Lillia A. Baird

1 Introduction Amyotrophic lateral sclerosis (ALS) is an incurable and rapidly fatal motor neuron disease causing progressive cranial, limb, and respiratory weakness [1]. Among the complex pathophysiology of ALS [1, 2], immune system dysregulation is consistently implicated [3, 4], and the immune system appears to contribute to ALS pathology both in mouse models [5, 6] and human patients [3, 7].

Christine V. Odom, Yuri Kim, Claire L. Burgess, Lillia A. Baird, Filiz T. Korkmaz, Elim Na, Anukul T. Shenoy, Emad I. Arafa, TuKiet T. Lam, Matthew R. Jones, Joseph P. Mizgerd, Katrina E. Traber and Lee J. Quinton J Immunol October 1, 2021, 207 (7) 1891-1902; DOI: https://doi.org/10.4049/jimmunol.2100254 Key Points Hepatic STAT3 activity remodels lung transcription and proteomics during endotoxemia. Cytokine responses to secondary lung infection are altered without intact liver input.

Christine V. Odom, Yuri Kim, Claire L. Burgess, Lillia A. Baird, Filiz T. Korkmaz, Elim Na, Anukul T. Shenoy, Emad I. Arafa, TuKiet T. Lam, Matthew R. Jones, Joseph P. Mizgerd, Katrina E. Traber and Lee J. Quinton J Immunol September 1, 2021, ji2100254; DOI: https://doi.org/10.4049/jimmunol.2100254 Key Points Hepatic STAT3 activity remodels lung transcription and proteomics during endotoxemia. Cytokine responses to secondary lung infection are altered without intact liver input.