{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T14:57:10Z","timestamp":1791125830720,"version":"4.1.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2015,4,1]],"date-time":"2015-04-01T00:00:00Z","timestamp":1427846400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The paracaspase MALT1 plays an important role in immune receptor-driven signaling pathways leading to NF-\u03baB activation. MALT1 promotes signaling by acting as a scaffold, recruiting downstream signaling proteins, as well as by proteolytic cleavage of multiple substrates. However, the relative contributions of these two different activities to T and B cell function are not well understood. To investigate how MALT1 proteolytic activity contributes to overall immune cell regulation, we generated MALT1 protease-deficient mice (Malt1PD\/PD) and compared their phenotype with that of MALT1 knockout animals (Malt1\u2212\/\u2212). Malt1PD\/PD mice displayed defects in multiple cell types including marginal zone B cells, B1 B cells, IL-10\u2013producing B cells, regulatory T cells, and mature T and B cells. In general, immune defects were more pronounced in Malt1\u2212\/\u2212 animals. Both mouse lines showed abrogated B cell responses upon immunization with T-dependent and T-independent Ags. In vitro, inactivation of MALT1 protease activity caused reduced stimulation-induced T cell proliferation, impaired IL-2 and TNF-\u03b1 production, as well as defective Th17 differentiation. Consequently, Malt1PD\/PD mice were protected in a Th17-dependent experimental autoimmune encephalomyelitis model. Surprisingly, Malt1PD\/PD animals developed a multiorgan inflammatory pathology, characterized by Th1 and Th2\/0 responses and enhanced IgG1 and IgE levels, which was delayed by wild-type regulatory T cell reconstitution. We therefore propose that the pathology characterizing Malt1PD\/PD animals arises from an immune imbalance featuring pathogenic Th1- and Th2\/0-skewed effector responses and reduced immunosuppressive compartments. These data uncover a previously unappreciated key function of MALT1 protease activity in immune homeostasis and underline its relevance in human health and disease.<\/jats:p>","DOI":"10.4049\/jimmunol.1402254","type":"journal-article","created":{"date-parts":[[2015,3,11]],"date-time":"2015-03-11T22:03:23Z","timestamp":1426111403000},"page":"3723-3734","source":"Crossref","is-referenced-by-count":131,"title":["Deficiency of MALT1 Paracaspase Activity Results in Unbalanced Regulatory and Effector T and B Cell Responses Leading to Multiorgan Inflammation"],"prefix":"10.1093","volume":"194","author":[{"given":"Fr\u00e9d\u00e9ric","family":"Bornancin","sequence":"first","affiliation":[{"name":"Novartis Institutes for BioMedical Research, Novartis Pharma AG , 4056 Basel ,","place":["Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Renner","sequence":"additional","affiliation":[{"name":"Novartis Institutes for BioMedical Research, Novartis 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