Human bone marrow lymphocytes. I. Distribution of lymphocyte subpopulations in the bone marrow of normal individuals.

Fauci, Anthony S.

doi:10.1172/jci108085

Cited by 91 publications

(48 citation statements)

References 29 publications

(31 reference statements)

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“…34 The effect of hemodilution on the distribution of major lymphocyte subsets has been demonstrated previously. [41][42][43] While we did not investigate the effects of hemodilution in this study, it was probably a factor in many of the cases with absent or minute numbers of hematogones. The overall effect of hemodilution on the mean percent hematogones for each of the 5 age groups was presumably minimized by the large number of cases analyzed.…”

Section: Total Specimens 53mentioning

confidence: 96%

Immunophenotypic analysis of hematogones (B-lymphocyte precursors) in 662 consecutive bone marrow specimens by 4-color flow cytometry

McKenna

Washington

Aquino

et al. 2001

Blood

338

281

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Bone marrow hematogones (B-lymphocyte precursors) may cause problems in diagnosis because of their morphologic and immunophenotypic similarities to neoplastic lymphoblasts. The purposes of this prospective, multiparametric flow cytometry study were to quantify hematogones across age groups and a spectrum of clinical conditions, to identify factors that affect the relative quantity of hematogones, and to compare their immunophenotype with that of neoplastic lymphoblasts. A total of 662 consecutive marrow specimens were analyzed for hematogones using one of two 4-color antibody combinations; hematogones were identified in 528 (79.8%). There was a significant decline in hematogones with increasing age (P < .001), but a broad range was found at all ages and many adults had a relatively high number. Specimens processed by density gradient had a higher mean percent hematogones than those processed by erythrocyte lysis (P < .001). There was a direct decline in hematogones with increasing marrow involvement with neoplastic cells. A total of 8% of the 662 specimens contained 5% or more hematogones: 24.6% of specimens from patients aged less than 16 years and 6.3% from those 16 and older (P < .000 01).

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Section: Total Specimens 53mentioning

confidence: 96%

Immunophenotypic analysis of hematogones (B-lymphocyte precursors) in 662 consecutive bone marrow specimens by 4-color flow cytometry

McKenna

Washington

Aquino

et al. 2001

Blood

338

281

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“…This has been achieved by altering the APC of the host (12) or by using fractionated irradiation of the lymphoid tissues (total lymphoid irradiation, TLI) that induces regulatory "natural suppressor" T cells in the host (13,14). However, it is not clear whether these host conditioning regimens can protect against severe GVHD induced by peripheral blood T cells, because in the case of human BM or mobilized hemopoietic progenitor transplantation there is a high level of contamination with these blood T cells (15,16).…”

mentioning

confidence: 99%

Predominance of NK1.1+TCRαβ+ or DX5+TCRαβ+ T Cells in Mice Conditioned with Fractionated Lymphoid Irradiation Protects Against Graft-Versus-Host Disease: “Natural Suppressor” Cells

Lan

Zeng

Higuchi

et al. 2001

The Journal of Immunology

169

161

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We developed a nonmyeloablative host conditioning regimen in a mouse model of MHC-mismatched bone marrow transplantation that not only reduces radiation toxicity, but also protects against graft-vs-host disease. The regimen of fractionated irradiation directed to the lymphoid tissues and depletive anti-T cell Abs results in a marked change in the residual host T cells, such that NK1.1+ or DX5+asialo-GM1+ T cells become the predominant T cell subset in the lymphoid tissues of C57BL/6 and BALB/c mice, respectively. The latter “natural suppressor” T cells protect hosts from graft-vs-host disease after the infusion of allogeneic bone marrow and peripheral blood cells that ordinarily kill hosts conditioned with sublethal or lethal total body irradiation. Protected hosts become stable mixed chimeras, but fail to show the early expansion and infiltration of donor T cells in the gut, liver, and blood associated with host tissue injury. Cytokine secretion and adoptive transfer studies using wild-type and IL-4−/− mice showed that protection afforded by NK1.1+ and DX5+asialo-GM1+ T cells derived from either donors or hosts conditioned with lymphoid irradiation is dependent on their secretion of high levels of IL-4.

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“…Since activated and antibody-secreting cells not found in the peripheral blood may be sequestered in other organs, it was possible that the triggered B cells in Sjogren's syndrome were not circulating, but were sequestered. The bone marrow contains large numbers of B cells in both animals and humans (26)(27)(28)(29). Since the bone marrow can serve as both a source of B cells in humans and a potential site of B cell sequestration, the present study examined the relative levels of B cell activation simultaneously in the peripheral blood and bone marrow of patients with SLE compared to patients with Sjogren's syndrome in order to determine: l) the relationship, if any, between polyclonally activated B cells in the blood and bone marrow and 2) the possibility that activated B cells are sequestered in the bone marrow of patients with Sjogren's syndrome.…”

mentioning

confidence: 99%

Polyclonally triggered B cells in the peripheral blood and bone marrow of normal individuals and in patients with systemic lupus erythematosus and primary sjögren's syndrome

Fauci

Moutsopoulos

1981

Arthritis & Rheumatism

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Numbers of B cells spontaneously secreting Ig (IgC, IgA, and IgM) were determined by a plaque-forming cell (PFC) assay simultaneously in the peripheral blood and bone marrow of normal individuals, patients with systemic lupus erythematosus (SLE), and patients with primary Sjogren's syndrome. Normal individuals had 382 (f 89) PFC per 106 mononuclear cells in peripheral blood. Patients with either active or inactive Sjcigren's syndrome had normal numbers of spontaneous Ig-secreting cells in peripheral blood (P > 0.2). Conversely, patients with inactive as well as active SLE had markedly increased spontaneous PFC (P < 0.05 and P c 0.001, respectively). Patients with active SLE had significantly greater PFC than patients with inactive SLE: 3,984 (+ 960) versus 1,605 (+ 527) PFC per 106 mononuclear cells (P < 0.05). The lack of increased numbers of activated B cells in the blood of patients with Sjogren's syndrome was not explained by a preferential sequestration of activated B cells in the bone marrow. However, of particular interest was the finding that the bone marrow served not only as a major source of virgin B cells but as a lymphoid organ of either in situ Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by bone marrow-derived (B) cell hyperreactivity with hypergammaglobulinemia and autoantibody production (1-5). In addition, abnormalities of thymus-derived (T) cell subsets, particularly a deficiency of suppressor T cells, have been reported in a number of studies (reviewed in reference 5). This association of hyperactive B cells and irnmunoregulatory T cell abnormalities is strongly analogous to the murine models of SLE (6,7). It has been unclear whether the B cell hyperreactivity in SLE is independent from and actually may precede the T cell abnormalities or whether the B cell hyperreactivity results from deficient suppressor cell activity. Of interest in this regard is the fact that certain studies in the murine mod-

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Human bone marrow lymphocytes. I. Distribution of lymphocyte subpopulations in the bone marrow of normal individuals.

Cited by 91 publications

References 29 publications

Immunophenotypic analysis of hematogones (B-lymphocyte precursors) in 662 consecutive bone marrow specimens by 4-color flow cytometry

Immunophenotypic analysis of hematogones (B-lymphocyte precursors) in 662 consecutive bone marrow specimens by 4-color flow cytometry

Predominance of NK1.1+TCRαβ+ or DX5+TCRαβ+ T Cells in Mice Conditioned with Fractionated Lymphoid Irradiation Protects Against Graft-Versus-Host Disease: “Natural Suppressor” Cells

Polyclonally triggered B cells in the peripheral blood and bone marrow of normal individuals and in patients with systemic lupus erythematosus and primary sjögren's syndrome

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