ArticleFrontiers in immunology2013
Roles for BLyS family members in meeting the distinct homeostatic demands of innate and adaptive B cells.
Article in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- IgM Plasma Cells Reside in Healthy Skin and Accumulate with Chronic Inflammation.The Journal of investigative dermatology · 2019Article
- Regulation of IgMFrontiers in immunology · 2018Article
- B Cell-Intrinsic Expression of the HuR RNA-Binding Protein Is Required for the T Cell-Dependent Immune Response In Vivo.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- APRIL mediates peritoneal B-1 cell homeostasis.Immunology letters · 2014Article
- New roles for the BLyS/BAFF family in antigen-experienced B cell niches.Cytokine & growth factor reviews · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-1 and B-2 B cell populations have different progenitors, receptor diversity, anatomic location, and functions - suggesting vastly differing requisites for homeostatic regulation. There is evidence that the B lymphocyte stimulator (BLyS) family of cytokines and receptors, key factors in the homeostatic regulation of B-2 B cell subsets, is also a major player in the B-1 compartment. Here we review the development and differentiation of these two primary B cell lineages and their immune functions. We discuss evidence that BLyS or a proliferation-inducing ligand (APRIL) availability in different anatomic sites, coupled with signature BLyS receptor expression patterns on different B cell subsets, may be important for homeostatic regulation of B-1 as well as B-2 populations. Finally, we extend our working model of B cell homeostasis to integrate B-1s.
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