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                <term xml:lang="en">DNA End-Joining Repair</term>
                <term xml:lang="en">V(D)J Recombination</term>
                <term xml:lang="en">VDJ recombination</term>
                <term xml:lang="en">Young Adult</term>
                <term xml:lang="en">DNA-dependent protein kinase catalytic subunit</term>
                <term xml:lang="en">DNA-Activated Protein Kinase</term>
                <term xml:lang="en">Transcription Factors</term>
                <term xml:lang="en">B-Lymphocytes</term>
                <term xml:lang="en">Autoimmunity</term>
                <term xml:lang="en">Autoimmune regulator</term>
                <term xml:lang="en">Autoantibodies</term>
                <term xml:lang="en">Animals</term>
                <term xml:lang="en">Adolescent</term>
                <term xml:lang="en">Nuclear Proteins</term>
                <term xml:lang="en">Gene Expression Regulation</term>
                <term xml:lang="en">Granuloma</term>
                <term xml:lang="en">Humans</term>
                <term xml:lang="en">Immune Tolerance</term>
                <term xml:lang="en">Immunologic Deficiency Syndromes</term>
                <term xml:lang="en">Male</term>
                <term xml:lang="en">Mice</term>
                <term xml:lang="en">Mutation</term>
                <term xml:lang="en">Female</term>
                <term xml:lang="en">PRKDC</term>
                <term xml:lang="en">recombination-activating gene</term>
                <term xml:lang="en">severe combined immunodeficiency</term>
                <term xml:lang="en">Skin Neoplasms</term>
                <term xml:lang="en">Th1 Cells</term>
                <term xml:lang="en">Th2 Cells</term>
                <term xml:lang="en">tolerance</term>
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              <p>BACKGROUND: PRKDC encodes for DNA-dependent protein kinase catalytic subunit (DNA-PKcs), a kinase that forms part of a complex (DNA-dependent protein kinase [DNA-PK]) crucial for DNA double-strand break repair and V(D)J recombination. In mice DNA-PK also interacts with the transcription factor autoimmune regulator (AIRE) to promote central T-cell tolerance. OBJECTIVE: We sought to understand the causes of an inflammatory disease with granuloma and autoimmunity associated with decreasing T- and B-cell counts over time that had been diagnosed in 2 unrelated patients. METHODS: Genetic, molecular, and functional analyses were performed to characterize an inflammatory disease evocative of a combined immunodeficiency. RESULTS: We identified PRKDC mutations in both patients. These patients exhibited a defect in DNA double-strand break repair and V(D)J recombination. Whole-blood mRNA analysis revealed a strong interferon signature. On activation, memory T~cells displayed a skewed cytokine response typical of TH2 and TH1 but not TH17. Moreover, mutated DNA-PKcs did not promote AIRE-dependent transcription of peripheral tissue antigens in~vitro. The latter defect correlated in~vivo with production of anti-calcium-sensing receptor autoantibodies, which are typically found in AIRE-deficient patients. In addition, 9 months after bone marrow transplantation, patient 1~had Hashimoto thyroiditis, suggesting that organ-specific autoimmunity might be linked to nonhematopoietic cells, such as AIRE-expressing thymic epithelial cells. CONCLUSION: Deficiency of DNA-PKcs, a key AIRE partner, can present as an inflammatory disease with organ-specific autoimmunity, suggesting a role for DNA-PKcs in regulating autoimmune responses and maintaining AIRE-dependent tolerance in human subjects.</p>
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