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Review
. 1999 Jun;97(2):188-96.
doi: 10.1046/j.1365-2567.1999.00772.x.

Do self-perpetuating B lymphocytes drive human autoimmune disease?

J C Edwards  1 , G Cambridge, V M Abrahams
Affiliations
Review

Do self-perpetuating B lymphocytes drive human autoimmune disease?

J C Edwards et al. Immunology. 1999 Jun.

Abstract

Normal immunological memory is thought to be underpinned by T lymphocytes. However, in rheumatoid arthritis there are indications that T-lymphocyte control has been subverted by self-perpetuating B lymphocytes. Potential mechanisms in other autoimmune states are less clear, but a number of observations suggest that misappropriation of immunological memory by B lymphocytes may be a common feature of human autoantibody-associated disease. Put simply, autoantibodies drive their own production. If so, the availability of safe B-lymphocyte-depleting agents provides a potential means for reversal of autoimmunity.

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Figures

Figure 1
Figure 1
A generalized mechanism for autoantibody-associated disease.
Figure 2
Figure 2
Comparison of IgG1 and IgG3 RF dimers showing the difference in hinge length.
Figure 3
Figure 3
A suggested basis for how the long hinge of IgG3 may inhibit IgG3 RF dimers from bringing the signalling γ-chains of FcγRIIIa into apposition.
Figure 4
Figure 4
The basis of ‘bystander’ T-cell help to RF-specific B lymphocytes.
Figure 5
Figure 5
Physiological RF in normal individuals (a); RF in rheumatoid arthritis (b); and RF in HPW (c).
Figure 6
Figure 6
Relative potency of survival signals for autoantigen-specific and RF-specific B cells. Cross-hatching of elements indicates reduced availability because of competition by other ligands.
See this image and copyright information in PMC

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