{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T18:30:15Z","timestamp":1789583415690,"version":"build-2803163510"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2025,2,26]],"date-time":"2025-02-26T00:00:00Z","timestamp":1740528000000},"content-version":"vor","delay-in-days":2279,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Mouse strains with specific deficiency of given hematopoietic lineages provide invaluable tools for understanding blood cell function in health and disease. Whereas neutrophils are dominant leukocytes in humans and mice, there are no widely useful genetic models of neutrophil deficiency in mice. In this study, we show that myeloid-specific deletion of the Mcl-1 antiapoptotic protein in Lyz2Cre\/CreMcl1flox\/flox (Mcl1\u0394Myelo) mice leads to dramatic reduction of circulating and tissue neutrophil counts without affecting circulating lymphocyte, monocyte, or eosinophil numbers. Surprisingly, Mcl1\u0394Myelo mice appeared normally, and their survival was mostly normal both under specific pathogen-free and conventional housing conditions. Mcl1\u0394Myelo mice were also able to breed in homozygous form, making them highly useful for in vivo experimental studies. The functional relevance of neutropenia was confirmed by the complete protection of Mcl1\u0394Myelo mice from arthritis development in the K\/B\u00d7N serum-transfer model and from skin inflammation in an autoantibody-induced mouse model of epidermolysis bullosa acquisita. Mcl1\u0394Myelo mice were also highly susceptible to systemic Staphylococcus aureus or Candida albicans infection, due to defective clearance of the invading pathogens. Although neutrophil-specific deletion of Mcl-1 in MRP8-CreMcl1flox\/flox (Mcl1\u0394PMN) mice also led to severe neutropenia, those mice showed an overt wasting phenotype and strongly reduced survival and breeding, limiting their use as an experimental model of neutrophil deficiency. Taken together, our results with the Mcl1\u0394Myelo mice indicate that severe neutropenia does not abrogate the viability and fertility of mice, and they provide a useful genetic mouse model for the analysis of the role of neutrophils in health and disease.<\/jats:p>","DOI":"10.4049\/jimmunol.1701803","type":"journal-article","created":{"date-parts":[[2018,11,21]],"date-time":"2018-11-21T19:29:36Z","timestamp":1542828576000},"page":"3793-3803","source":"Crossref","is-referenced-by-count":53,"title":["Myeloid-Specific Deletion of Mcl-1 Yields Severely Neutropenic Mice That Survive and Breed in Homozygous Form"],"prefix":"10.1093","volume":"201","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8009-139X","authenticated-orcid":false,"given":"Janka Zs\u00f3fia","family":"Csepregi","sequence":"first","affiliation":[{"name":"Department of Physiology, Semmelweis University School of Medicine , 1094 Budapest ,","place":["Hungary"]},{"name":"MTA-SE \u201cLend\u00fclet\u201d Inflammation Physiology Research Group of the Hungarian Academy of Sciences and Semmelweis University , 1094 Budapest ,","place":["Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6839-964X","authenticated-orcid":false,"given":"Anita","family":"Orosz","sequence":"additional","affiliation":[{"name":"Department of Physiology, Semmelweis University School of Medicine , 1094 Budapest ,","place":["Hungary"]},{"name":"MTA-SE \u201cLend\u00fclet\u201d Inflammation Physiology Research Group of the Hungarian Academy of Sciences and Semmelweis University , 1094 Budapest ,","place":["Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Zajta","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Szeged , 6726 Szeged 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