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Previously, we developed a panel of <jats:italic>H2<\/jats:italic>\u2010congenic mouse strains differing by small segments of the major histocompatibility complex Class II (MHC\u2010II) region from TB\u2010susceptible <jats:italic>H2<\/jats:italic><jats:sup>j<\/jats:sup> mice transferred onto the genetic background of the TB\u2010resistant C57BL\/6 (<jats:italic>H2<\/jats:italic><jats:sup>b<\/jats:sup>) strain. Susceptible B6.I\u20109.3 mice differ from B6 progenitors by the alleles of their only classical MHC\u2010II <jats:italic>H2\u2010A\u03b2<\/jats:italic> gene. The goals of the present study were to: (i) comprehensively characterise the differences in TB\u2010related phenotypes between mice of the two strains and (ii) decipher interactions between the <jats:italic>H2\u2010A\u03b2<\/jats:italic> and <jats:italic>S100A8\/9<\/jats:italic> genes. Here, we describe the dynamics of TB\u2010related phenotypes differentiating B6.I\u20109.3 and B6 mice (colony forming units\u00a0counts, histopathology, lung immune cell infiltration and cytokine profiles). We show that disproportionally diminished CD4<jats:sup>+<\/jats:sup> T\u2010cell population, an enlarged S100A8\/9\u2010positive neutrophil population and higher S100A8\/9 serum levels in B6.I\u20109.3 mice collectively form the \u2018susceptible\u2019 phenotype before infection. An increase in IL\u201017 and a decrease in intrferon\u2010gamma production by CD4<jats:sup>+<\/jats:sup> T\u2010cells in these mice provide a mechanistic explanation of this phenotype. Using F2 segregation analysis, we show that the number of S100A8\/9\u2010producing neutrophils in lungs and spleens and the proportion of Th17 CD4<jats:sup>+<\/jats:sup> T\u2010cells in lungs are significantly lower in the presence of the <jats:italic>MHC\u2010II<\/jats:italic> dominant \u2018resistant\u2019 <jats:italic>b<\/jats:italic> allele compared to the recessive \u2018susceptible\u2019 <jats:italic>j\/j<\/jats:italic> genotype. This provides direct genetic evidence that MHC\u2010II\u2010regulated CD4<jats:sup>+<\/jats:sup> T\u2010cell landscapes determine neutrophil abundance before infection, an important pathogenic factor in TB immunity.<\/jats:p>","DOI":"10.1111\/imm.13836","type":"journal-article","created":{"date-parts":[[2024,7,14]],"date-time":"2024-07-14T14:48:45Z","timestamp":1720968525000},"page":"381-393","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Polygenic <scp>TB<\/scp> control and the sequence of innate\/adaptive immune responses to infection: <scp>MHC<\/scp>\u2010<scp>II<\/scp> alleles determine the size of the <scp>S100A8<\/scp>\/9\u2010producing neutrophil population"],"prefix":"10.1111","volume":"173","author":[{"given":"Nadezhda","family":"Logunova","sequence":"first","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marina","family":"Kapina","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Dyatlov","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatiana","family":"Kondratieva","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elvira","family":"Rubakova","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Konstantin","family":"Majorov","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Kondratieva","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1535-5800","authenticated-orcid":false,"given":"Irina","family":"Linge","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3683-3085","authenticated-orcid":false,"given":"Alexander","family":"Apt","sequence":"additional","affiliation":[{"name":"Laboratory for Immunogenetics Central Tuberculosis Research Institute  Moscow Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,7,14]]},"reference":[{"key":"e_1_2_9_2_1","unstructured":"WHO.Global tuberculosis report.https:\/\/creativecommons.org\/licenses\/by-nc-sa\/3.0\/igo(2019). 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