Reply to Choubey et al. | Genes & Immunity

Access through your institution Buy or subscribe 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). This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive 6 digital issues and online

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taxes which are calculated during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Gubbels Bupp

MR, Li M, Pashine A, Aud D, Peng SL . The candidate lupus susceptibility gene Ifi202a is largely dispensable for B-cell function. _Rheumatology (Oxford)_ 2008; 47: 103–104. Article  CAS 

Google Scholar  * Wang H, Chatterjee G, Meyer JJ, Liu CJ, Manjunath NA, Bray-Ward P _et al_. Characteristics of three homologous 202 genes (Ifi202a, Ifi202b, and Ifi202c) from the murine

interferon-activatable gene 200 cluster. _Genomics_ 1999; 60: 281–294. Article  CAS  PubMed  Google Scholar  * Rozzo SJ, Allard JD, Choubey D, Vyse TJ, Izui S, Peltz G _et al_. Evidence for

an interferon-inducible gene, Ifi202, in the susceptibility to systemic lupus. _Immunity_ 2001; 15: 435–443. Article  CAS  PubMed  Google Scholar  * Kono DH, Baccala R, Theofilopoulos AN .

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protects against murine lupus. _J Immunol_ 2004; 173: 2134–2142. Article  CAS  PubMed  Google Scholar  Download references AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * 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 Authors

* R Dniesh View author publications You can also search for this author inPubMed Google Scholar * B H Hahn View author publications You can also search for this author inPubMed Google

Scholar * A La Cava View author publications You can also search for this author inPubMed Google Scholar * R P Singh View author publications You can also search for this author inPubMed 

Google Scholar CORRESPONDING AUTHOR Correspondence to R P Singh. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no conflict of interest. RIGHTS AND PERMISSIONS Reprints and

permissions ABOUT THIS ARTICLE CITE THIS ARTICLE 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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