• Title/Summary/Keyword: IgG subclass containing cell

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AN IMMUNOHISTOCHEMICAL STUDY ON THE IMMUNOGLOBULIN G SUBCLASSES OF THE EXPERIMENTALLY INDUCED RAT PULP AND PERIAPICAL PATHOSES (실험적 백서 치수 및 치근단 병소에서의 면역글로불린 G 아강분포에 관한 면역조직화학적 연구)

  • Baek, Seung-Ho;Lim, Sung-Sam
    • Restorative Dentistry and Endodontics
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    • v.16 no.1
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    • pp.41-59
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    • 1991
  • This study was performed to elucidate the distribution and correlation of immunoglobulin G subclasses with the degree of inflammation in the experimentally induced rat pulp and periapical pathoses. The pulp exposures were made in 108 mandibular 1st molars of 54 rats and the teeth were left open to the oral environment The animals were sacrified at 3, 7, 15, 30, 60 and 90 days after pulp exposure, and examined microscopically and radiographically Seventy one specimens were routinely sectioned at the thickness of 4 - $6{\mu}$ and stained with Hematoxylin - eosin for histologic examination, with toluidine blue for mast cells, and with the primary antibodies against rat IgG subclasses by using the Avidin - Biotin complex method. The following results were obtained: 1. As the degree of inflammation of rat pulp and periapeces intensified, the number of IgG subclass containing cells per unit area, especially IgG2a and IgG2c, decresased. 2. The IgG2c cells were most predominantly found in the lesions with slight inflammation, IgG1 cells in mild or severe inflammation, and IgG2a cells in moderate inflammation. 3. IgG subclass containg cells were more predominantly observed in the periapical granuloma than periapical abscess or cyst(p<0.01). 4. IgG2a containing cells were predominant in pulp inflammation, IgG1 containing cells in periapical granuloma, IgG2a cells and IgG1 cells in periapical abscess, and IgG2a cells were significantly predominant in periapical cyst. 5. The number of IgG subclass containing cells and mast cells in periapical tissue decreased with time lapse after pulp exposure. And correlation index between mast cells and IgG1, IgG2a, IgG2b was stastically high.

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A Novel Anti-PD-L1 Antibody Exhibits Antitumor Effects on Multiple Myeloma in Murine Models via Antibody-Dependent Cellular Cytotoxicity

  • Ahn, Jae-Hee;Lee, Byung-Hyun;Kim, Seong-Eun;Kwon, Bo-Eun;Jeong, Hyunjin;Choi, Jong Rip;Kim, Min Jung;Park, Yong;Kim, Byung Soo;Kim, Dae Hee;Ko, Hyun-Jeong
    • Biomolecules & Therapeutics
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    • v.29 no.2
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    • pp.166-174
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    • 2021
  • Multiple myeloma is a malignant cancer of plasma cells. Despite recent progress with immunomodulatory drugs and proteasome inhibitors, it remains an incurable disease that requires other strategies to overcome its recurrence and non-response. Based on the high expression levels of programmed death-ligand 1 (PD-L1) in human multiple myeloma isolated from bone marrow and the murine myeloma cell lines, NS-1 and MOPC-315, we propose PD-L1 molecule as a target of anti-multiple myeloma therapy. We developed a novel anti-PD-L1 antibody containing a murine immunoglobulin G subclass 2a (IgG2a) fragment crystallizable (Fc) domain that can induce antibody-dependent cellular cytotoxicity. The newly developed anti-PD-L1 antibody showed significant antitumor effects against multiple myeloma in mice subcutaneously, intraperitoneally, or intravenously inoculated with NS-1 and MOPC-315 cells. The anti-PD-L1 effects on multiple myeloma may be related to a decrease in the immunosuppressive myeloid-derived suppressor cells (MDSCs), but there were no changes in the splenic MDSCs after combined treatment with lenalidomide and the anti-PD-L1 antibody. Interestingly, the newly developed anti-PD-L1 antibody can induce antibody-dependent cellular cytotoxicity in the myeloma cells, which differs from the existing anti-PD-L1 antibodies. Collectively, we have developed a new anti-PD-L1 antibody that binds to mouse and human PD-L1 and demonstrated the antitumor effects of the antibody in several syngeneic murine myeloma models. Thus, PD-L1 is a promising target to treat multiple myeloma, and the novel anti-PD-L1 antibody may be an effective anti-myeloma drug via antibody-dependent cellular cytotoxicity effects.