Absence of major histocompatibility class II expression does not impair hematopoiesis in mice

Objective Major histocompatibility class II (MHC II) molecules are among the earliest antigens to be expressed in hematopoietic progenitor cells; however, the functional role of these molecules in hematopoiesis remains controversial. We examined the role of MHC II antigens during hematopoiesis using a mouse model of MHC II deficiency related to the absence of the critical transcriptional activator, CIITA. Methods Sca-1−, Sca-1+lin+, and Sca-1+lin− populations of marrow cells from CIITA−/− and wild-type mice were analyzed by immunofluorescence for MHC II expression. Hematopoietic capacity was assessed in CIITA−/− and wild-type mice by CFU-S, CFU-GM, and radiation sensitivity assays. Results Flow cytometric characteristics of hematopoietic progenitors from CIITA−/− and wild-type mice were identical except for the absence of MHC II expression in CIITA null mice. There were no significant differences in capacity for hematopoietic reconstitution and clonogenicity as measured by radiation sensitivity, CFU-S, and CFU-GM assays among CIITA−/− and wild-type mice. Conclusions These experiments show that downregulation of MHC II gene transcription does not effectively alter normal hematopoiesis, and provide strong evidence that MHC II expression on hematopoietic progenitors is not required for normal hematopoietic development.