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ABSTRACT: Rosai-Dorfman disease (RDD) can present in any anatomic site, but breast involvement is rarely reported. Recently, a relationship between RDD and IgG4-related sclerosing disease has been suggested. Here we report another case of RDD with overlapping features of IgG4-related sclerosing disease occurring in a right breast of a 62-year-old female. On microscopic examination, the mass demonstrated a characteristic zonal pattern of proliferation of large polygonal histiocytes and lymphoplasma cells with stromal fibrosis. Emperipolesis was observed in histiocytes with abundant cytoplasm, which showed immunoreactivity for S-100 protein and CD68; the diagnosis of RDD was made. Sheets of plasma cells in the fibrotic stroma demonstrated positive reactions for IgG and IgG4. The mean count of IgG4-positive plasma cells was 100.2/high power field, and the ratio of IgG4/IgG was 56.7%. Additional findings of stromal fibrosis and obliteration of preexisting breast lobules suggested overlapping features with IgG4-related sclerosing disease.
Korean journal of pathology. 10/2012; 46(5):489-93.
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ABSTRACT: CD1d is an MHC class I-like molecule that presents glycolipid Ags to types I and II NKT cells. The YxxI motif in the cytoplasmic tail of CD1d contributes to its intracellular localization to the endolysosomal compartment and is important for Ag presentation to type I NKT cells. In this study, we identified the (327-329)RRR motif in CD1d and showed that it is critical for the control of CD1d intracellular trafficking and Ag presentation. The replacement of the arginines in this motif with alanines resulted in the extensive accumulation of CD1d in lysosomes but did not affect the cell surface expression. The defect in its cellular localization was accompanied by defects in Ag presentation to both type I and type II NKT cells. These results demonstrated that the (327-329)RRR motif of CD1d is required for proper cellular distribution of CD1d and optimal Ag presentation to both type I and type II NKT cells.
The Journal of Immunology 03/2012; 188(5):2235-43. · 5.79 Impact Factor
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Won Suck Yoon,
Seung Rel Ryu,
Seung Seok Lee,
Yang Seok Chae,
Eun Jae Kim,
Ji Hyun Choi,
Sejin Oh, Se Ho Park,
Ji Tae Choung,
Young Yoo,
Yong Keun Park
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ABSTRACT: Atopic dermatitis (AD) is an inflammatory, chronically relapsing, puritic skin disorder. These syndromes result from multifactorial inheritance, with interaction between genetic and environmental factors. In particular, the macrophage-derived chemokine CCL22 is directly implicated in skin inflammatory reactions and its levels are significantly elevated in serum and correlated with disease severity in AD. We tested the suppression of the CCL22 gene by microRNA (miRNA) and observed the effects in mice with inflammation similar to AD. We used Salmonella as a vector to deliver miRNA. The recombinant strain of Salmonella typhimurium expressing CCL22 miRNA (ST-miRCCL22) was prepared for in vivo knockdown of CCL22. ST-miRCCL22 was orally inoculated into mice and the CCL22 gene suppressed with CCL22 miRNA in the activated lymphocytes. IgE and interleukin-4 were inhibited and interferon-γ was induced after treatments with ST-miRCCL22 and CCL22 was suppressed. Further, Th17 cells were suppressed in the atopic mice treated with ST-miRCCL22. These results suggested that suppression of the CCL22 gene using Salmonella induced anti-inflammatory effects.
DNA and cell biology 08/2011; 31(3):290-7. · 2.28 Impact Factor
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ABSTRACT: Recent reports have provided evidence for cross-talk between regulatory T (Treg) cells and natural killer T (NKT) cells. However, it is unclear whether NKT cells play a role in the differentiation of Treg cells. By employing NKT cell-abundant Vα14 TCR transgenic (Tg) and NKT cell-deficient CD1d knock-out (KO) mice, we examined the effects of NKT cells on the in vitro differentiation of induced Treg (iTreg) cells with IL2 and TGFβ. We found that iTreg induction from CD1d KO mice was significantly increased compared to the control. Also, the addition of isolated NKT cells from Vα14 TCR Tg mice to naïve CD4(+) T cells from CD1d KO mice during iTreg differentiation caused a remarkable reduction of iTreg cells. Through IFNγ neutralization, we showed that this reduction was mediated by IFNγ. Furthermore, the main source of IFNγ during iTreg differentiation was NK1.1(-)CD4(+)Foxp3(-) T cells. This finding implied that early-activated NKT cells induced Th1-type cells and subsequently underwent apoptosis. Taken together, our results suggest that NKT cells inhibit the in vitro development of iTreg cells by increasing IFNγ.
Biochemical and Biophysical Research Communications 08/2011; 411(3):599-606. · 2.48 Impact Factor
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ABSTRACT: Krüppel-like factor 4 (KLF4) is a transcription factor that plays an important role in cell differentiation, proliferation, and survival, especially in the context of cancers. This study revealed that KLF4 activates glycolytic metabolism in breast cancer cells by up-regulating the platelet isoform of phosphofructokinase (PFKP). KLF4 activated the transcription of the PFKP gene by directly binding to the PFKP promoter. Whereas glucose uptake and lactate production were inhibited by the knockdown of KLF4, they were activated by the overexpression of KLF4. Unlike PFKP, the expressions of the other isoforms of phosphofructokinase and glycolytic genes were unaffected by KLF4. The human breast cancer tissues showed a close correlation between KLF4 and PFKP expression. This study also showed that PFKP plays a critical role in cell proliferation in breast cancer cells. In conclusion, it is suggested that KLF4 plays a role in maintenance of high glycolytic metabolism by transcriptional activation of the PFKP gene in breast cancer cells.
Journal of Biological Chemistry 05/2011; 286(27):23808-16. · 4.77 Impact Factor
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ABSTRACT: Pathologic complete response (pCR) is the most predictive factor for patients with neoadjuvant chemotherapy and we investigated the rate of pCR according to molecular subtypes defined by immunohistochemical staining.
Our subjects comprised 257 breast cancer patients who received 3 cycles of anthracycline/taxane-based neoadjuvant chemotherapy. The patients were classified into 4 subtypes: luminal A, luminal B, HER2 and triple negative. We analyzed the pCR rate and treatment outcome according to these subtypes.
Of a total of 257 patients, the pCR rate of luminal A, luminal B, HER2 and triple negative was 3.9, 5.0, 10.5 and 21.1%, respectively (p = 0.001). The 5-year disease-free survival of the pCR group (88.4%) was higher than that of the non-pCR group (65.6%), but it was not significant (p = 0.228). Among patients who have residual disease, the 5-year disease-free survival of luminal A, luminal B, HER2 and triple negative was 64.0, 65.7, 75.2 and 66.5%, respectively (p = 0.243). Triple negative and HER2 subtypes are more sensitive to neoadjuvant chemotherapy.
To increase the pCR rate, type-specific approaches according to subtypes, such as an addition of trastuzumab, increasing the number of cycles or a novel regimen, should be considered.
Oncology 03/2011; 79(5-6):324-30. · 2.27 Impact Factor
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ABSTRACT: TGF-beta-induced tolerogenic-antigen presenting cells (Tol-APCs) could induce suppression of autoimmune diseases such as collagen-induced arthritis (CIA) and allergic asthma. In contrast, many studies have shown that NKT cells are involved in the pathogenesis of Th1-mediated autoimmune joint inflammation and Th2-mediated allergic pulmonary inflammation. In this study, we investigated the effect of CD1d-restricted NKT cells in the Tol-APCs-mediated suppression of autoimmune disease using a murine CIA model. When CIA-induced mice were treated with Tol-APCs obtained from CD1d+/- or CD1d-/- mice, unlike CD1d+/- APCs, CD1d-/- Tol-APCs failed to suppress CIA. More specifically, CD1d-/- Tol-APCs failed to suppress the production of inflammatory cytokines and the induction of Th2 responses by antigen-specific CD4 T cells both in vitro and in vivo. Our results demonstrate that the presence of CD1d-restricted NKT cells is critical for the induction of Tol-APCs-mediated suppression of CIA.
Experimental and Molecular Medicine 08/2010; 42(8):547-54. · 2.48 Impact Factor
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ABSTRACT: NKT cells are considered to be innate-like regulatory cells. However, their regulatory functions in adaptive immune responses have not been studied in detail. In this study, we investigated the immunoregulatory functions of NKT cells during the secondary phase of an Ag-specific CD4(+) T cell response. When compared with OVA-specific effector CD4(+) T cells adoptively transferred into NKT cell-deficient naive CD1d(-/-) mice, the same T cells transferred into naive CD1d(+/-) mice exhibited substantially stronger immune responses on OVA challenge. The enhanced immune response of the transferred CD4(+) T cells in the presence of NKT cells correlated with an increase in their proliferation in vivo. In addition, T cells transferred into CD1d(+/-) recipients showed enhanced cytokine productions relative to T cells in CD1d(-/-) recipients. To elucidate the physiological relevance of the regulatory role of NKT cells in a disease setting, OVA-specific asthma was induced in recipient mice after adoptive transfer of OVA-specific CD4(+) T cells. CD1d(+/-) recipients showed stronger asthmatic phenotypes in all indications when compared with CD1d(-/-) recipients. Taken together, these results suggest that NKT cells are critical for the regulation of Ag-specific, conventional CD4(+) T cells during the secondary phase of an adaptive immune response.
The Journal of Immunology 04/2010; 184(10):5589-94. · 5.79 Impact Factor
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ABSTRACT: Collagen-induced arthritis (CIA) is mediated by self-reactive CD4(+) T cells that produce inflammatory cytokines. TGF-beta(2)-treated tolerogenic antigen-presenting cells (Tol-APCs) are known to induce tolerance in various autoimmune diseases. In this study, we investigated whether collagen-specific Tol-APCs could induce suppression of CIA. We observed that Tol-APCs could suppress the development and severity of CIA and delay the onset of CIA. Treatment of Tol-APCs reduced the number of IFN-gamma- and IL-17-producing CD4(+) T cells and increased IL-4- and IL-5-producing CD4(+) T cells upon collagen antigen stimulation in vitro. The suppression of CIA conferred by Tol-APCs correlated with their ability to selectively induce IL-10 production. We also observed that treatment of Tol-APCs inhibited not only cellular immune responses but also humoral immune responses in the process of CIA. Our results suggest that in vitro-generated Tol-APCs have potential therapeutic value for the treatment of rheumatoid arthritis as well as other autoimmune diseases.
Experimental and Molecular Medicine 02/2010; 42(3):187-94. · 2.48 Impact Factor
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ABSTRACT: In this study, we report the development of a new dual reporter vector system for the analysis of promoter activity. This system employs green fluorescence emitting protein, EGFP, as a reporter, and uses red fluorescence emitting protein, DsRed, as a transfection control in a single vector. The expression of those two proteins can be readily detected via flow cytometry in a single analysis, with no need for any further manipulation after transfection. As this system allows for the simultaneous detection of both the control and reporter proteins in the same cells, only transfected cells which express the control protein, DsRed, can be subjected to promoter activity analysis, via the gating out of all un-transfected cells. This results in a dramatic increase in the promoter activity detection sensitivity. This novel reporter vector system should prove to be a simple and efficient method for the analysis of promoter activity.
Immune Network 12/2009; 9(6):243-7.
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ABSTRACT: The role of NKT cells in the pathogenesis of collagen-induced arthritis (CIA) remains unclear since most studies have used C57BL/6 (B6) mice, which are less susceptible to CIA than mice with a DBA/1 background. To clarify the immunological functions of NKT cells in CIA, it is necessary to analyze in detail the effects of NKT cell deficiency on CIA development in DBA/1 mice. The incidence and severity of CIA were significantly exacerbated in DBA/1CD1d(+/-) mice as compared to DBA/1CD1d(-/-) mice. In DBA/1CD1d(+/-) mice, antigen-specific responses of B and T cells against CII were remarkably increased and inflammatory cytokine levels were also increased in vivo and in vitro. The number of IL-17-producing NKT cells significantly increased in DBA/1CD1d(+/-) mice as the disease progressed. Our results clearly show that NKT cells are involved not only in accelerating the severity and incidence of CIA but also in perpetuating the disease progression.
Biochemical and Biophysical Research Communications 10/2009; 390(3):399-403. · 2.48 Impact Factor
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ABSTRACT: The physiologic function of natural killer T (NKT) cells in adaptive immunity remains largely unknown because most studies have used NKT cell agonists. In the present study, the role of NKT cells during the secondary effector phase was investigated separately from the primary immunization phase via adoptive transfer of differentiated effector T cells into naive recipients. We found that secondary antitumor CD8(+) T-cell responses were optimal when NKT cells were present. Tumor-specific CD8(+) effector T cells responded less strongly to tumor cell challenge in NKT cell-deficient recipients than in recipients with intact NKT cells. NKT cell-mediated enhancement of the secondary antitumor CD8(+) T-cell response was concurrent with increased number and activity of tumor-specific CD8(+) T cells. These findings provide the first demonstration of a direct role for NKT cells in the regulation of antigen-specific secondary T-cell responses without the use of exogenous NKT cell agonists such as alpha-galactosylceramide (alpha-GalCer). Furthermore, forced activation of NKT cells with alpha-GalCer during the secondary immune response in suboptimally immunized animals enhanced otherwise poor tumor rejection responses. Taken together, our findings strongly emphasize the importance of NKT cells in secondary CD8(+) T-cell immune responses.
Cancer Research 05/2009; 69(10):4301-8. · 7.86 Impact Factor
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ABSTRACT: As a part of our ongoing search for a safe and efficient anti-tumor vaccine, we attempted to determine whether the molecular nature of certain tumor antigens would influence immune responses against tumor cells. As compared with freeze-thawed or formaldehyde-fixed tumor antigens, heat-denatured tumor antigens elicited profound anti-tumor immune responses and greatly inhibited the growth of live tumor cells. The heat-denatured tumor antigens induced a substantial increase in the anti-tumor CTL response in the absence of any adjuvant material. This response appears to be initiated by strong activation of the antigen-presenting cells, which may recognize heat-denatured protein antigens. Upon recognition of the heat-denatured tumor antigens, macrophages and dendritic cells were found to acutely upregulate the expression of co-stimulatory molecules such as B7.2, as well as the secretion of inflammatory cytokines such as IL-12 and TNF-alpha. The results of this study indicate that heat-denatured tumor extracts might elicit protective anti-tumor adaptive immune responses and also raise the possibility that a safe and efficient adjuvant-free tumor vaccine might be developed in conjunction with a dendritic cell-based tumor vaccine.
Experimental and Molecular Medicine 03/2008; 40(1):130-44. · 2.48 Impact Factor
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ABSTRACT: Human thymic stromal lymphopoietin (TSLP) activates dendritic cells (DCs), which promote the proliferation and differentiation of CD4+ T cells. However, murine TSLP (mTSLP) can act directly on CD4+ T cells and bring about their differentiation. We studied the role of mTSLP in the generation of CD4+CD25+FoxP3+ T cells from thymocytes. mTSLP promoted the differentiation of CD4+ single-positive thymocytes into CD4+CD25+FoxP3+ T cells. Although we cannot exclude an effect of TSLP mediated through DCs due to co-stimulatory effects, mTSLP appears to act directly on thymocytes. T-cell receptor and TSLP receptor signaling act synergistically on thymocytes to generate CD4+CD25+FoxP3+ T cells. mTSLP may play an important role in maintaining immune tolerance by promoting the conversion of thymocytes into natural regulatory T cells via escape from negative selection.
Immunology and Cell Biology 03/2008; 86(2):206-13. · 3.66 Impact Factor
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ABSTRACT: We assessed whether the sublingual (s.l.) route would be an effective means of delivering vaccines against influenza virus in mice by using either formalin-inactivated or live influenza A/PR/8 virus (H1N1). Sublingual administration of inactivated influenza virus given on two occasions induced both systemic and mucosal antibody responses and conferred protection against a lethal intranasal (i.n.) challenge with influenza virus. Coadministration of a mucosal adjuvant (mCTA-LTB) enhanced these responses and resulted in complete protection against respiratory viral challenge. In addition, s.l. administration of formalin-inactivated A/PR/8 plus mCTA-LTB induced systemic expansion of IFN-gamma-secreting T cells and virus-specific cytotoxic T lymphocyte responses. Importantly, a single s.l. administration of live A/PR/8 virus was not pathogenic and induced protection mediated by both acquired and innate immunity. Moreover, s.l. administration of live A/PR/8 virus conferred heterosubtypic protection against respiratory challenge with H3N2 virus. Unlike the i.n. route, the A/PR/8 virus, whether live or inactivated, did not migrate to or replicate in the CNS after s.l. administration. Based on these promising findings, we propose that the s.l. mucosal route offers an attractive alternative to mucosal routes for administering influenza vaccines.
Proceedings of the National Academy of Sciences 03/2008; 105(5):1644-9. · 9.68 Impact Factor
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ABSTRACT: It is well known that interferon (IFN)-alpha is important to the pathogenesis of systemic lupus erythematosus (SLE). However, several reports have indicated that the number of IFN-alpha producing cells are decreased or that their function is defective in patients with SLE. We studied the function of plasmacytoid dendritic cells (pDCs) under persistent stimulation of Toll-like receptor (TLR)9 via a TLR9 ligand (CpG ODN2216) or SLE serum.
The concentrations of IFN-alpha were determined in serum and culture supernatant of peripheral blood mononuclear cells (PBMCs) from SLE patients and healthy controls after stimulation with CpG ODN2216 or SLE serum. The numbers of circulating pDCs were analyzed by fluoresence-activated cell sorting analysis. pDCs were treated with CpG ODN2216 and SLE serum repeatedly, and levels of produced IFN-alpha were measured. The expression of IFN-alpha signature genes and inhibitory molecules of TLR signaling were examined in PBMCs from SLE patients and healthy control individuals.
Although there was no significant difference in serum concentration of IFN-alpha and number of circulating pDCs between SLE patients and healthy control individuals, the IFN-alpha producing capacity of PBMCs was significantly reduced in SLE patients. Interestingly, the degree which TLR9 ligand-induced IFN-alpha production in SLE PBMCs was inversely correlated with the SLE serum-induced production of IFN-alpha in healthy PMBCs. Because repeated stimulation pDCs with TLR9 ligands showed decreased level of IFN-alpha production, continuous TLR9 stimulation may lead to decreased production of IFN-alpha in SLE PBMCs. In addition, PBMCs isolated from SLE patients exhibited higher expression of IFN-alpha signature genes and inhibitory molecules of TLR signaling, indicating that these cells had already undergone IFN-alpha stimulation and had become desensitized to TLR signaling.
We suggest that the persistent presence of endogenous IFN-alpha inducing factors induces TLR tolerance in pDCs of SLE patients, leading to impaired production of IFN-alpha.
Arthritis research & therapy 02/2008; 10(2):R29. · 4.27 Impact Factor
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ABSTRACT: NKT cells are a unique subset of T cells that recognize glycolipid antigens presented by CD1d molecules. NKT cells have the potential to produce key cytokines of both Th1 and Th2 T cells and are involved in the control of several types of immune response. Furthermore, NKT cells perform spontaneous tumor immunosurveillance. Upon specific activation with alpha-GalCer, NKT cells show strong antitumor immune responses through direct cytotoxicity and indirect activation of a cascade of antitumor effector cells such as natural killer (NK) cells and CD8+ cytotoxic T cells. In addition to alpha-GalCer, many other CD1d ligands, including self and bacterial glycolipids and modified synthetic glycolipid antigens, have also been discovered. Structurally different glycolipid antigens have the distinct ability to activate NKT cells. Thus, it seems that we are now close to a position in which we can control the activation status of NKT cells; this makes NKT cells an ideal target of anticancer immunotherapies. Clinical trials with soluble alpha-GalCer or alpha-GalCer-pulsed dendritic cells aimed at in vivo reconstitution and activation of human NKT cells have provided both promising and challenging results. In this review, we discuss NKT-cell-mediated antitumor immune responses, as well as the early outcomes and implications of recent clinical studies.
Critical Reviews in Immunology 02/2007; 27(6):511-25. · 3.32 Impact Factor
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ABSTRACT: We present our surgical experiences with functioning neuroendocrine neoplasms of the pancreas to define its natural history, and to suggest its proper management. From June 1990 to June 2005, patients with diagnosis of functioning neuroendocrine (islet cell) neoplasms of the pancreas were retrospectively reviewed. Fourteen patients (5 men and 9 women) with a median age of 49 years (range, 12 - 68 years) were identified. Twelve patients (86%) had insulinoma, two (14%) had gastrinoma. One (7%) with pancreatic insulinoma was multiple endocrine neoplasia type 1. Intraoperative ultrasound scan (sensitivity, 83%) was the most powerful modality for tumor localization. Fifteen neoplasms with median tumor size 1 cm (range 0-3 cm) were resected. Four insulinomas (26.7%) were located in the head of the pancreas and 5 (36%), in the tail. Another 5 (36%) insulinomas and 1 (7%) gastrinoma were located around the neck area near the SMV or PV. Eleven patients (79%) underwent enucleation, and 2 patients (14%), distal pancreatectomy with splenectomy. 100% of patients with functioning neuroendocrine neoplasms of the pancreas have survived. The overall disease free 10-year survival was found to be about 81%. Exact localization of tumor by intraoperative ultrasound and surgical removal are promising for good prognosis.
Yonsei Medical Journal 01/2007; 47(6):833-9. · 1.14 Impact Factor
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ABSTRACT: NKT cells perform crucial roles in tumor surveillance, functioning as regulators of early host response. In this study, we have assessed the effects of NKT activation at the time of tumor Ag immunization, and have evaluated the contributions of CD4+ and CD8+ T cells in tumor rejection during adaptive immune response against live tumor cells. Our data indicate that CD4+ T cells play critical roles, not only in assisting CTL, but also in the orchestration of host response against the tumor. The CD4+ T cells were found to reject the transplanted tumor cells very efficiently under conditions in which the CTLs were removed either genetically, or via the action of anti-CD8 Ab in mice that had been immunized with tumor extracts and alpha-galactosylceramide. Immunization resulted in an NKT cell-dependent antitumor adaptive immune response, which was associated with both CD4+ T cells and cytokine IFN-gamma.
The Journal of Immunology 12/2006; 177(10):6747-57. · 5.79 Impact Factor
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Seok Goo Cho,
So-Youn Min,
Min Jung Park,
Kyung Wha Lee,
Young-Gyu Cho,
Mi-La Cho,
Hong Seok Chang, Se-Ho Park,
Jong Wook Lee,
Woo Sung Min,
Chun Choo Kim,
Ho-Youn Kim
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ABSTRACT: To investigate the immunoregulatory effects of allogeneic mixed chimerism induced by T cell-depleted, nonmyeloablative bone marrow transplantation (BMT) on chronic inflammatory arthritis and autoimmunity in mice deficient in interleukin-1 receptor antagonist (IL-1Ra).
IL-1Ra(-/-) mice (H-2K(d)) were treated with antibody to asialoganglioside G(M1) (anti-natural killer cell), total body irradiation (500 cGy), and T cell-depleted, nonmyeloablative BMT derived from C57BL/6 mice (H-2K(b)). Engraftment and chimerism were evaluated in peripheral blood, lymph nodes, and spleen by multicolor flow cytometry. The severity of arthritis was evaluated by clinical scoring and histopathologic assessment. Levels of IgG1 and IgG2a subtypes of anti-type II collagen (anti-CII) antibodies were measured in serum samples. After T cells were stimulated with CII, ovalbumin, and phytohemagglutinin, T cell proliferative responses and levels of cytokine production (interferon-gamma [IFNgamma], tumor necrosis factor alpha [TNFalpha], interleukin-10 [IL-10], and IL-17) were assayed in culture supernatants.
All IL-1Ra(-/-) mice receiving BMT showed marked improvement in arthritis within 3 weeks, as well as successful induction of mixed chimerism. These mice showed higher levels of IgG1, and lower levels of IgG2a anti-CII antibodies and weaker T cell proliferative responses than did mice in the control groups (either no treatment or conditioning alone without bone marrow rescue). In mixed chimeras, the levels of IFNgamma, TNFalpha, and IL-17 produced from CII-stimulated T cells were significantly suppressed and IL-10 production was significantly higher as compared with controls.
The introduction of allogeneic mixed chimerism showed a strong immunoregulatory potential to correct established chronic inflammatory arthritis and autoimmunity originating from a dysregulated proinflammatory cytokine network.
Arthritis & Rheumatism 07/2006; 54(6):1878-87. · 7.87 Impact Factor
