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Germline CARD11 mutations cause at least three types of primary immunodeficiency including CARD11 deficiency, B cell expansion with NF-\u03baB and T cell anergy (BENTA), and CARD11-associated atopy with dominant interference of NF-\u03baB signaling (CADINS). CADINS is uniquely caused by heterozygous loss-of-function CARD11 alleles that act as dominant negatives. CADINS patients present with frequent respiratory and skin infections, asthma, allergies, and atopic dermatitis. However, precisely how a heterozygous dominant negative CARD11 allele leads to the development of this CADINS-specific cluster of symptoms remains poorly understood. To address this, we generated mice expressing the CARD11 R30W allele originally identified in patients. We find that CARD11R30W\/+ mice exhibit impaired signaling downstream of CARD11 that leads to defects in T, B, and NK cell function and immunodeficiency. CARD11R30W\/+ mice develop elevated serum IgE levels with 50% penetrance that becomes more pronounced with age, but do not develop spontaneous atopic dermatitis. CARD11R30W\/+ mice display reduced regulatory T cell numbers, but not the Th2 expansion observed in other mice with diminished CARD11 activity. Interestingly, the presence of mixed CARD11 oligomers in CARD11R30W\/+ mice causes more severe signaling defects in T cells than in B cells, and specifically impacts IFN-\u03b3 production by NK cells, but not NK cell cytotoxicity. Our findings help explain the high susceptibility of CADINS patients to infection and suggest that the development of high serum IgE is not sufficient to induce overt atopic symptoms.<\/jats:p>","DOI":"10.4049\/jimmunol.2001233","type":"journal-article","created":{"date-parts":[[2021,8,2]],"date-time":"2021-08-02T16:20:43Z","timestamp":1627921243000},"page":"1150-1164","source":"Crossref","is-referenced-by-count":22,"title":["Pathway-Specific Defects in T, B, and NK Cells and Age-Dependent Development of High IgE in Mice Heterozygous for a CADINS-Associated Dominant Negative CARD11 Allele"],"prefix":"10.1093","volume":"207","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8380-5012","authenticated-orcid":false,"given":"Shelby M","family":"Hutcherson","sequence":"first","affiliation":[{"name":"Department of Biological Chemistry and Institute for Cell Engineering, The Johns Hopkins University School of Medicine , Baltimore, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacquelyn R","family":"Bedsaul","sequence":"additional","affiliation":[{"name":"Department of Biological Chemistry and Institute for Cell Engineering, The Johns Hopkins University School of Medicine , Baltimore, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5030-1018","authenticated-orcid":false,"given":"Joel L","family":"Pomerantz","sequence":"additional","affiliation":[{"name":"Department of Biological Chemistry and Institute for Cell Engineering, The Johns Hopkins University School of Medicine , Baltimore, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,8,15]]},"reference":[{"key":"2025022610320670200_r1","doi-asserted-by":"crossref","first-page":"2105","DOI":"10.3389\/fimmu.2018.02105","article-title":"Mechanisms of Regulated and Dysregulated CARD11 Signaling in Adaptive Immunity and Disease","volume":"9","author":"Bedsaul","year":"2018","journal-title":"Front. 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