HAX1 deficiency: Impact on lymphopoiesis and B-cell development

Doris Peckl-Schmid, Susanne Wolkerstorfer, Sebastian Königsberger, Gertrude Achatz-Straussberger, Stefan Feichtner, Elisabeth Schwaiger, Nadja Zaborsky, Michael Huemer, Iris K. Gratz, Roger Schibli, Marinus Lamers, Reto Crameri, Katrin Moser, Elke O. Luger, Gernot Achatz*

*Corresponding author for this work
16 Citations (Scopus)


HAX1 was originally described as HS1-associated protein with a suggested function in receptor-mediated apoptotic and proliferative responses of lymphoid cells. Recent publications refer to a complex and multifunctional role of this protein. To investigate the in vivo function of HAX1 (HS1-associated protein X1) in B cells, we generated a Hax1-deficient mouse strain. Targeted deletion of Hax1 resulted in premature death around the age of 12 wk accompanied by a severe reduction of lymphocytes in spleen, thymus and bone marrow. In the bone marrow, all B-cell populations were lost comparably. In the spleen, B220 + cells were reduced by almost 70%. However, as investigated by adoptive transfer experiments, this impairment is not exclusively B-cell intrinsic and we hypothesize that a HAX1-deficient environment cannot sufficiently provide the essential factors for proper lymphocyte development, trafficking and survival. Hax1 -/- B cells show a significantly reduced expression of CXCR4, which might have an influence on the observed defects in B-cell development.

Original languageEnglish
JournalEuropean Journal of Immunology
Issue number11
Pages (from-to)3161-3172
Number of pages12
Publication statusPublished - 01.12.2010

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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