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Murine γδ T Cells Render B Cells Refractory to Commitment of IgA Isotype Switching
- Han, Hye-Ju;
- Jang, Young-Saeng;
- Seo, Goo-Young;
- Park, Sung-Gyoo;
- Kang, Seung Goo;
- ... Yoon, Sung-il;
- ... Ko, Hyun-Jeong;
- ... Lee, Geun-Shik;
- 외 1명
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4초록
gamma delta T cells are abundant in the gut mucosa and play an important role in adaptive immunity as well as innate immunity. Although gamma delta T cells are supposed to be associated with the enhancement of Ab production, the status of gamma delta T cells, particularly in the synthesis of IgA isotype, remains unclear. We compared Ig expression in T cell receptor delta chain deficient (TCRd(-/-)) mice with wild-type mice. The amount of IgA in fecal pellets was substantially elevated in TCRd(-/-) mice. This was paralleled by an increase in surface IgA expression and total IgA production by Peyer's patches (PPs) and mesenteric lymph node (MLN) cells. Likewise, the TCRd(-/-) mice produced much higher levels of serum IgA isotype. Here, surface IgA expression and number of IgA secreting cells were also elevated in the culture of spleen and bone marrow (BM) B cells. Germ-line alpha transcript, an indicator of IgA class switch recombination, higher in PP and MLN B cells from TCRd(-/-) mice, while it was not seen in inactivated B cells. Nevertheless, the frequency of IgA(+) B cells was much higher in the spleen from TCRd(-/-) mice. These results suggest that gamma delta T cells control the early phase of B cells, in order to prevent unnecessary IgA isotype switching. Furthermore, this regulatory role of gamma delta T cells had lasting effects on the long-lived IgA-producing plasma cells in the BM.
키워드
- 제목
- Murine γδ T Cells Render B Cells Refractory to Commitment of IgA Isotype Switching
- 저자
- Han, Hye-Ju; Jang, Young-Saeng; Seo, Goo-Young; Park, Sung-Gyoo; Kang, Seung Goo; Yoon, Sung-il; Ko, Hyun-Jeong; Lee, Geun-Shik; Kim, Pyeung-Hyeun
- 발행일
- 2018-08
- 유형
- Article
- 저널명
- Immune Network
- 권
- 18
- 호
- 4
- 언어
- ENG
- 출판사
- KOREA ASSOC IMMUNOLOGISTS
- 발행국가
- 대한민국
- ISSN
- E 2092-6685
P 1598-2629