| First Author | Beamer GL | Year | 2011 |
| Journal | Cell Immunol | Volume | 271 |
| Issue | 1 | Pages | 53-61 |
| PubMed ID | 21714962 | Mgi Jnum | J:176750 |
| Mgi Id | MGI:5292605 | Doi | 10.1016/j.cellimm.2011.06.002 |
| Citation | Beamer GL, et al. (2011) H-2 alleles contribute to antigen 85-specific interferon-gamma responses during Mycobacterium tuberculosis infection. Cell Immunol 271(1):53-61 |
| abstractText | The in vitro immune responses to mycobacterial antigens have been linked to the H-2 loci in mice. We evaluated in vitro and in vivo immune responses during early Mycobacterium tuberculosis (M.tb) pulmonary infection of C57BL/6 (H-2(b)), C57BL/6 (H-2(k)), CBA/J (H-2(k)), and C3H/HeJ (H-2(k)) mice to determine H-2(k)-dependent and -independent effects. H-2(k)-dependent effects included delayed and diminished Ag85-specific Th1 cell priming, a reduced frequency of Ag85-specific IFN-gamma producing cells, reduced IFN-gamma protein in vivo, and increased M.tb lung burden as demonstrated by C57BL/6 H-2(k) mice vs. C57BL/6 mice. H-2(k)-independent factors controlled the amount of Ag85-specific IFN-gamma produced by each cell, T cell numbers, granuloma size, and lymphocytic infiltrates in the lungs. Overall, these results suggest that an H-2(k)-dependent suboptimal generation of Ag85-specific cells impairs control of early M.tb growth in the lungs. H-2(k)-independent factors influence the potency of IFN-gamma producing cells and immune cell trafficking during pulmonary M.tb infection. |
