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17 beta-estradiol expands IgA-Producing b cells in mice deficient for the mu chain

Lagerquist, M. K. ; Erlandsson, M. C. ; Islander, U. ; Svensson, L. ; Holmdahl, Rikard LU and Carlsten, H. (2008) In Scandinavian Journal of Immunology 67(1). p.12-17
Abstract
Oestrogen is not only a sex hormone but also an important regulator of the immune system. Expression of the heavy chain of IgM (mu) is essential for B-cell differentiation. However, a small number of IgA-positive B cells can be found in mice lacking the mu chain (mu MT-/-). The aim of this study was to investigate the effects of oestrogen on this alternative B-cell pathway in mu MT-/- mice. Our results clearly demonstrate that oestrogen increases the frequency of IgA-producing B cells in mu MT-/- mice in both bone marrow and spleen cells. We also show that mature IgM-producing B cells are not required for oestrogen-mediated suppression of granulocyte-mediated inflammation or thymic involution. In conclusion, we demonstrate that 17... (More)
Oestrogen is not only a sex hormone but also an important regulator of the immune system. Expression of the heavy chain of IgM (mu) is essential for B-cell differentiation. However, a small number of IgA-positive B cells can be found in mice lacking the mu chain (mu MT-/-). The aim of this study was to investigate the effects of oestrogen on this alternative B-cell pathway in mu MT-/- mice. Our results clearly demonstrate that oestrogen increases the frequency of IgA-producing B cells in mu MT-/- mice in both bone marrow and spleen cells. We also show that mature IgM-producing B cells are not required for oestrogen-mediated suppression of granulocyte-mediated inflammation or thymic involution. In conclusion, we demonstrate that 17 beta-estradiol benzoate increases the frequency of IgA-producing B cells in mu MT-/- mice, suggesting that oestrogen can influence the alternative B-cell pathway found in mu MT-/- mice. (Less)
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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Scandinavian Journal of Immunology
volume
67
issue
1
pages
12 - 17
publisher
Wiley-Blackwell
external identifiers
  • wos:000251329700002
  • scopus:36749043215
  • pmid:18021189
ISSN
1365-3083
DOI
10.1111/j.1365-3083.2007.02027.x
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: Medical Inflammation Research (013212019)
id
0630c844-4980-4b79-aec1-f2d92a0358d4 (old id 966473)
date added to LUP
2016-04-01 12:52:55
date last changed
2022-01-27 08:07:03
@article{0630c844-4980-4b79-aec1-f2d92a0358d4,
  abstract     = {{Oestrogen is not only a sex hormone but also an important regulator of the immune system. Expression of the heavy chain of IgM (mu) is essential for B-cell differentiation. However, a small number of IgA-positive B cells can be found in mice lacking the mu chain (mu MT-/-). The aim of this study was to investigate the effects of oestrogen on this alternative B-cell pathway in mu MT-/- mice. Our results clearly demonstrate that oestrogen increases the frequency of IgA-producing B cells in mu MT-/- mice in both bone marrow and spleen cells. We also show that mature IgM-producing B cells are not required for oestrogen-mediated suppression of granulocyte-mediated inflammation or thymic involution. In conclusion, we demonstrate that 17 beta-estradiol benzoate increases the frequency of IgA-producing B cells in mu MT-/- mice, suggesting that oestrogen can influence the alternative B-cell pathway found in mu MT-/- mice.}},
  author       = {{Lagerquist, M. K. and Erlandsson, M. C. and Islander, U. and Svensson, L. and Holmdahl, Rikard and Carlsten, H.}},
  issn         = {{1365-3083}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{12--17}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Scandinavian Journal of Immunology}},
  title        = {{17 beta-estradiol expands IgA-Producing b cells in mice deficient for the mu chain}},
  url          = {{http://dx.doi.org/10.1111/j.1365-3083.2007.02027.x}},
  doi          = {{10.1111/j.1365-3083.2007.02027.x}},
  volume       = {{67}},
  year         = {{2008}},
}