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Jung, In-Hyuk,Choi, Jae-Hoon,Jin, Jing,Jeong, Se-Jin,Jeon, Sejin,Lim, Chaeji,Lee, Mi-Ran,Yoo, Ji-Young,Sonn, Seong-Keun,Kim, Young Ho,Choi, Beom Kyu,Kwon, Byoung S.,Seoh, Ju-Young,Lee, Cheol Whan,Kim, The Federation of American Societies for Experimen 2014 The FASEB Journal Vol.28 No.11
<P>CD137 (4-1BB), a member of the tumor necrosis factor receptor superfamily, has been reported to be expressed in atherosclerotic plaques, and to promote lesion formation. However, the role of CD137 in mediating atherosclerotic plaque stability and the possible underlying molecular and cellular mechanisms are poorly understood. Here, apolipoprotein E-deficient (<I>ApoE</I><SUP>−/−</SUP>) and CD137-deficient <I>ApoE</I><SUP>−/−</SUP> (<I>ApoE</I><SUP>−/−</SUP>CD137<SUP>−/−</SUP>) mice fed a chow diet for 66 wk were used. CD137 induces plaque instability, which is characterized by increased plaque necrosis, decreased collagen content, decreased vascular smooth muscle cell (VSMC) content, and increased macrophage infiltration. CD137 also increases the infiltration of effector T (T<SUB>eff</SUB>) cells into plaque lesion sites, resulting in increased interferon-γ (IFN-γ) expression. Interestingly, T<SUB>eff</SUB>-cell-derived IFN-γ inhibits collagen synthesis in atherosclerotic plaques. Furthermore, CD137 activation increases the apoptosis of VSMCs, possibly by decreasing the antiapoptotic regulator, Bcl-2, and subsequently up-regulating cleaved caspase-3. In macrophages, activation of CD137 signaling boosted the oxidized low density lipoprotein-induced expression of matrix metalloproteinase 9 <I>via</I> the p38 mitogen-activated protein kinase and extracellular signal-regulated kinase1/2 signaling pathways. In summary, activation of CD137 signaling decreases the stability of advanced atherosclerotic plaques <I>via</I> its combined effects on T<SUB>eff</SUB> cells, VSMCs, and macrophages.—Jung, I.-H., Choi, J.-H., Jin, J., Jeong, S.-J., Jeon, S., Lim, C., Lee, M.-R., Yoo, J.-Y., Sonn, S.-K., Kim, Y. H., Choi, B. K., Kwon, B. S., Seoh, J.-Y., Lee, C. W., Kim, D.-Y., Oh, G. T. CD137-inducing factors from T cells and macrophages accelerate the destabilization of atherosclerotic plaques in hyperlipidemic mice.</P>
A MELANOCYTE-SPECIFIC cDNA WHOSE EXPRESSION IS INDUCIBLE BY α-MSH AND IBMX
Kwon, Byoung S,Ruth Halaban,Kim, Gwan Shik,Seymour Pomerantz,Asifa K. Haq 대한구강생물학회 1987 International Journal of Oral Biology Vol.11 No.1
Normal human melanocyte의 λgtll cDNA library를 tyrosinase항체를 이용하여 검 색, 16 cDNA clones을 분리하였다. 이중 albino locus혹은 그인접부위에 존재하는 13clones는 tyrosinase gene으로 여겨지며 나머지 3clones는 상호간 상동성(homology)을 보이고 있으나 tyrosinase gene과 는 상이하였다. 이들 3clones의 대표적인 Pmel 17 - 1에 상응하는 mRNA(cRNA)는 사람과 mouse melanocyte에서만 특이하게 표현되며 크기는 약 2.4kb, 표현도는 melanin양과 비례 하였다. 여러종류의 melanoma cell을 αMSH 또는 IBMX로 자극시 Pmel 17 - 1의 cRNA표현은 증가되었으며 단일항체를 이용한 면역학적 실험으로 Pmel 17 - 1은 tyrosinase와 면역학적 동질성을 갖는 75KD glycoprotein을 합성함이 판명되었다. 또한 genomic DNA blot실험결과 Pmel 17 - 1 cDNA는 mouse albino locus 혹은 인접부위에 위치하지는 않으나 mouse와 사람에 single gene으로 존재하며 evolutionarily conserved gene임을 볼 수 있어 중요한 기능을 가지고 있을 것으로 사료된다.
Amelioration of mercury-induced autoimmunity by 4-1BB.
Vinay, Dass S,Kim, Jung D,Kwon, Byoung S American Association of Immunologists 2006 Journal of Immunology Vol.177 No.8
<P>In certain strains of mice, subtoxic doses of HgCl2 (mercuric chloride; mercury) induce a complex autoimmune condition characterized by the production of antinucleolar IgG Abs, lymphoproliferation, increased serum levels of IgG1/IgE Abs, and deposition of renal immune complexes. 4-1BB is an important T cell costimulatory molecule that has been implicated in T cell proliferation and cytokine production, especially production of IFN-gamma. To elucidate T cell control mediated by the 4-1BB signaling pathway in this syndrome, we assessed the effect of administering agonistic anti-4-1BB mAb on mercury-induced autoimmunity. Groups of A.SW mice (H-2s) received mercury/control Ig or mercury/anti-4-1BB or PBS alone. Anti-4-1BB mAb treatment resulted in a dramatic reduction of mercury-induced antinucleolar Ab titers, serum IgG1/IgE induction, and renal Ig deposition. These effects may be related to the present finding that anti-4-1BB mAb decreases B cell numbers and function. The anti-4-1BB mAb-treated mercury group also showed a marked reduction in Th2-type cytokines but an increase in Th1-type cytokines and chemokines. Increased IFN-gamma production due to anti-4-1BB mAb treatment appears to be responsible for the observed B cell defects because neutralization of IFN-gamma in vivo substantially restored B cell numbers and partly restored IgG1/IgE. Collectively, our results indicate that 4-1BB mAb can down-regulate mercury-induced autoimmunity by affecting B cell function in an IFN-gamma-dependent manner and thus, preventing the development of autoantibody production and tissue Ig deposition.</P>
Kim, Juyang,Choi, Woon S.,La, Soojin,Suh, Jae-Hee,Kim, Byoung-Sam,Cho, Hong R.,Kwon, Byoung S.,Kwon, Byungsuk American Society of Hematology 2005 Blood Vol.105 No.5
<B>Abstract</B><P>4-1BB, a member of the tumor necrosis factor (TNF) receptor superfamily, is a costimulator for activated T cells. Previous studies have established that treatment with agonistic anti-4-BB monoclonal antibody (3H3) is effective in reversing the progression of spontaneous systemic lupus erythematosus. Its therapeutic effect is mediated by suppression of autoantibody production. In this report, we show that a single injection of 3H3 blocks chronic graft-versus-host disease (cGVHD) in the parent-into-F1 model. In particular, donor CD4+ T cells are rapidly eliminated from host spleens by activation-induced cell death after 4-1BB triggering. Since donor CD4+ T cells are required for the development of cGVHD, and 3H3-mediated inhibition of autoantibody production occurs without donor CD8+ T cells, 3H3 blocks cGVHD by preventing alloreactive donor CD4+ T cells from activating host B cells. Importantly, 3H3 treatment can reverse the progression of advanced cGVHD. Our findings indicate that agonistic anti-4-1BB monoclonal antibody has potential as an immunotherapeutic agent for preventing and treating cGVHD.</P>
Kim, Hye J.,Lee, Jong S.,Kim, Ahra,Koo, Sumi,Cha, Hee J.,Han, Jae-A,Do, Yoonkyung,Kim, Kyung M.,Kwon, Byoung S.,Mittler, Robert S.,Cho, Hong R.,Kwon, Byungsuk The American Association of Immunologists, Inc. 2013 JOURNAL OF IMMUNOLOGY Vol.191 No.5
<P>Damage-associated molecular patterns released from damaged kidney cells initiate postischemic inflammation, an essential step in the progression of kidney ischemia–reperfusion injury (IRI). However, the mechanism that coordinates this highly specific process in ischemic kidneys remains to be clarified. Previously, we demonstrated that CD137 from NK cells specifically stimulates CD137 ligand (CD137L) on tubular epithelial cells (TECs) such that TECs produced the high CXCR2 chemokine levels required for neutrophil chemotaxis. We report in the present study that endogenous TLR2 ligands released from ischemic TECs induce CCR5 chemokine expression, which is critical to promoting NK cell recruitment. By implanting CD137L<SUP>−/−</SUP> TECs into the kidney capsule of TLR2<SUP>−/−</SUP> mice, we further showed that TLR2-mediated NK cell recruitment is an uncoupled event that can occur independently of CD137L signaling in TECs, which is responsible for recruiting neutrophils. Therefore, our findings identify TECs as both a target for kidney damage and also as a master regulator that actively modulates stepwise signaling, leading to the initiation and amplification of acute sterile inflammation that inflicts kidney IRI. Being clinically important, the signaling pathway of innate receptors in epithelial cells may therefore be a good target to block acute sterile inflammation resulting from tissue damage, including kidney IRI.</P>