Jacob Markiewicz

Kevin M.-C. Lee, Andrew Jarnicki, Adrian Achuthan, Andrew J. Fleetwood, Gary P. Anderson, Christian Ellson, Maria Feeney, Louise K. Modis, Julia E. Smith, John A. Hamilton and Andrew Cook J Immunol July 1, 2020, 205 (1) 213-222; DOI: https://doi.org/10.4049/jimmunol.2000315 Key Points GM-CSF–dependent CCL17 is expressed predominantly in macrophage lineage populations. CCL17 acts on CCR4+ non–bone marrow–derived cells for arthritic pain development.

Kevin M.-C. Lee, Andrew Jarnicki, Adrian Achuthan, Andrew J. Fleetwood, Gary P. Anderson, Christian Ellson, Maria Feeney, Louise K. Modis, Julia E. Smith, John A. Hamilton and Andrew Cook J Immunol May 27, 2020, ji2000315; DOI: https://doi.org/10.4049/jimmunol.2000315 Key Points GM-CSF–dependent CCL17 is expressed predominantly in macrophage lineage populations. CCL17 acts on CCR4+ non–bone marrow–derived cells for arthritic pain development.

The JAK/STAT signaling is critical for the initiation, regulation and termination of immune responses, and dysregulation of JAK/STAT signaling is associated with many pathological conditions such as multiple sclerosis. We previously demonstrated that myeloid lineage–specific deletion of SOCS3, a negative regulator of STAT3, resulted in a severe, non-resolving atypical form of experimental autoimmune encephalomyelitis (EAE).