I used the mice reported by Kitamura et al. (PMID: 1901381, from Jax #002288) as B cell deficient mice, but I heard once that some mature B cells 'escape' in this strain - allegedly especially in some non-lymphoid organs. However, I could not find any reference. Any hint would be appreciated. Thanks!
In the absence of mu Ig heavy chain IgA B cells can still develop by using alpha chain as a surrogate. These IgA B cells require commensal bacteria and peripheral lymphoid tissue to develop and can make up 1-2% of lymphocytes in lymph nodes:
Macpherson, A. J., A. Lamarre, K. McCoy, G. R. Harriman, B. Odermatt,
G. Dougan, H. Hengartner, and R. M. Zinkernagel. 2001. IgA production without mu or delta chain expression in developing B cells. Nat. Immunol. 2: 625–631.
These IgA B1 cells can also switch to IgG and IgE isotypes eg:
Sumit Ghosh, Scott A. Hoselton and Jane M. Schuh. 2012. μ-Chain−Deficient Mice Possess B-1 Cells and Produce IgG and IgE, but Not IgA, following Systemic Sensitization and Inhalational Challenge in a Fungal Asthma Model J Immunol.189:1322-1329.
In the absence of mu Ig heavy chain IgA B cells can still develop by using alpha chain as a surrogate. These IgA B cells require commensal bacteria and peripheral lymphoid tissue to develop and can make up 1-2% of lymphocytes in lymph nodes:
Macpherson, A. J., A. Lamarre, K. McCoy, G. R. Harriman, B. Odermatt,
G. Dougan, H. Hengartner, and R. M. Zinkernagel. 2001. IgA production without mu or delta chain expression in developing B cells. Nat. Immunol. 2: 625–631.
These IgA B1 cells can also switch to IgG and IgE isotypes eg:
Sumit Ghosh, Scott A. Hoselton and Jane M. Schuh. 2012. μ-Chain−Deficient Mice Possess B-1 Cells and Produce IgG and IgE, but Not IgA, following Systemic Sensitization and Inhalational Challenge in a Fungal Asthma Model J Immunol.189:1322-1329.
The earliest observation was by D. Melamed et al. (with David Nemazee as a nearby source for you) in JI 2000. Melamed has gone on to characterize further the phenomenon.
Note that there seem to be genetic (or possibly microbial flora-dependent) factors regulating the extent of the leakiness. Milena Hasan and coworkers (EJI 32: 3463) described that in their animal house BALB/c but not C57BL/6 mice showed leakiness with formation of B cells and production of Ig of most classes except IgM. This is in contrast to Macpherson et al. who found IgA only (but not other classes) in C57BL/6 mice.
Thanks so much. Your help and references are greatly appreciated!
This question and answer complex is of interest in the hematopoietic stem cell (HSC) field. I have met practitioners who consider uMT-/- mice uni-laterally as B cell deficient. The impression of reliable conclusion is insinuated that HSCs in such mice do not/cannot differentiate into the B lymphoid lineage. That "leakage" occurs in BALB/c, but not in C57BL/6, casts doubt on this inference - like all absolutes in the face of biology. In your opinion, how would you interpret the strain-discrepancy in the context of hematopoiesis? I have formed an opinion of my own coming from the stem cell field, yet I would like to know the thoughts of immunologists and genome specialists.
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