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Host genetics significantly impacts tuberculosis outcomes. A specific mouse strain (CC042) shows high susceptibility due to a novel mutation in the Itgal gene, impairing T cell function and increasing bacterial load.

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Area of Science:

  • Immunology
  • Genetics
  • Microbiology

Background:

  • Host genetics influences tuberculosis (TB) infection outcomes.
  • Collaborative Cross (CC) mouse strains exhibit varied susceptibility to Mycobacterium tuberculosis.
  • The CC042 strain displays rapid disease progression and impaired gamma interferon (IFN-γ) production.

Purpose of the Study:

  • Investigate the genetic and immunological basis of CC042 mouse susceptibility to M. tuberculosis.
  • Identify quantitative trait loci (QTL) associated with TB immunophenotypes.
  • Characterize the role of specific gene variants in disease pathogenesis.

Main Methods:

  • Crossbreeding CC001 and CC042 mouse strains to create an intercross population.
  • Mapping quantitative trait loci (QTL) for TB immunophenotypes (Tip1-Tip4).
  • Immunological characterization of T cell recruitment and integrin alpha L (CD11a) expression in CC042 mice.
  • Genetic analysis of the Itgal gene and its variants.

Main Results:

  • Four QTL (Tip1-Tip4) were mapped, influencing bacterial burden, IFN-γ production, and IFN-γ-independent bacterial control.
  • CC042 mice showed reduced recruitment of antigen-specific T cells to the lung.
  • A CC042-specific deletion in the Itgal gene (encoding CD11a) caused aberrant mRNA splicing and predicted truncated protein.
  • This Itgal variant was strongly associated with all measured disease traits, indicating a major role in susceptibility.

Conclusions:

  • A novel loss-of-function mutation in the Itgal gene is a primary driver of CC042 mouse susceptibility to M. tuberculosis.
  • Multigenic factors, including distinct Tip variants, contribute to the severe TB phenotype in CC042 mice.
  • The Collaborative Cross mouse resource is valuable for dissecting the genetic control of mycobacterial disease and host-pathogen interactions.