B220: a B cell-specific member of the T200 glycoprotein family

Coffman, Robert L.

doi:10.1038/289681a0

Cited by 476 publications

(193 citation statements)

References 11 publications

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“…Recent studies have shown that B220, one of murine CD45 isoforms [4], was rapidly induced on the majority of splenic T cells of mice following IL-2 and anti-CD3 mAb stimulation [18]. These activated B220 + cells were undergoing apoptosis.…”

Section: Discussionmentioning

confidence: 99%

B220 is Expressed on Apoptotic Thymocytes Induced by X-Irradiation.

Oka

Kubo

Matsuyama

et al. 1999

The Journal of Veterinary Medical Science

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ABSTRACT. CD45 is cell surface glycoprotein and expressed on all haematopoietic cells except mature erythrocytes and platelets. Eight isoforms of CD45 are generated by alternative splicing of exons 4-6. B220 including all three exons is expressed specifically on pan-B cell lineage. Recently, it was reported that B220 was expressed on apoptotic T cells induced by staphylococcal enterotoxin B (SEB). In the present study, we investigated the expression of B220 on murine thymocytes after whole-body X-irradiation. We used the forward light scattering of flow cytometry as a parameter of cell size, and defined two populations; FSC high (normal cell size) and FSC low (correspond to apoptotic cell in size) fraction. B220 + cells in FSC high fraction reached a maximum value (35%) at 18 hr after irradiation. In FSC low fraction, 40-60% cells were positive for B220 at any time points. These results suggest that B220 is expressed on thymocytes in the pre-apoptotic stage, because B220 was expressed on not only FSC low cells but also FSC high cells.-KEY WORDS: apoptosis, B220, mouse, thymocyte, X-irradiation.J. Vet. Med. Sci. 61(4): [337][338][339][340][341] 1999 kept in a room at a temperature 22 ± 1°C and in a relative humidity of 50 ± 5%, and the room was lighted for 12 hr/ day. Mice were provided commercial NMF diet (Oriental Yeast Co., Ltd., Tokyo, Japan) and acidified water (pH 3) ad libitum. In the present study, each point in the figure is the mean ± standard deviation of three to seven mice. Irradiation: Female 6-week-old mice were exposed to 6.8 Gy of whole-body X-irradiation at a dose rate of 0.46Gy/ min with X-ray irradiator (Radioflex-350; Rigaku Denki Co., Ltd., Tokyo, Japan) operated at 250 kV and 12.5 mA with of 0.3 mm Cu and 0.5 mm Al filtration. Mice were subsequently killed at 0 (control), 3,6,9,12,18, 24, 36, 48, 72 and 168 hr after the irradiation, and then thymi were excised and weighted. Thymocyte suspensions were prepared by gently teasing the thymus with forceps in

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Section: Discussionmentioning

confidence: 99%

B220 is Expressed on Apoptotic Thymocytes Induced by X-Irradiation.

Oka

Kubo

Matsuyama

et al. 1999

The Journal of Veterinary Medical Science

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“…Rat antibody RA3-3A1/6.1 (anti-B220 [16]) was obtained from American Type Culture Collection (Rockville, MD). Biotin-labehd goat anti-hamster IgG antibody (Caltag Laboratories), FITC-conjugated affinity-purified F(ab')2 fragment of rabbit anti-mouse IgG Fc, and biotin-conjugated a~nity-purified F(ab')2 fragment of goat anti-rat IgM (Jackson Immunoresearch, Avondale, PA) were used as second antibodies.…”

Section: Methodsmentioning

confidence: 99%

The development of autoimmunity in C57BL/6 lpr mice correlates with the disappearance of natural killer type 1-positive cells: evidence for their suppressive action on bone marrow stem cell proliferation, B cell immunoglobulin secretion, and autoimmune symptoms.

Takeda

Dennert

1993

The Journal of Experimental Medicine

203

135

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SummaryF1 hybrid mice are able to acutely reject parental marrow grafts, a phenomenon that is due to natural killer type 1-positive (NKI+) cells. Circumstantial evidence had suggested that the antigenic determinants recognized by these cells are self-antigens, leading to the hypothesis that the physiological role of NK1 + cells is a downregulatory or suppressive function on bone marrow stem cell proliferation and lymphocyte function. In analyzing this hypothesis it is shown here that in young mice there is a temporal correlation between appearance of NK1 + cells in the spleen and the ability to reject allogeneic marrow or to suppress endogenous stem cell proliferation. The reverse situation exists in mice expressing the homozygous Ipr gene. Whereas in young mice cells with NK1 + phenotype are demonstrable, these cells disappear with age, i.e., at the time autoimmunity develops. Concomitant with the disappearance of NK1 + cells, the ability to reject marrow grafts and to control endogenous stem cell proliferation also vanishes. The suggestion that the development of autoimmunity is causally related to the disappearance of NK1 + cells is supported by experiments in which NK1 + cells were either eliminated by antibody injection or increased by adoptively transferring cell populations enriched for NK1 + cells into Ipr mice. It is shown that removal of cells enhances autoimmunity, whereas injection of NK1 + cells delays the onset of autoimmunity. In vitro assays are presented that demonstrate that suppression of autoantibody-secreting B cells is due to two NK1 § cell populations, one that expresses CD3 and causes specific suppression and one that lacks CD3 and causes nonspecific suppression.

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“…Christa and Cheryl and I decided to quantitate the colony-forming cells that included B-lineage outcomes, and then to use monoclonal antibodies to prospectively divide the whole bone marrow nonadherent fraction to find the B cell precursors. We used the B220 antibodies that Coffman and I had generated (123), and I remember the evening that Christa and I first looked at the results: B220 + cells were NOT the precursors of the B-lineage colonies, but the B220-negative fraction contained them, enriched appropriately. I realized at that time that we were no longer looking for B cell progenitors, but HSCs, because if B220 + cells were too late in the lineage to make B colonies, marrow cells with T cell and granulocyte and monocyte and other lineage markers would also not make B cell colonies.…”

Section: Wwwannualreviewsorg • How One Thing Led To Anothermentioning

confidence: 99%

How One Thing Led to Another

Weissman

2016

Annu. Rev. Immunol.

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I started research in high school, experimenting on immunological tolerance to transplantation antigens. This led to studies of the thymus as the site of maturation of T cells, which led to the discovery, isolation, and clinical transplantation of purified hematopoietic stem cells (HSCs). The induction of immune tolerance with HSCs has led to isolation of other tissue-specific stem cells for regenerative medicine. Our studies of circulating competing germline stem cells in colonial protochordates led us to document competing HSCs. In human acute myelogenous leukemia we showed that all preleukemic mutations occur in HSCs, and determined their order; the final mutations occur in a multipotent progenitor derived from the preleukemic HSC clone. With these, we discovered that CD47 is an upregulated gene in all human cancers and is a “don't eat me” signal; blocking it with antibodies leads to cancer cell phagocytosis. CD47 is the first known gene common to all cancers and is a target for cancer immunotherapy.

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B220: a B cell-specific member of the T200 glycoprotein family

Cited by 476 publications

References 11 publications

B220 is Expressed on Apoptotic Thymocytes Induced by X-Irradiation.

B220 is Expressed on Apoptotic Thymocytes Induced by X-Irradiation.

The development of autoimmunity in C57BL/6 lpr mice correlates with the disappearance of natural killer type 1-positive cells: evidence for their suppressive action on bone marrow stem cell proliferation, B cell immunoglobulin secretion, and autoimmune symptoms.

How One Thing Led to Another

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