CD11b expression distinguishes sequential stages of peritoneal B-1 development

Ghosn, Eliver; Yang, Yang; Tung, James W.; Herzenberg, Leonard A.; Herzenberg, Leonore A.

doi:10.1073/pnas.0712350105

Cited by 90 publications

(87 citation statements)

References 25 publications

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“…CD11b expression was variable between the groups. CD11b Ϫ B1b cells have been reported previously, at similar proportions to those described here, and have the potential to become CD11b ϩ after transfer into lymphopenic recipients (12). The T-independence of this B1b induction was shown by giving porins or STm to TCR␤␦-deficient mice (Fig.…”

Section: B220supporting

confidence: 88%

The porin OmpD from nontyphoidal Salmonella is a key target for a protective B1b cell antibody response

Gil‐Cruz

Bobat

Marshall

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

155

172

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Section: B220supporting

confidence: 88%

The porin OmpD from nontyphoidal Salmonella is a key target for a protective B1b cell antibody response

Gil‐Cruz

Bobat

Marshall

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

155

172

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“…S1). We also examined the CLP compartment for determinants that would segregate B-1-specified CLPs, like CD138 (17), CD11b (Mac-1) (35), and MHC class II antigens (17,36). However, neither CD138 nor CD11b selectively identified B-1-or B-2-specified CLPs (Figs.…”

Section: Discussionmentioning

confidence: 99%

Reduced production of B-1–specified common lymphoid progenitors results in diminished potential of adult marrow to generate B-1 cells

Barber

Montecino‐Rodriguez

Dorshkind

2011

Proc. Natl. Acad. Sci. U.S.A.

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B-1 B cells have been proposed to be preferentially generated from fetal progenitors, but this view is challenged by studies concluding that B-1 production is sustained throughout adult life. To address this controversy, we compared the efficiency with which hematopoietic stem cells (HSCs) and common lymphoid progenitors (CLPs) from neonates and adults generated B-1 cells in vivo and developed a clonal in vitro assay to quantify B-1 progenitor production from CLPs. Adult HSCs and CLPs generated fewer B-1 cells in vivo compared with their neonatal counterparts, a finding corroborated by the clonal studies that showed that the CLP compartment includes B-1-and B-2-specified subpopulations and that the former cells decrease in number after birth. Together, these data indicate that B-1 lymphopoiesis is not sustained at constant levels throughout life and define a heretofore unappreciated developmental heterogeneity within the CLP compartment.bone marrow | clonal analysis | hematopoiesis I mmune system development has been hypothesized to be a layered process in which lymphoid populations of increased complexity are produced in successive waves in the fetus, neonate, and adult. The initial wave of fetal lymphopoiesis has been proposed to generate lymphocytes involved in innate immunity, whereas waves appearing later produce cells involved in adaptive immune responses (1). A corollary of the layered immune system hypothesis is that, after peaking in the fetus/neonate, the initial wave(s) of lymphopoiesis wanes as the adult wave establishes.The layered immune system hypothesis arose from studies aimed at defining the origin of two types of B lymphocytes, termed B-1 and B-2 cells (2). B-1 cells are innate effectors distinguished by their preferential localization in serous cavities and an unusual sIgM high CD11b + CD5 + B-1a and sIgM high CD11b + CD5 − B-1b phenotype (3, 4). B-1a cells spontaneously secrete IgM natural antibodies, whereas production of Ig by B-1b cells can be induced by antigen exposure, and the latter cells exhibit immunologic memory (5, 6). Human B-1 cells with properties similar to those described in mice have recently been described (7). In contrast, conventional B cells, referred to as B-2 cells, are mediators of adaptive immune responses, predominate in the spleen and lymph nodes, and undergo somatic hypermutation after antigen encounter (8, 9).Studies showing that cells from fetal liver are more efficient than cells from adult bone marrow at reconstituting B-1 cells in irradiated recipients initially suggested that innate B cells arise from progenitors that appear during a fetal wave of development (10, 11). CD5 + B-1a cells, in particular, were preferentially generated from fetal sources (2, 12, 13). These early findings are supported by more recent studies showing the existence of lineage negative (Lin − ) CD45R −/low CD19 + B-1-specified progenitors that arise in the embryonic yolk sac, peak in number in the fetal liver, and then decline in the adult (14-17). Taken together with data showing th...

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“…B1c cells may be a heterogeneous population comprised of transitional cells that develop into B1a cells, splenic B1a cells that have just migrated into the peritoneum, or a unique subset (46,47). The loss of Blc cells induced by B. crocidurae without an associated increase in B1a cells in the peritoneal cavity may be explained if they migrate and then differentiate into either B1a cells or plasma cells outside the peritoneal cavity.…”

Section: Discussionmentioning

confidence: 99%

“…B1b cells can also elicit inducible and long-lasting memory (20). A third subset of Mac1 Ϫ CD5 ϩ B cells has been described as a unique population and termed B1c cells, although they can develop into B1a cells (46,47). Their role during infection has not been studied.…”

mentioning

confidence: 99%

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

Malkiel

Kuhlow

Mena

et al. 2009

The Journal of Immunology

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T cell-independent Abs are protective against Lyme disease and relapsing fever, illnesses caused by Borrelia spirochetes with distinct blood-borne phases of infection. To understand this protective response, we characterized splenic and peritoneal B cell compartments during infection using flow cytometry and immunohistochemistry. In the spleen, early after infection, Borrelia crocidurae, a relapsing fever species, induced a striking loss of marginal zone (MZ) B cells from the MZ, while Borrelia burgdorferi, the agent of Lyme disease, induced the expansion of this subset. At the same time, no significant changes were observed in follicular B cells in response to either species of Borrelia. In the peritoneal cavity, a further loss was demonstrated early in response to B. crocidurae in the B1b, B1c, and B2 cell subsets, but B1a cells were not significantly altered. The loss of B1c and B2 cells was sustained through subsequent peaks of spirochetemia, suggesting these subsets may be important in resolving relapsing episodes. In contrast, an early and significant increase in peritoneal B1a, B1b, and B1c cells, but not B2 cells, occurred in response to B. burgdorferi. Later in the course of infection, both species of Borrelia induced the selective expansion of peritoneal B1b cells, suggesting that B1b cells may participate in long-lasting immunity to Lyme and relapsing fever spirochetes. Our data demonstrate that different Borrelia can activate the same B cell subsets in distinct ways and they each elicit a complex interplay of MZ and multiple peritoneal B cell subsets in the early response to infection.

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CD11b expression distinguishes sequential stages of peritoneal B-1 development

Cited by 90 publications

References 25 publications

The porin OmpD from nontyphoidal Salmonella is a key target for a protective B1b cell antibody response

The porin OmpD from nontyphoidal Salmonella is a key target for a protective B1b cell antibody response

Reduced production of B-1–specified common lymphoid progenitors results in diminished potential of adult marrow to generate B-1 cells

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

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