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Contrasting Roles of Different Endoglin Forms in Atherosclerosis
장영생,최인홍 대한면역학회 2014 Immune Network Vol.14 No.5
Endoglin (also known as CD105 or TGF-β type III receptor)is a co-receptor involved in TGF-β signaling. In atherosclerosis,TGF-β signaling is crucial in regulating diseaseprogression owing to its anti-inflammatory effects as well asits inhibitory effects on smooth muscle cell proliferation andmigration. Endoglin is a regulator of TGF-β signaling, but itsrole in atherosclerosis has yet to be defined. This review focuseson the roles of the various forms of endoglin inatherosclerosis. The expression of the two isoforms of endoglin(long-form and short-form) is increased in atheroscleroticlesions, and the expression of the soluble forms ofendoglin is upregulated in sera of patients with hypercholesterolemiaand atherosclerosis. Interestingly, long-formendoglin shows an atheroprotective effect via the inductionof eNOS expression, while short-form and soluble endoglinenhance atherogenesis by inhibiting eNOS expression andTGF-β signaling. This review summarizes evidence suggestingthat the different forms of endoglin have distinct roles inatherosclerosis.
IgA Isotype Switching 연구를 위한 마우스 B Lymphoma Cell (CH12F3-2A)의 특성 연구
장영생,최서현,박석래,김현아,박재봉,김평현 대한면역학회 2004 Immune Network Vol.4 No.4
Background: It is well known that IgA isotype switching is induced by TGF-β1. LPS-activated mouse normal B cells well differentiate into IgA secreting plasma cells under the influence of TGF-β1. Nevertheless, there are lots of difficulties in studying normal B cells in detail because it is not simple to obtain highly purified B cells, showing low reproducibility and transfection efficacy, moreover impossible to keep continuous culture. To overcome these obstacles, it is desperately needed to develop B cell line which acts like normal B cells. In the present study, we investigated whether CH12F3-2A lymphoma cells are appropriate for studying IgA isotype switching event. Methods: CH12F3-2A B cell line was treated with LPS and TGF-β1, then levels of germ-line (GL) transcripts were measured by RT-PCR, and GLα promoter activity was measured by luciferase assay. In addition, membrane IgA (mIgA) expression and IgA secretion were determined by FACS and ELISA, respectively. Results: TGF-β1, regardless of the presence of LPS, increased level of GLα transcripts but not GLγ2b transcripts. However, IgA secretion was increased dramatically by co-stimulation of LPS and TGF-β1. Both mIgA and IgA secretion in the presence of TGF-β1 were further increased by over-expression of Smad3/4. Finally, GLα promoter activity was increased by TGF-β1. Conclusion: CH12F3-2A cell line acts quite similarly to the normal B cells which have been previously reported regarding IgA expression. Thus, CH12F3-2A lymphoma cell line appears to be adequate for the investigation of the mechanism(s) of IgA isotype switching at the cellular and molecular levels. (Immune Network 2004;4(4):216-223)
Murine γδ T Cells Render B Cells Refractory to Commitment of IgA Isotype Switching
한혜주,장영생,서구영,박성규,강승구,윤성일,고현정,이근식,김평현 대한면역학회 2018 Immune Network Vol.18 No.4
γδ T cells are abundant in the gut mucosa and play an important role in adaptive immunity as well as innate immunity. Although γδ T cells are supposed to be associated with the enhancement of Ab production, the status of γδ T cells, particularly in the synthesis of IgA isotype, remains unclear. We compared Ig expression in T cell receptor delta chain deficient (TCRδ−/−) mice with wild-type mice. The amount of IgA in fecal pellets was substantially elevated in TCRδ−/− 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 TCRδ−/− 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 α transcript, an indicator of IgA class switch recombination, higher in PP and MLN B cells from TCRδ−/− mice, while it was not seen in inactivated B cells. Nevertheless, the frequency of IgA+ B cells was much higher in the spleen from TCRδ−/− mice. These results suggest that γδ T cells control the early phase of B cells, in order to prevent unnecessary IgA isotype switching. Furthermore, this regulatory role of γδ T cells had lasting effects on the long-lived IgA-producing plasma cells in the BM.
TGF-β and BAFF derived from CD4+CD25+Foxp3+ T cells mediate mouse IgA isotype switching
박경훈,서구영,장영생,김평현 한국유전학회 2012 Genes & Genomics Vol.34 No.6
TGF-β1 is generally accepted as the physiological IgA isotype switch factor. Nevertheless, it is unclear as to which cells in mucus-associated lymphoid tissue provide this cytokine to B cells. Regulatory T cells (Tregs) play immune-suppressive roles by secreting inhibitory cytokines such as TGF-β and IL-10. Thus, it is plausible that Tregs are involved in IgA class switch recombination (CSR) in MALT. We explored, in the present study, the possibility that CD4+CD25+ T cells facilitate IgA CSR in murine B cells. In cocultures,CD4+CD25+Foxp3+ T cells stimulated IgA production by splenic B cells to a greater extent than did CD4+CD25-Foxp3-T cells. This effect was markedly abrogated by the addition of anti-TGF-β1 Ab. Additionally, IgA production was paralleled by an increase in germ line transcript α (GLTα), an indicator of IgA CSR. In contrast, CD4+CD25-Foxp3- T cells were more potent at inducing GLTγ1 and GLTε production by cocultured splenic B cells than were CD4+CD25+Foxp3+T cells. Consistent with these results, phenotypic analyses revealed that TGF-β1 and IL-4 were predominantly expressed by CD4+CD25+Foxp3+ T cells and CD4+CD25-Foxp3- T cells,respectively. Furthermore, CD4+CD25+ T cells strongly expressed BAFF, which led to activation-induced deaminase (AID) expression in B cells. Taken together, our results suggest that CD4+CD25+ Tregs have an important effect on IgA isotype commitment by expressing TGF-β1 and BAFF in MALT.
강성호,진보라,김현진,서구영,장영생,김선진,안선진,박석래,김완섭,김평현 대한면역학회 2015 Immune Network Vol.15 No.1
It is well established that TGF-β1 and retinoic acid (RA)cause IgA isotype switching in mice. We recently found thatlactoferrin (LF) also has an activity of IgA isotype switchingin spleen B cells. The present study explored the effect of LFon the Ig production by mouse peritoneal B cells. LF, likeTGF-β1, substantially increased IgA production in peritonealB1 cells but little in peritoneal B2 cells. In contrast, LF increasedIgG2b production in peritoneal B2 cells much morestrongly than in peritoneal B1 cells. LF in combination withRA further enhanced the IgA production and, interestingly,this enhancement was restricted to IgA isotype and B1 cells. Similarly, the combination of the two molecules also led toexpression of gut homing molecules α4β7 and CCR9 onperitoneal B1 cells, but not on peritoneal B2 cells. Thus,these results indicate that LF and RA can contribute to gutIgA response through stimulating IgA isotype switching andexpression of gut-homing molecules in peritoneal B1 cells.
Alum Directly Modulates Murine B Lymphocytes to Produce IgG1 Isotype
진보라,서구영,김평현,김선진,이정민,강성호,한혜주,장영생 대한면역학회 2013 Immune Network Vol.13 No.1
Aluminum hydroxide (alum) is the most widely used adjuvant in human vaccines. Nevertheless, it is virtually unknown whether alum acts on B cells. In the present study, we explored the direct effect of alum on Ig expression by murine B cells in vitro. LPS-activated mouse spleen B cells were cultured with alum, and the level of isotype-specific Ig secretion,IgG1 secreting cell numbers, and Ig germ-line transcripts (GLT) were measured using ELISA, ELISPOT, and RT-PCR,respectively. Alum consistently enhanced total IgG1 production,numbers of IgG1 secreting cells, and GLTγ1expression. These results demonstrate that alum can directly cause IgG1 isotype switching leading to IgG1 production.