GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation

Abstract GATA-binding factor 1 (GATA1) is a transcription that governs the development and function of multiple hematopoietic cell lineages. GATA1 expressed in stem progenitor cells (HSPCs) essential for erythroid lineage commitment; however, whether it plays role (HSC) biology myeloid cells, what might be, remains unclear. We initially set out to test eosinophils experimental autoimmune encephalomyelitis (EAE), model central nervous system autoimmunity, using mice lacking double GATA-site (ΔdblGATA), which lacks due deletion dblGATA enhancer Gata1, alters its expression. ΔdblGATA were resistant EAE, but not because lack eosinophils, suggesting these have an additional defect. with EAE had fewer inflammatory than control mice, resistance caused by defect cells. Naïve also showed reduced frequency CD11b +myeloid blood, indicating production. Examination HSPCs revealed HSCs progenitors bone marrow (BM), competitive BM chimera experiments capacity reconstitute immune numbers cause functional deficit during inflammation. Taken together, our data show regulates number expression results diminished response following challenge. This work was supported grant from National Institute Allergy Infectious Diseases, Institutes Health (T32 training T32AI134646).