| First Author | Shahaf G | Year | 2012 |
| Journal | Eur J Immunol | Volume | 42 |
| Issue | 2 | Pages | 511-21 |
| PubMed ID | 22057631 | Mgi Jnum | J:179824 |
| Mgi Id | MGI:5304220 | Doi | 10.1002/eji.201141940 |
| Citation | Shahaf G, et al. (2012) Lyn deficiency affects B-cell maturation as well as survival. Eur J Immunol 42(2):511-21 |
| abstractText | Lyn, an Src-family protein tyrosine kinase expressed in B lymphocytes, contributes to initiation of BCR signaling and is also responsible for feedback inhibition of BCR signaling. Lyn-deficient mice have a decreased number of follicular B cells and also spontaneously develop a lupus-like autoimmunity. We used flow cytometric analysis, BrdU labeling and our mathematical models of B-cell population dynamics, to analyze how Lyn deficiency impacts B-cell maturation and survival. We found that Lyn-deficient transitional 1 (T1) cells develop normally, but T2 cells develop primarily from the T1 subset in the spleen and fail to also develop directly from BM immature B cells. Lyn-deficient T2 cells either mature to the follicular B-cell type at a close to normal rate, or die in this compartment rather than access the T3 anergic subset. The approximately 40% of WT follicular cells that were short-lived exited primarily by joining the T3 anergic subset, whereas the approximately 15% Lyn(-/-) follicular cells that were not long lived had a high death rate and died in this compartment rather than entering the T3 subset. We hypothesize that exaggerated BCR signaling resulting from weak interactions with self-antigens is largely responsible for these alterations in Lyn-deficient B cells. |
