Am J Blood Res 2013;3(2):124-140
Original Article
MyD88 is involved in myeloid as well as lymphoid hematopoiesis independent
of the presence of a pathogen
Katja Fiedler, Enikö Kokai, Susanne Bresch, Cornelia Brunner
Ulm University, Institute of Physiological Chemistry, D-89081 Ulm, Germany
Received February 11, 2013; Accepted April 6, 2013; Epub May 5, 2013; Published May 15, 2013
Abstract: MyD88 was originally described as a primary response gene up-regulated during myeloid differentiation after IL-6
induction. Later, MyD88 was shown to be a key molecule necessary for IL1, IL18 and Toll-like receptor signaling. Since these
receptors recognize abundantly produced cytokines during infection or molecular patterns of pathogens, MyD88 itself was
suggested to be an important regulator of the first line of defense against invading pathogens, including the differentiation and
maturation of myeloid cells. Here we describe that MyD88 is important for early and late hematopoietic events that occur
independently of antigen under steady-state conditions. In MyD88-deficient mice the earliest alteration in hematopoiesis was
found at the level of long-term hematopoietic stem cells. Moreover, we found that MyD88 influences not only the development
of the myeloid lineage but also the differentiation of B cells. The B cell defect observed in Btk-deficient mice is further
enhanced when both molecules, Btk and MyD88, are not expressed. Therefore, MyD88 affects myeloid as well as lymphoid
hematopoiesis. Since Btk and MyD88 deficiencies influence differentially myeloid and lymphoid development, both molecules
seem to act in different signaling pathways important for appropriate developmental events during myelo- and lymphopoiesis.
(AJBR1302002).
Keywords: MyD88, Btk, hematopoiesis, myelopoiesis, lymphopoiesis
Address correspondence to: Dr. Cornelia Brunner, Ulm University, Institute of Physiological Chemistry, Albert-Einstein-Allee
11, D-89081 Ulm, Germany. Tel: +49-731-500-33846; Fax: +49-731-500-22892; E-mail: cornelia.brunner@uni-ulm.de
Original Article
MyD88 is involved in myeloid as well as lymphoid hematopoiesis independent
of the presence of a pathogen
Katja Fiedler, Enikö Kokai, Susanne Bresch, Cornelia Brunner
Ulm University, Institute of Physiological Chemistry, D-89081 Ulm, Germany
Received February 11, 2013; Accepted April 6, 2013; Epub May 5, 2013; Published May 15, 2013
Abstract: MyD88 was originally described as a primary response gene up-regulated during myeloid differentiation after IL-6
induction. Later, MyD88 was shown to be a key molecule necessary for IL1, IL18 and Toll-like receptor signaling. Since these
receptors recognize abundantly produced cytokines during infection or molecular patterns of pathogens, MyD88 itself was
suggested to be an important regulator of the first line of defense against invading pathogens, including the differentiation and
maturation of myeloid cells. Here we describe that MyD88 is important for early and late hematopoietic events that occur
independently of antigen under steady-state conditions. In MyD88-deficient mice the earliest alteration in hematopoiesis was
found at the level of long-term hematopoietic stem cells. Moreover, we found that MyD88 influences not only the development
of the myeloid lineage but also the differentiation of B cells. The B cell defect observed in Btk-deficient mice is further
enhanced when both molecules, Btk and MyD88, are not expressed. Therefore, MyD88 affects myeloid as well as lymphoid
hematopoiesis. Since Btk and MyD88 deficiencies influence differentially myeloid and lymphoid development, both molecules
seem to act in different signaling pathways important for appropriate developmental events during myelo- and lymphopoiesis.
(AJBR1302002).
Keywords: MyD88, Btk, hematopoiesis, myelopoiesis, lymphopoiesis
Address correspondence to: Dr. Cornelia Brunner, Ulm University, Institute of Physiological Chemistry, Albert-Einstein-Allee
11, D-89081 Ulm, Germany. Tel: +49-731-500-33846; Fax: +49-731-500-22892; E-mail: cornelia.brunner@uni-ulm.de
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