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Reply to Choubey et al.

Genes & Immunity volume 12, page 496 (2011)Cite this article

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A Corrigendum to this article was published on 01 December 2011

The work cited in our manuscript states that Ifi202a is dispensable for B-cell functions and it suppresses inflammatory responses, B cell activation, proliferation and immunoglobulin production.1 The authors used Ifi202a knockout mouse cells compared with Ifi202 wild-type mice. The mechanisms described included Rb, E2F2 and nuclear factor-κB.3 The main focus of our work was to define the role of Ifi202b in peptide-induced CD8+ regulatory T cells in (NZBX NZW) F1 lupus mice. This gene came up together with interferon (IFN)AR1 in our microarray analyses. Its expression was upregulated in tolerized CD8+T cells as compared with non-tolerized or negative control peptide-treated CD8+ T cells from BWF1 mice. In this manuscript, we did not explore the whole family of Ifi200 cluster genes, and thus the issues raised by Dr Choubey are beyond the scope of our manuscript. It has to be kept in mind that other family members of Ifi200 (currently 10 or more), such as Ifi203, Ifi204, Ifi205, p204, p205, p206, AIM2, IFI16, MNDA and so on, may also have an additional role in the protection versus susceptibility from systemic lupus erythematosis (SLE), and that it may also depend on the mouse strain. For example, SLE was prevented or reduced in NZB mice in which IFNAR1, the RI receptor for type I IFNs such as IFNα, was knocked out.4 In contrast, knockout of the RI receptor in MRL/lpr mice worsened autoimmune disease.5 We are not disputing and agree with Dr Choubey on the fact that Ifi200 antibody can detect both Ifi 202a and Ifi200b. In our experiments, we tested four antibodies (Ifi200 (S-19-sc-6054), (Ifi200 (F-7-sc-166253), Ifi200 (M-70)-sc-50358 and Ifi200 (M-20) sc-6048), and found that the antibody from clone F-7 works the best in our model. The positive control to detect Ifi202b was 293T whole-cell lysates.

Regarding the comments on the RT-PCR nucleotide sequences used in our experiments, we used both custom-designed and validated primers and probes (assay ID for Ifi202b is Mm 00839397_M1). The NCBI database is constantly being updated, yet it does not mean the sequence is not specific. There are several reasons not to get specific blast results, such as masking of some of the BLAST programs by default, and not increasing the expected threshold to see shorter alignments. BLAST 2 sequences use the size of the current nucleotide or protein database to calculate expected values. There are other reasons that blast result may fail, and we relied upon the validated Applied Biosystem primers and probes for real-time PCR (Applied Biosystems, Foster City, CA, USA).

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References

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Authors and Affiliations

  1. Division of Rheumatology, Department of Medicine at the David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA

    R Dniesh, B H Hahn, A La Cava & R P Singh

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  1. R Dniesh
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  2. B H Hahn
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  3. A La Cava
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  4. R P Singh
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Correspondence to R P Singh.

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Dniesh, R., Hahn, B., La Cava, A. et al. Reply to Choubey et al.. Genes Immun 12, 496 (2011). https://doi.org/10.1038/gene.2011.48

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