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Review
. 2003 Mar;108(3):263-73.
doi: 10.1046/j.1365-2567.2003.01592.x.

B cell inhibitory receptors and autoimmunity

Nicholas R Pritchard  1 , Kenneth G C Smith
Affiliations
Review

B cell inhibitory receptors and autoimmunity

Nicholas R Pritchard et al. Immunology. 2003 Mar.
No abstract available

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Figures

Figure 1
Figure 1
B cell inhibitory receptors.
Figure 2
Figure 2
The FcγRII inhibitory pathway. Cross-linking of FcγRII to the BCR by immune complexes containing IgG inhibits B cell activation. This occurs through a number of mechanisms that are mediated by SHIP and lyn at key stages.
Figure 3
Figure 3
The CD22 inhibitory pathway. Ligation of CD22 to the BCR and subsequent SHP-1 activation by lyn inhibits B cell activation through a number of mechanisms.
Figure 4
Figure 4
SLE in mice and humans. (a) Antinuclear antibodies in the serum of Lyn deficient mice, shown binding to HEp2 cells (courtesy of Dr D. M. Tarlinton). (b) Immunofluorescence microscopy for IgG demonstrating the deposition of immune complexes in a glomerulus from an SLE patient with membranous (Type V) lupus nephritis. (c) A normal glomerulus. (d) A glomerulus from a patient with SLE showing the inflammatory response to immune complex deposition (diffuse proliferative glomerulonephritis). (e) Crescentic glomerulonephritis with scarring following lupus glomerulonephritis. (f) Discoid lupus; a form of skin rash seen in SLE.
Figure 5
Figure 5
The pathogenesis of SLE. The breakdown in tolerance responsible for the development of autoantibodies (upper panel) is necessary but insufficient to cause disease in the absence of an abnormal inflammatory response to immune complexes (lower panel). Cell types in which FcγRIIb is likely to control antibody production or immune complex handling are shown in red.
See this image and copyright information in PMC

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