Abstract
Immature B cells are the first B cell progenitors to express a fully formed B cell receptor and are therefore subject to extensive selection processes that act to mitigate the emergence of autoreactive clones. While it is well appreciated that most B cell generation in the bone marrow is highly dependent on access to molecules present in the local milieu, the existence of extrinsically provided factors that modulate immature B cell biology is ambiguous. Nonetheless, a population of CD49b+CD90lo cells has demonstrated in vitro potential to promote immature B cell survival. Using a mouse basophil reporter strain we confirmed the identity of these CD49b+CD90lo supportive cells as basophils. However, analysis of bone marrow B cell populations following lineage specific basophil depletion demonstrates that basophils do not have a significant role in vivo in modulating immature B cell biology during steady-state conditions.
Highlights
The bone marrow microenvironment is critical in supporting B lymphopoiesis and mature B cell function
This issue is of particular significance because it is at the immature stage that central tolerance is enforced though negative selection of autoreactive B cell receptors (BCR) [8]
Staining bone marrow from Basoph8 mice for CD49b, CD90, CD200R3, and the high affinity IgE receptor revealed a dramatic enrichment of basophils (YFP+CD200R3+FcεRIα+) in the CD49b+CD90lo flow cytometry gate as compared to other cell populations (Fig 1A)
Summary
The bone marrow microenvironment is critical in supporting B lymphopoiesis and mature B cell function. While immature B cells are found enriched within and around the bone marrow sinusoids, a definitive cellular niche supportive of their biology has not been characterized in vivo [6,7]. This issue is of particular significance because it is at the immature stage that central tolerance is enforced though negative selection of autoreactive B cell receptors (BCR) [8]. Maturing B cells expressing an autoreactive BCR are able to reexpress the recombinase genes RAG1 and RAG2; in doing so such cells have the opportunity to undergo a secondary rearrangement process termed receptor editing [9,10,11].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
