Induction of autoimmune gastritis by neonatal thymectomy requires autoantibodies and is prevented by anti-FcγR antibodies

Tsubasa Saito; Satoru Suenaga; Masato Fujii; Yoshihiro Kushida; Yusuke Kawauchi; Kenji Suzuki; Maki Touma; Masamichi Hosono

doi:10.1016/j.cellimm.2015.10.004

Induction of autoimmune gastritis by neonatal thymectomy requires autoantibodies and is prevented by anti-FcγR antibodies

Tsubasa Saito, Satoru Suenaga, Masato Fujii, Yoshihiro Kushida, Yusuke Kawauchi, Kenji Suzuki, Maki Touma, Masamichi Hosono

Research output: Contribution to journal › Article › peer-review

1 Citation (Scopus)

Abstract

The autoantibodies (auto-Abs) that are a hallmark of neonatally thymectomized (NTx) mice with autoimmune gastritis (AIG) have been poorly explored. We investigated their immune significance using B cell-deficient (B^-) mice and found that B^- mice are totally resistant to AIG but become susceptible to AIG after receiving bone marrow cells from B⁺ mice. This susceptibility is most likely caused by the production of auto-Abs by B cells because B^- pups also became susceptible to AIG when nourished by an AIG dam producing auto-Abs of the IgG class during the suckling period. NTx B^- mice receiving purified IgG auto-Abs at this developmental stage similarly developed AIG. Auto-Abs probably act on antigen handling for antigen presentation because the treatment of NTx B⁺ mice with anti-FcγR Abs prevented the development of AIG. Auto-Abs are indispensable for AIG development but are not sufficient because auto-Ab treatment did not increase AIG incidence in NTx B⁺ mice above the baseline.

Original language	English
Pages (from-to)	1-8
Number of pages	8
Journal	Cellular Immunology
Volume	300
DOIs	https://doi.org/10.1016/j.cellimm.2015.10.004
Publication status	Published - 2016 Feb 1
Externally published	Yes

Keywords

Anti-FcγR antibodies
Autoantibodies
Autoimmune gastritis
B cell-deficient mice
Neonatal thymectomy

ASJC Scopus subject areas

Immunology

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10.1016/j.cellimm.2015.10.004

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title = "Induction of autoimmune gastritis by neonatal thymectomy requires autoantibodies and is prevented by anti-FcγR antibodies",

abstract = "The autoantibodies (auto-Abs) that are a hallmark of neonatally thymectomized (NTx) mice with autoimmune gastritis (AIG) have been poorly explored. We investigated their immune significance using B cell-deficient (B-) mice and found that B- mice are totally resistant to AIG but become susceptible to AIG after receiving bone marrow cells from B+ mice. This susceptibility is most likely caused by the production of auto-Abs by B cells because B- pups also became susceptible to AIG when nourished by an AIG dam producing auto-Abs of the IgG class during the suckling period. NTx B- mice receiving purified IgG auto-Abs at this developmental stage similarly developed AIG. Auto-Abs probably act on antigen handling for antigen presentation because the treatment of NTx B+ mice with anti-FcγR Abs prevented the development of AIG. Auto-Abs are indispensable for AIG development but are not sufficient because auto-Ab treatment did not increase AIG incidence in NTx B+ mice above the baseline.",

keywords = "Anti-FcγR antibodies, Autoantibodies, Autoimmune gastritis, B cell-deficient mice, Neonatal thymectomy",

author = "Tsubasa Saito and Satoru Suenaga and Masato Fujii and Yoshihiro Kushida and Yusuke Kawauchi and Kenji Suzuki and Maki Touma and Masamichi Hosono",

note = "Funding Information: We thank Dr. Tohru Masuda, deceased, for his encouragements and advices thorough out this study. We thank Dr. S. Nagafuchi (Kyushu University) for providing pairs of μMT/+ AKR mice, Dr. M. Kadowaki (Niigata University) for continuous supply of normal rat serum, Dr. M. Inaba (Kansai Medical University) and Dr. Y. Ikarashi (National Cancer Institute, Tokyo) for providing hybridomas, Mr. T. Kumata and Mr. T. Narumi for their technical advices in antigen-administration and handlings of newborn mice, and Mr. I. Kehara for the animal housing. This work was supported by a Grant from the Promotion of Niigata University Education and Research Project , and partly by JSPS KAKENHI Grant Number 26460570 to MT . Publisher Copyright: {\textcopyright} 2015 Elsevier Inc.",

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doi = "10.1016/j.cellimm.2015.10.004",

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AU - Saito, Tsubasa

AU - Suenaga, Satoru

AU - Fujii, Masato

AU - Kushida, Yoshihiro

AU - Kawauchi, Yusuke

AU - Suzuki, Kenji

AU - Touma, Maki

AU - Hosono, Masamichi

N1 - Funding Information: We thank Dr. Tohru Masuda, deceased, for his encouragements and advices thorough out this study. We thank Dr. S. Nagafuchi (Kyushu University) for providing pairs of μMT/+ AKR mice, Dr. M. Kadowaki (Niigata University) for continuous supply of normal rat serum, Dr. M. Inaba (Kansai Medical University) and Dr. Y. Ikarashi (National Cancer Institute, Tokyo) for providing hybridomas, Mr. T. Kumata and Mr. T. Narumi for their technical advices in antigen-administration and handlings of newborn mice, and Mr. I. Kehara for the animal housing. This work was supported by a Grant from the Promotion of Niigata University Education and Research Project , and partly by JSPS KAKENHI Grant Number 26460570 to MT . Publisher Copyright: © 2015 Elsevier Inc.

PY - 2016/2/1

Y1 - 2016/2/1

N2 - The autoantibodies (auto-Abs) that are a hallmark of neonatally thymectomized (NTx) mice with autoimmune gastritis (AIG) have been poorly explored. We investigated their immune significance using B cell-deficient (B-) mice and found that B- mice are totally resistant to AIG but become susceptible to AIG after receiving bone marrow cells from B+ mice. This susceptibility is most likely caused by the production of auto-Abs by B cells because B- pups also became susceptible to AIG when nourished by an AIG dam producing auto-Abs of the IgG class during the suckling period. NTx B- mice receiving purified IgG auto-Abs at this developmental stage similarly developed AIG. Auto-Abs probably act on antigen handling for antigen presentation because the treatment of NTx B+ mice with anti-FcγR Abs prevented the development of AIG. Auto-Abs are indispensable for AIG development but are not sufficient because auto-Ab treatment did not increase AIG incidence in NTx B+ mice above the baseline.

AB - The autoantibodies (auto-Abs) that are a hallmark of neonatally thymectomized (NTx) mice with autoimmune gastritis (AIG) have been poorly explored. We investigated their immune significance using B cell-deficient (B-) mice and found that B- mice are totally resistant to AIG but become susceptible to AIG after receiving bone marrow cells from B+ mice. This susceptibility is most likely caused by the production of auto-Abs by B cells because B- pups also became susceptible to AIG when nourished by an AIG dam producing auto-Abs of the IgG class during the suckling period. NTx B- mice receiving purified IgG auto-Abs at this developmental stage similarly developed AIG. Auto-Abs probably act on antigen handling for antigen presentation because the treatment of NTx B+ mice with anti-FcγR Abs prevented the development of AIG. Auto-Abs are indispensable for AIG development but are not sufficient because auto-Ab treatment did not increase AIG incidence in NTx B+ mice above the baseline.

KW - Anti-FcγR antibodies

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KW - Autoimmune gastritis

KW - B cell-deficient mice

KW - Neonatal thymectomy

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JO - Cellular Immunology

JF - Cellular Immunology

ER -

Induction of autoimmune gastritis by neonatal thymectomy requires autoantibodies and is prevented by anti-FcγR antibodies

Abstract

Keywords

ASJC Scopus subject areas

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