Beta1 integrin is not essential for hematopoiesis but is necessary for the T cell-dependent IgM antibody response.
(2002) In Immunity 16(3). p.465-477- Abstract
- Several experimental evidences suggested that beta1 integrin-mediated adhesion of hematopoietic stem cells (HSC) is important for their function in the bone marrow (BM). Using induced deletion of the beta1 integrin gene restricted to the hematopoietic system, we show that beta1 integrin is not essential for HSC retention in the BM, hematopoiesis, and trafficking of lymphocytes. However, immunization with a T cell-dependent antigen resulted in virtually no IgM production and an increased secretion of IgG in mutant mice, while the response to a T cell-independent type 2 antigen showed decreases in both IgM and IgG. These data suggest that beta1 integrins are necessary for the primary IgM antibody response.
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/107139
- author
- Brakebusch, Cord LU ; Fillatreau, Simon ; Potocnik, Alexandre J ; Bungartz, Gerd ; Wilhelm, Patricia ; Svensson Frej, Marcus LU ; Kearney, Phil ; Körner, Heinrich ; Gray, David and Fässler, Reinhard LU
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- CD29 : immunology, Antigens, CD29 : genetics, Hematopoiesis : genetics, Gene Expression Regulation : immunology, Gene Deletion, B-Lymphocytes : immunology, Immunoglobulin M : biosynthesis, Immunoglobulin M : genetics, Immunoglobulin M : immunology, Mice, Support, Non-U.S. Gov't, T-Lymphocytes : immunology, Antibody Formation : immunology, Animal, Antibody Formation : genetics
- in
- Immunity
- volume
- 16
- issue
- 3
- pages
- 465 - 477
- publisher
- Cell Press
- external identifiers
-
- wos:000174572800014
- pmid:11911830
- scopus:18344384036
- ISSN
- 1074-7613
- DOI
- 10.1016/S1074-7613(02)00281-9
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Pathology, (Lund) (013030000), Eosinophil Biology (013210067)
- id
- b15bb13e-a559-428c-80d8-b76d94c43e97 (old id 107139)
- alternative location
- http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11911830&dopt=Abstract
- date added to LUP
- 2016-04-01 12:17:55
- date last changed
- 2022-03-13 08:01:26
@article{b15bb13e-a559-428c-80d8-b76d94c43e97, abstract = {{Several experimental evidences suggested that beta1 integrin-mediated adhesion of hematopoietic stem cells (HSC) is important for their function in the bone marrow (BM). Using induced deletion of the beta1 integrin gene restricted to the hematopoietic system, we show that beta1 integrin is not essential for HSC retention in the BM, hematopoiesis, and trafficking of lymphocytes. However, immunization with a T cell-dependent antigen resulted in virtually no IgM production and an increased secretion of IgG in mutant mice, while the response to a T cell-independent type 2 antigen showed decreases in both IgM and IgG. These data suggest that beta1 integrins are necessary for the primary IgM antibody response.}}, author = {{Brakebusch, Cord and Fillatreau, Simon and Potocnik, Alexandre J and Bungartz, Gerd and Wilhelm, Patricia and Svensson Frej, Marcus and Kearney, Phil and Körner, Heinrich and Gray, David and Fässler, Reinhard}}, issn = {{1074-7613}}, keywords = {{CD29 : immunology; Antigens; CD29 : genetics; Hematopoiesis : genetics; Gene Expression Regulation : immunology; Gene Deletion; B-Lymphocytes : immunology; Immunoglobulin M : biosynthesis; Immunoglobulin M : genetics; Immunoglobulin M : immunology; Mice; Support; Non-U.S. Gov't; T-Lymphocytes : immunology; Antibody Formation : immunology; Animal; Antibody Formation : genetics}}, language = {{eng}}, number = {{3}}, pages = {{465--477}}, publisher = {{Cell Press}}, series = {{Immunity}}, title = {{Beta1 integrin is not essential for hematopoiesis but is necessary for the T cell-dependent IgM antibody response.}}, url = {{http://dx.doi.org/10.1016/S1074-7613(02)00281-9}}, doi = {{10.1016/S1074-7613(02)00281-9}}, volume = {{16}}, year = {{2002}}, }