Wheat germ agglutinin-positive cells in a stem cell-enriched fraction of mouse bone marrow have potent natural suppressor activity.

Sugiura, Kikuya; Inaba, Muneo; Ogata, Hiroaki; Yasumizu, Ryoji; Inaba, Kayo; Good, Robert A.; Ikehara, Susumu

doi:10.1073/pnas.85.13.4824

Cited by 76 publications

(43 citation statements)

References 13 publications

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“…Thus, the Gr-1 ϩ suppressor cells described in this work are different from those found to be expanded in response to a schistosome-expressed immunomodulatory glycoconjugate and to suppress the proliferative activity of naive CD4 ϩ T cells via an IFN-␥ and NO dependent mechanism (24). A population of alternatively activated macrophages that suppress CD4 ϩ T cells reactivity by an as-yet-unknown mechanism, but in an IFN-␥/NO-independent manner, has been reported (53).…”

Section: On Cd4mentioning

confidence: 68%

“…Two distinct subpopulations of myeloid suppressors have been characterized. CA MSC are NO and IFN-␥ dependent (24,28), whereas alternatively activated MSC are IL-4 dependent (17,18,26,29,30,52). An immature myeloid cell line strongly up-regulated its suppressive functions after exposure to IL-4 (26) and, interestingly, the exposure to IL-4 also up-regulated CD80 expression on these cells (26), whereas exposure to IFN-␥ did not up-regulate CD80 expression on human PMN (32).…”

Section: Discussionmentioning

confidence: 99%

“…Two distinct subpopulations of MSC have been characterized. Classically activated (CA) MSC are NO and IFN-␥ dependent (23,24), whereas alternatively activated MSC are IL-4 dependent (16,17,28,29).…”

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confidence: 99%

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CD80+Gr-1+ Myeloid Cells Inhibit Development of Antifungal Th1 Immunity in Mice with Candidiasis

Mencacci

Montagnoli

Bacci

et al. 2002

The Journal of Immunology

124

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To find out whether polymorphonuclear neutrophils (PMN), abundantly recruited in disseminated Candida albicans infection, could directly affect the activation of Th cells we addressed the issues as to whether murine PMN, like their human counterparts, express costimulatory molecules and the functional consequence of this expression in terms of antifungal immune resistance. To this purpose, we assessed 1) the expression of CD80 (B7-1) and CD86 (B7-2) molecules on peripheral, splenic, and inflammatory murine Gr-1+ PMN; 2) its modulation upon interaction with C. albicans in vitro, in vivo, and in human PMN; 3) the effect of Candida exposure on the ability of murine PMN to affect CD4+ Th1 cell proliferation and cytokine production; and 4) the mechanism responsible for this effect. Murine PMN constitutively expressed CD80 molecules on both the surface and intracellularly; however, in both murine and human PMN, CD80 expression was differentially modulated upon interaction with Candida yeasts or hyphae in vitro as well as in infected mice. The expression of the CD86 molecule was neither constitutive nor inducible upon exposure to the fungus. In vitro, Gr-1+ PMN were found to inhibit the activation of IFN-γ-producing CD4+ T cells and to induce apoptosis through a CD80/CD28-dependent mechanism. A population of CD80+Gr-1+ myeloid cells was found to be expanded in conventional as well as in bone marrow-transplanted mice with disseminated candidiasis, but its depletion increased the IFN-γ-mediated antifungal resistance. These data indicate that alternatively activated PMN expressing CD80 may adversely affect Th1-dependent resistance in fungal infections.

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Section: On Cd4mentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

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CD80+Gr-1+ Myeloid Cells Inhibit Development of Antifungal Th1 Immunity in Mice with Candidiasis

Mencacci

Montagnoli

Bacci

et al. 2002

The Journal of Immunology

124

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“…T cells were depleted from the whole BMCs by treatment with the monoclonal antibody (mAb) against Thy1.2 (clone HO-13-4, ATCC; Rockville, MD) and rabbit complement (Perfreeze; Brown Deer, WI). The wheat germ agglutinin (WGA)-positive (HSC-enriched) BMC fraction was prepared as previously described [17,18] with a minor modification. In brief, low-density BMCs ([LDBMCs]; 1.060-1.073 g/ml) were separated from whole BMCs by equilibrium density centrifugation (1,000 g, 30 min, 4°C) on discontinuous density gradients of Percoll (Pharmacia-LKB; Uppsala, Sweden) solution.…”

Section: Preparation Of Bmcsmentioning

confidence: 99%

Requirement of Major Histocompatibility Complex‐Compatible Microenvironment for Spleen Colony Formation (CFU‐S on day 12 but not on day 8)

Sugiura¹,

Inaba²,

Hisha³

et al. 1997

STEM CELLS

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To clarify major histocompatibility complex (MHC) restriction between hematopoietic stem cells (HSCs) and microenvironments, T cell-depleted bone marrow cells (BMCs) were transplanted into MHC-compatible and MHC-incompatible recipients. A significantly large number of spleen colony-forming units (CFU-S) on day 12 were noted in MHC-compatible recipients, while only a small number were observed in MHC-incompatible recipients. There was, however, no significant difference in CFU-S counts on day 8 between the two groups. A large number of CFU-S counts on day 12 were also observed in F1 hybrid recipients, as seen in syngeneic recipients. The decrease in CFU-S counts on day 12 in MHC-incompatible recipients was also observed even after in vivo abrogation of T and NK cells. The difference in CFU-S counts on day 12 became more prominent when HSC-enriched cells were transferred. These results suggest that an MHC restriction exists between pluripotent HSCs (P-HSCs) and spleen microenvironments. Furthermore, experiments using B10.A recombinant strains revealed that H-2D and S loci play a crucial role in the MHC restriction. The experiments of serial transplantation suggest that the differentiation and proliferation of P-HSCs are inhibited in MHC-incompatible microenvironments. It is therefore likely that the MHC-compatible microenvironment is essential to the differentiation and proliferation of P-HSCs.

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“…Moreover, when the total bone marrow cells were fractionated by Percoll density-gradient centrifugation, APO-H gene expression was detected in STIL-3 C5-CM stimulated fraction (Fr.) 2 (1.064<ρ<1.074), which has been reported to be a hematopoietic stem cell rich fraction (Sugiura et al, 1988).…”

Section: Pcr Analysismentioning

confidence: 99%

Identification of Negative Regulator of Interleukin-3 (NIL-3) in Bone Marrow.

Adachi

Sugimoto²,

Sato³

et al. 2002

Cell Struct. Funct.

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ABSTRACT. We have reported that an inhibitor of interleukin-3 (NIL-3) is produced from murine bone marrow cells in response to excess stimulation of interleukin-3. In this report, we attempted the purification of the NIL-3 activity from bone marrow culture supernatant in the presence of interleukin-3. The purified NIL-3 activity was a protein with relative molecular weight of 54.5 kDa (SDS-PAGE), which inhibited the growth of IL-3 dependent DA-1 cell growth in a dose dependent manner. The N-terminal amino acid sequence of purified NIL-3 activity was determined to be homologous to beta-2 glycoprotein I (apolipoprotein H: APO-H). The gene expression of APO-H was detected by nested-PCR in STIL-3 C5-CM stimulated total bone marrow cells and STIL-3 C5-CM stimulated bone marrow fraction 2 (Fr. 2) which has been reported as a hematopoietic stem cell rich fraction. These observations indicate the possibility that the APO-H is the NIL-3 which was produced from bone marrow cells in response to excess IL-3 stimuli.

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Wheat germ agglutinin-positive cells in a stem cell-enriched fraction of mouse bone marrow have potent natural suppressor activity.

Abstract: In the present study we have characterized natural suppressor (NS) cells, which nonspeciflically suppress mitogen responses and mixed-lymphocyte reaction. The strongest NS activity was found in a fraction of relatively low-density cells (1.

Cited by 76 publications

References 13 publications

CD80+Gr-1+ Myeloid Cells Inhibit Development of Antifungal Th1 Immunity in Mice with Candidiasis

CD80+Gr-1+ Myeloid Cells Inhibit Development of Antifungal Th1 Immunity in Mice with Candidiasis

Requirement of Major Histocompatibility Complex‐Compatible Microenvironment for Spleen Colony Formation (CFU‐S on day 12 but not on day 8)

Identification of Negative Regulator of Interleukin-3 (NIL-3) in Bone Marrow.

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