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HAX1 deficiency: Impact on lymphopoiesis and B-cell development


Peckl-Schmid, D; Wolkerstorfer, S; Königsberger, S; Achatz-Straussberger, G; Feichtner, S; Schwaiger, E; Zaborsky, N; Huemer, M; Gratz, I K; Schibli, R; Lamers, M; Crameri, R; Moser, K; Luger, E O; Achatz, G (2010). HAX1 deficiency: Impact on lymphopoiesis and B-cell development. European Journal of Immunology, 40(11):3161-3172.

Abstract

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.
Copyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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.
Copyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Swiss Institute of Allergy and Asthma Research
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2010
Deposited On:28 Feb 2011 13:24
Last Modified:05 Apr 2016 14:50
Publisher:Wiley-Blackwell
ISSN:0014-2980
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:10.1002/eji.200940221
PubMed ID:20865787
Permanent URL: http://doi.org/10.5167/uzh-46915

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