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Comment
. 2014 Jun 24;111(25):9022-3.
doi: 10.1073/pnas.1407877111. Epub 2014 Jun 11.

Redemption of autoreactive B cells

Barton F Haynes  1 , Laurent Verkoczy  2 , Garnett Kelsoe  3
Affiliations
Comment

Redemption of autoreactive B cells

Barton F Haynes et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
Experimental demonstration of autoantibody redemption in the HEL transgenic mouse system. (A) The immunization schema that allowed detection of rescued anergic autoreactive B cells following HEL-RBC immunization. HEL-specific B cells from double-transgenic mice, rendered anergic because of their prior encounter with soluble-expressed HEL, were injected into HEL transgenic mice, together with a HEL-SRBC immunogen. Immunized mice driven to generate anergic HEL-specific GC B cells were induced to acquire mutations in the HEL antibody HCDR2 region that resulted in decreased affinity for HEL and increased B-cell survival. (B) An illustration of how such a mechanism may contribute to bnAb responses during HIV-1 infection, and how B-cell populations generated by this process could be harnessed in the setting of HIV-1 vaccination. Vaccination with HIV-1 Env may result in either a population of anergic GC B cells, which have accumulated somatic mutations that generate bnAb specifcity (red) and self-reactivity (black), but may also generate rare B cells with BCR that harbor decreased self-reactivity, while retaining bnAb HIV-1 Env affinity. The hypothesis is that Env vaccination targeted at disfavored bnAb B-cell clonal lineages could drive otherwise unfavored and rare HIV-1–specific B-cell clones in GC to survive and proliferate.
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