Amano, H.

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  • Amano, H. (2)
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Author's Bibliography

Differential activation of anti-erythrocyte and anti-DNA autoreactive B lymphocytes by the Yaa mutation

Moll, T.; Martinez-Soria, E.; Santiago-Raber, ML; Amano, H.; Pihlgren-Bosch, M; Marinković, Dragan; Izui, S

(Amer Assoc Immunologists, Bethesda, 2005)

TY  - JOUR
AU  - Moll, T.
AU  - Martinez-Soria, E.
AU  - Santiago-Raber, ML
AU  - Amano, H.
AU  - Pihlgren-Bosch, M
AU  - Marinković, Dragan
AU  - Izui, S
PY  - 2005
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/36
AB  - An as-yet-unidentified mutation, Y-linked autoimmune acceleration (Yaa), is responsible for the accelerated development of lupus-like autoimmune syndrome in mice. In view of a possible role for Yaa as a positive regulator of BCR signaling, we have explored whether the expression of the Yaa mutation affects the development and activation of transgenic autoreactive B cells expressing either 4C8 IgM anti-RBC or Sp6 IgM anti-DNA. In this study, we show that the expression of the Yaa mutation induced a lethal form of autoimmune hemolytic anemia in 4C8 transgenic C57BL/6 mice, likely as a result of activation of 4C8 anti-RBC autoreactive B cells early in life. This was further supported, although indirectly, by increased T cell-independent IgM production in spleens of nontransgenic C57BL/6 mice bearing the Yaa mutation. In contrast, Yaa failed to induce activation of Sp6 anti-DNA autoreactive B cells, consistent with a lack of increased IgM anti-DNA production in nontransgenic C57BL/6 Yaa mice. Our results suggest that Yaa can activate autoreactive B cells in a BCR-dependent manner, related to differences in the form and nature of autoantigens.
PB  - Amer Assoc Immunologists, Bethesda
T2  - Journal of Immunology
T1  - Differential activation of anti-erythrocyte and anti-DNA autoreactive B lymphocytes by the Yaa mutation
EP  - 709
IS  - 2
SP  - 702
VL  - 174
DO  - 10.4049/jimmunol.174.2.702
ER  - 
@article{
author = "Moll, T. and Martinez-Soria, E. and Santiago-Raber, ML and Amano, H. and Pihlgren-Bosch, M and Marinković, Dragan and Izui, S",
year = "2005",
abstract = "An as-yet-unidentified mutation, Y-linked autoimmune acceleration (Yaa), is responsible for the accelerated development of lupus-like autoimmune syndrome in mice. In view of a possible role for Yaa as a positive regulator of BCR signaling, we have explored whether the expression of the Yaa mutation affects the development and activation of transgenic autoreactive B cells expressing either 4C8 IgM anti-RBC or Sp6 IgM anti-DNA. In this study, we show that the expression of the Yaa mutation induced a lethal form of autoimmune hemolytic anemia in 4C8 transgenic C57BL/6 mice, likely as a result of activation of 4C8 anti-RBC autoreactive B cells early in life. This was further supported, although indirectly, by increased T cell-independent IgM production in spleens of nontransgenic C57BL/6 mice bearing the Yaa mutation. In contrast, Yaa failed to induce activation of Sp6 anti-DNA autoreactive B cells, consistent with a lack of increased IgM anti-DNA production in nontransgenic C57BL/6 Yaa mice. Our results suggest that Yaa can activate autoreactive B cells in a BCR-dependent manner, related to differences in the form and nature of autoantigens.",
publisher = "Amer Assoc Immunologists, Bethesda",
journal = "Journal of Immunology",
title = "Differential activation of anti-erythrocyte and anti-DNA autoreactive B lymphocytes by the Yaa mutation",
pages = "709-702",
number = "2",
volume = "174",
doi = "10.4049/jimmunol.174.2.702"
}
Moll, T., Martinez-Soria, E., Santiago-Raber, M., Amano, H., Pihlgren-Bosch, M., Marinković, D.,& Izui, S.. (2005). Differential activation of anti-erythrocyte and anti-DNA autoreactive B lymphocytes by the Yaa mutation. in Journal of Immunology
Amer Assoc Immunologists, Bethesda., 174(2), 702-709.
https://doi.org/10.4049/jimmunol.174.2.702
Moll T, Martinez-Soria E, Santiago-Raber M, Amano H, Pihlgren-Bosch M, Marinković D, Izui S. Differential activation of anti-erythrocyte and anti-DNA autoreactive B lymphocytes by the Yaa mutation. in Journal of Immunology. 2005;174(2):702-709.
doi:10.4049/jimmunol.174.2.702 .
Moll, T., Martinez-Soria, E., Santiago-Raber, ML, Amano, H., Pihlgren-Bosch, M, Marinković, Dragan, Izui, S, "Differential activation of anti-erythrocyte and anti-DNA autoreactive B lymphocytes by the Yaa mutation" in Journal of Immunology, 174, no. 2 (2005):702-709,
https://doi.org/10.4049/jimmunol.174.2.702 . .
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The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells

Amano, H.; Amano, E.; Moll, T.; Marinković, Dragan; Ibnou-Zekri, N; Martinez-Soria, E.; Semac, I; Wirth, Thomas; Nitschke, L.; Izui, S

(Amer Assoc Immunologists, Bethesda, 2003)

TY  - JOUR
AU  - Amano, H.
AU  - Amano, E.
AU  - Moll, T.
AU  - Marinković, Dragan
AU  - Ibnou-Zekri, N
AU  - Martinez-Soria, E.
AU  - Semac, I
AU  - Wirth, Thomas
AU  - Nitschke, L.
AU  - Izui, S
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/32
AB  - The accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of an as yet unidentified mutant gene, Yaa (Y-linked autoimmune acceleration). In view of a possible role of marginal zone (MZ) B cells in murine SLE, we have explored whether the expression of the Yaa mutation affects the differentiation of MZ and follicular B cells, thereby implicating the acceleration of the disease. In this study, we show that both BXSB and C57BL/6 Yaa mice, including two different substrains of BXSB Yaa males that are protected from SLE, displayed an impaired development of MZ B cells early in life. Studies in bone marrow chimeras revealed that the loss of MZ B cells resulted from a defect intrinsic to B cells expressing the Yaa mutation. The lack of selective expansion of MZ B cells in diseased BXSB Yaa males strongly argues against a major role of MZ B cells in the generation of pathogenic autoantibodies in the BXSB model of SLE. Furthermore, a comparative analysis with mice deficient in CD22 or expressing an IgM anti-trinitrophenyl/DNA transgene suggests that the hyperreactive phenotype of Yaa B cells, as judged by a markedly increased spontaneous IgM secretion, is likely to contribute to the enhanced maturation toward follicular B cells and the block in the MZ B cell generation.
PB  - Amer Assoc Immunologists, Bethesda
T2  - Journal of Immunology
T1  - The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells
EP  - 2301
IS  - 5
SP  - 2293
VL  - 170
DO  - 10.4049/jimmunol.170.5.2293
ER  - 
@article{
author = "Amano, H. and Amano, E. and Moll, T. and Marinković, Dragan and Ibnou-Zekri, N and Martinez-Soria, E. and Semac, I and Wirth, Thomas and Nitschke, L. and Izui, S",
year = "2003",
abstract = "The accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of an as yet unidentified mutant gene, Yaa (Y-linked autoimmune acceleration). In view of a possible role of marginal zone (MZ) B cells in murine SLE, we have explored whether the expression of the Yaa mutation affects the differentiation of MZ and follicular B cells, thereby implicating the acceleration of the disease. In this study, we show that both BXSB and C57BL/6 Yaa mice, including two different substrains of BXSB Yaa males that are protected from SLE, displayed an impaired development of MZ B cells early in life. Studies in bone marrow chimeras revealed that the loss of MZ B cells resulted from a defect intrinsic to B cells expressing the Yaa mutation. The lack of selective expansion of MZ B cells in diseased BXSB Yaa males strongly argues against a major role of MZ B cells in the generation of pathogenic autoantibodies in the BXSB model of SLE. Furthermore, a comparative analysis with mice deficient in CD22 or expressing an IgM anti-trinitrophenyl/DNA transgene suggests that the hyperreactive phenotype of Yaa B cells, as judged by a markedly increased spontaneous IgM secretion, is likely to contribute to the enhanced maturation toward follicular B cells and the block in the MZ B cell generation.",
publisher = "Amer Assoc Immunologists, Bethesda",
journal = "Journal of Immunology",
title = "The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells",
pages = "2301-2293",
number = "5",
volume = "170",
doi = "10.4049/jimmunol.170.5.2293"
}
Amano, H., Amano, E., Moll, T., Marinković, D., Ibnou-Zekri, N., Martinez-Soria, E., Semac, I., Wirth, T., Nitschke, L.,& Izui, S.. (2003). The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells. in Journal of Immunology
Amer Assoc Immunologists, Bethesda., 170(5), 2293-2301.
https://doi.org/10.4049/jimmunol.170.5.2293
Amano H, Amano E, Moll T, Marinković D, Ibnou-Zekri N, Martinez-Soria E, Semac I, Wirth T, Nitschke L, Izui S. The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells. in Journal of Immunology. 2003;170(5):2293-2301.
doi:10.4049/jimmunol.170.5.2293 .
Amano, H., Amano, E., Moll, T., Marinković, Dragan, Ibnou-Zekri, N, Martinez-Soria, E., Semac, I, Wirth, Thomas, Nitschke, L., Izui, S, "The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells" in Journal of Immunology, 170, no. 5 (2003):2293-2301,
https://doi.org/10.4049/jimmunol.170.5.2293 . .
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