| Autor: |
Mahmoudi Aliabadi, Pedram, Al‐Qaisi, Khlowd, Jani, Peter K., Honjo, Kazuhito, Klemm, Uwe, Lee, Kyeong‐Hee, Baumgarth, Nicole, Radbruch, Andreas, Melchers, Fritz, Kubagawa, Hiromi |
| Předmět: |
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| Zdroj: |
European Journal of Immunology; Jul2023, Vol. 53 Issue 7, p1-13, 13p |
| Abstrakt: |
In previous studies, Mott cells, an unusual form of plasma cells containing Ig‐inclusion bodies, were frequently observed in peripheral lymphoid tissues in our IgM Fc receptor (FcμR)‐deficient (KO) mouse strain. Because of discrepancies in the reported phenotypes of different Fcmr KO mouse strains, we here examined two additional available mutant strains and confirmed that such enhanced Mott‐cell formation was a general phenomenon associated with FcμR deficiency. Splenic B cells from Fcmr KO mice clearly generated more Mott cells than those from WT mice when stimulated in vitro with LPS alone or a B‐1, but not B‐2, activation cocktail. Nucleotide sequence analysis of the Ig variable regions of a single IgMλ+ Mott‐hybridoma clone developed from splenic B‐1 B cells of Fcmr KO mice revealed the near (VH) or complete (Vλ) identity with the corresponding germline gene segments and the addition of six or five nucleotides at the VH/DH and DH/JH junctions, respectively. Transduction of an FcμR cDNA into the Mott hybridoma significantly reduced cells containing IgM‐inclusion bodies with a concomitant increase in IgM secretion, leading to secreted IgM binding to FcμR expressed on Mott transductants. These findings suggest a regulatory role of FcμR in the formation of Mott cells and IgM‐inclusion bodies. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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