammatory responses.These mice develop a spontaneous disease that resembles lupus in humans, but only in certain genetic backgrounds. We are studying genetic modifiers that augment susceptibility and severity of disease so that we can understand cellular mechanisms that induce these pathologies and identify new genes that can be used as therapeutic targets.
Figure 2. Addition of the Y chromosome-linked Yaa modifier in the FcγRII-ko lupus model results in aggravated glomerulonephritis and a switch from anti-chromatin to anti-nucleolar autoantibodies. Figure 2. Addition of the Y chromosome-linked Yaa modifier in the FcγRII-ko lupus model results in aggravated glomerulonephritis and a switch from anti-chromatin to anti-nucleolar autoantibodies. Figure 2. Addition of the Y chromosome-linked Yaa modifier in the FcγRII-ko lupus model results in aggravated glomerulonephritis and a switch from anti-chromatin to anti-nucleolar autoantibodies.Figure 3. We have shown that the nucleolar specificity of Yaa-derived antibodies is a B-cell-intrinsic feature resulting from a large genomic duplication that includes the TLR7 gene. Our future experiments will explore expression levels of Toll-like receptors and other genetic factors that regulate the development of autoimmunity.
Biography
Dr. Bolland received her Ph.D. in molecular biology from the University of Cantabria, Spain, and received postdoctoral training at Harvard and The Rockefeller University. She joined the NIAID Laboratory of Immunogenetics in September 2001. She is the recipient of an S.L.E. Foundation Career Development Award and a Novel Research Grant Award from the Lupus Research Institute.
Selected Publications
- Amo L, Kole HK, Scott B, Qi CF, Wu J, Bolland S. CCL17-producing cDC2s are essential in end-stage lupus nephritis and averted by a parasitic infection. J Clin Invest. 2021;131(11).
- Sun W, Wang H, Qi CF, Wu J, Scott B, Bolland S. Antiviral Adaptor MAVS Promotes Murine Lupus With a B Cell Autonomous Role. Front Immunol. 2019;10:2452.
- Walsh ER, Pisitkun P, Voynova E, Deane JA, Scott BL, Caspi RR, Bolland S. Dual signaling by innate and adaptive immune receptors is required for TLR7-induced B-cell-mediated autoimmunity. Proc Natl Acad Sci U S A. 2012;109(40):16276-81.
- Pisitkun P, Deane JA, Difilippantonio MJ, Tarasenko T, Satterthwaite AB, Bolland S. Autoreactive B cell responses to RNA-related antigens due to TLR7 gene duplication. Science. 2006;312(5780):1669-72.
- Amo L, Kole HK, Scott B, Qi CF, Krymskaya L, Wang H, Miller LH, Janse CJ, Bolland S. Plasmodium curtails autoimmune nephritis via lasting bone marrow alterations, independent of hemozoin accumulation. Front Immunol. 2023;14:1192819.
Related Scientific Focus Areas
This page was last updated on Thursday, August 22, 2024