B1 cell
B1 cells are a sub-class of B cell lymphocytes that are involved in the humoral immune response. They are not part of the adaptive immune system, as they have no memory, but otherwise, B1 cells perform many of the same roles as other B cells: making antibodies against antigens and acting as antigen presenting cells. Notably, most B1 cells do not develop into memory B cells.
Origin
B1 cells are first produced in the fetus and most B1 cells undergo self-renewal in the periphery, unlike conventional B cells (B2 cells) that are produced after birth and replaced in the bone marrow.
Types
In January 2011, human B1 cells were found to have marker profile of CD20+CD27+CD43+CD70- and could either be CD5+ or CD5-, which has been debated since.[1] CD5-CD72 is thought to mediate B cell-B cell interaction. B-1 B cells, in the mouse, can be further subdivided into B-1a (CD5+) and B-1b (CD5−) subtypes. Unlike B1a B cells, the B-1b subtype can be generated from precursors in the adult bone marrow. The B1a and B1b precursors have been reported to differ in the expression levels of CD138.[2]
Recent functional studies indicate a further subdivision of labor assigning B1a cells as the precursors of natural serum antibody (7). In contrast, B1b cells appear to be the primary source of dynamic T cell independent (TI) antibody production and long-term protection after bacterial infection such as Borrelia hermsii[3] and Streptococcus pneumoniae .[4] These studies indicate preexisting subset differences in B cell receptor (BCR) specificity and antigen-driven B cell fate that remain important unresolved features of the system.
Role in immune response
B1 cells express IgM in greater quantities than IgG and its receptors show polyspecificity, meaning that they have low affinities for many different antigens. These polyspecific immunoglobulins often have a preference for other immunoglobulins, self antigens and common bacterial polysaccharides. B1 cells are present in low numbers in the lymph nodes and spleen and are instead found predominantly in the peritoneal and pleural cavities. B1 cells generate diversity mainly via recombinatorial recombination (there is a preferential recombination between D-proximal VH gene segments).
B1 B cells characteristically express high levels of secreted IgM (sIgM), demonstrable CD11b, and low levels of secreted IgD (sIgD), CD21, CD23, and the B cell isoform of CD45R (B220).[5] In adult mice, B1 B cells constitute a minor fraction of the spleen and secondary lymphoid tissues but are enriched in the pleural and peritoneal cavities.[6],[7] B1 B cells were shown to arise from precursors in the fetal liver and neonatal but not adult bone marrow and constitute the earliest wave of mature peripheral B cells.
B1 B cells express a separable BCR repertoire.[8] Sequence analysis indicates antibodies with restricted sets of V region genes and an increased usage of λ light chains.[9] B1 B cells sequences also show no evidence for somatic hypermutation (SHM), and few non-templated nucleotide (N) sequence insertions, a pattern typical of neonatal B cells. Efficient B1 B cell development appears to be dependent on positive regulators of BCR signaling and the loss of negative regulators promotes greater accumulation of B1 B cells.[10] Hence, there appears to be a role for self or foreign antigen in shaping the repertoire of the B-1 B cell compartment.[11]
B1 B cells self-renew and spontaneously secrete IgM and IgG3 serum antibodies. These natural serum antibodies display extensive polyreactivity, demonstrable self-reactivity and bind to many common pathogen-associated carbohydrates.[8] Natural serum antibodies play an important early role in the immune response to many bacteria and viruses but require complement fixation for effective antigen clearance. Innate sensing mechanisms can rapidly mobilize B1 B cells regardless of specificity, highlighting the innate-like activity of this separate B cell compartment.
Laboratory isolation
In research laboratories, B1 B cells can be easily isolated from a mouse by injecting cell medium or PBS into the peritoneal cavity of the mouse and then draining it off via a technique mirroring diagnostic peritoneal lavage. Cells can be identified and placed into two categories "B1a" or B1b" using flow cytometry looking for surface expression of CD19, B220, and CD5. B1a expresses high CD5 level, while B1b expresses low CD5 to almost-absent levels; both are CD19+ and B220+.
References
- ^ Griffin DO, Holodick NE, Rothstein TL (January 2011). "Human B1 cells in umbilical cord and adult peripheral blood express the novel phenotype CD20+ CD27+ CD43+ CD70-". J. Exp. Med. 208 (1): 67–80. doi:10.1084/jem.20101499. PMC 3023138. PMID 21220451.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Tung JW, Mrazek MD, Yang Y, Herzenberg LA, Herzenberg LA (April 2006). "Phenotypically distinct B cell development pathways map to the three B cell lineages in the mouse". Proc. Natl. Acad. Sci. U.S.A. 103 (16): 6293–8. doi:10.1073/pnas.0511305103. PMC 1458871. PMID 16606838. Retrieved 2009-12-12.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Alugupalli KR, Leong JM, Woodland RT, Muramatsu M, Honjo T, Gerstein RM (September 2004). "B1b lymphocytes confer T cell-independent long-lasting immunity". Immunity. 21 (3): 379–90. doi:10.1016/j.immuni.2004.06.019. PMID 15357949. Retrieved 2009-12-12.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Haas KM, Poe JC, Steeber DA, Tedder TF (July 2005). "B-1a and B-1b cells exhibit distinct developmental requirements and have unique functional roles in innate and adaptive immunity to S. pneumoniae". Immunity. 23 (1): 7–18. doi:10.1016/j.immuni.2005.04.011. PMID 16039575. Retrieved 2009-12-12.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Ghosn EE, Yang Y, Tung J, Herzenberg LA, Herzenberg LA (April 2008). "CD11b expression distinguishes sequential stages of peritoneal B1 development". Proc. Natl. Acad. Sci. U.S.A. 105 (13): 5195–200. doi:10.1073/pnas.0712350105. PMC 2278228. PMID 18375763. Retrieved 2009-12-12.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Hayakawa K, Hardy RR, Herzenberg LA, Herzenberg LA (June 1985). "Progenitors for Ly1 B cells are distinct from progenitors for other B cells". J. Exp. Med. 161 (6): 1554–68. doi:10.1084/jem.161.6.1554. PMC 2187623. PMID 3874257.
{{cite journal}}:|access-date=requires|url=(help)CS1 maint: multiple names: authors list (link) - ^ Lalor PA, Stall AM, Adams S, Herzenberg LA (March 1989). "Permanent alteration of the murine Ly-1 B repertoire due to selective depletion of Ly1 B cells in neonatal animals". Eur. J. Immunol. 19 (3): 501–6. doi:10.1002/eji.1830190314. PMID 2785045.
{{cite journal}}:|access-date=requires|url=(help)CS1 maint: multiple names: authors list (link) - ^ a b Kantor AB, Herzenberg LA (1993). "Origin of murine B cell lineages". Annu. Rev. Immunol. 11: 501–38. doi:10.1146/annurev.iy.11.040193.002441. PMID 8476571. Retrieved 2009-12-12.
- ^ Hayakawa K., Hardy R.R., Herzenberg L.A. (1986). "Peritoneal Ly-1 B cells: genetic control, autoantibody production, increased lambda light chain expression". Eur J Immunol. 16: 450–456. doi:10.1002/eji.1830160423.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Martin F, Kearney JF (April 2001). "B1 cells: similarities and differences with other B cell subsets". Curr. Opin. Immunol. 13 (2): 195–201. doi:10.1016/S0952-7915(00)00204-1. PMID 11228413. Retrieved 2009-12-12.
- ^ Bendelac A, Bonneville M, Kearney JF (December 2001). "Autoreactivity by design: innate B and T lymphocytes". Nat. Rev. Immunol. 1 (3): 177–86. doi:10.1038/35105052. PMID 11905826.
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