Japanese Journal of Clinical Immunology

Online ISSN : 1349-7413
Print ISSN : 0911-4300
ISSN-L : 0911-4300

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Volume 35, Issue 4

The 40th Annual Meeting of the Japan Society for Clinical Immunology

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2012Volume 35Issue 4 Pages 306a
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DOIhttps://doi.org/10.2177/jsci.35.306a

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2012Volume 35Issue 4 Pages 306b
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DOIhttps://doi.org/10.2177/jsci.35.306b

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2012Volume 35Issue 4 Pages 307a
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2012Volume 35Issue 4 Pages 307b
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2012Volume 35Issue 4 Pages 308a
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W5-2 Lymphopenia-induced proliferation (LIP) triggers the development of follicular helper T (T_FH) cells which have a distinctive ontogeny and a critical role in aberrant B cell responses

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2012Volume 35Issue 4 Pages 308b
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  Lymphopenia results in the homeostatic peripheral expansion of lymphocytes to maintain T cell homeostasis. Accumulating data show that lymphopenia-induced proliferation (LIP) has a pathogenic role in the development of autoimmunity in animal models and human systemic autoimmune diseases such as systemic lupus erythematosus, Sjögren's syndrome and rheumatoid arthritis.
  To clarify the mechanism of anti-nuclear antibodies (ANA) production, we established a lymphopenic mouse model in which CD4⁺ T cell subsets from wild-type BALB/c mice were adoptively injected into BALB/c nude mice, which induced IgG-type ANA production. We observed that class switching and ANA production were enhanced when regulatory T cells were depleted. We identified IL-21-producing PD-1⁺ T_FH cells which develop from conventional T cells during LIP and drive germinal center reactions with aberrant B cell responses. Compared with traditional T_FH cells, this subset has a distinctive ontogeny and a critical role in breaking B cell tolerance.
  This study reveals the physiological mechanism how immunological tolerance is maintained during LIP and would help to understand the pathogenesis of systemic autoimmune diseases.

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2012Volume 35Issue 4 Pages 309a
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DOIhttps://doi.org/10.2177/jsci.35.309a

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2012Volume 35Issue 4 Pages 309b
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2012Volume 35Issue 4 Pages 310a
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DOIhttps://doi.org/10.2177/jsci.35.310a

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2012Volume 35Issue 4 Pages 310b
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DOIhttps://doi.org/10.2177/jsci.35.310b

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2012Volume 35Issue 4 Pages 311a
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DOIhttps://doi.org/10.2177/jsci.35.311a

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2012Volume 35Issue 4 Pages 311b
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DOIhttps://doi.org/10.2177/jsci.35.311b

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2012Volume 35Issue 4 Pages 312a
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DOIhttps://doi.org/10.2177/jsci.35.312a

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2012Volume 35Issue 4 Pages 312b
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DOIhttps://doi.org/10.2177/jsci.35.312b

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2012Volume 35Issue 4 Pages 313a
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DOIhttps://doi.org/10.2177/jsci.35.313a

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2012Volume 35Issue 4 Pages 313b
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DOIhttps://doi.org/10.2177/jsci.35.313b

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2012Volume 35Issue 4 Pages 314a
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DOIhttps://doi.org/10.2177/jsci.35.314a

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2012Volume 35Issue 4 Pages 314b
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DOIhttps://doi.org/10.2177/jsci.35.314b

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2012Volume 35Issue 4 Pages 315a
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DOIhttps://doi.org/10.2177/jsci.35.315a

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2012Volume 35Issue 4 Pages 315b
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DOIhttps://doi.org/10.2177/jsci.35.315b

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2012Volume 35Issue 4 Pages 316a
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DOIhttps://doi.org/10.2177/jsci.35.316a

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2012Volume 35Issue 4 Pages 316b
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DOIhttps://doi.org/10.2177/jsci.35.316b

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W8-3 Ceramide deficiency in the epidermis leads to development of psoriasis-like lesions associated with IL-23-dependent proliferation of γ d-17 cells

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2012Volume 35Issue 4 Pages 317a
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DOIhttps://doi.org/10.2177/jsci.35.317a

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It has been recognized that ceramide levels are decreased in the epidermis of patients with atopic dermatitis and psoriasis. However, the underlying mechanism by which ceramide deficiency leads to skin inflammation still remains unclear. Here, we generated Sptlc2 targeted mice under control of the keratin 5 promoter, by which their keratinocytes were devoid of serine palmitoyltransferase (SPT), the rate-limiting enzyme for de novo sphingolipid synthesis. K5-SPT-KO mice have demonstrated barrier dysfunction. From 2 weeks of age, they develop the skin lesion, showing psoriasis-like histopathologic changes. Transcriptional levels of IL-17 and IL-22 were increased in the skin and draining lymph nodes. Strikingly, K5-SPT-KO mice showed increased numbers of gd-T cells that produce IL-17 (gd-17) in the skin lesion and lymph nodes and most of them also produce IL-22, similar to Th17 cells. In vivo administration of anti-IL-12/23p40 antibody ameliorated the skin lesions and reduced the number of gd-17 cells in K5-SPT-KO mice. Therefore, we conclude that ceramide deficiency in the epidermis results in the development of psoriasis-like lesions, mediated by IL-23-dependent gd-17 cells in mice.

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2012Volume 35Issue 4 Pages 317b
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DOIhttps://doi.org/10.2177/jsci.35.317b

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W8-5 Advanced delivery system of mesenchymal stem cells using nano-fiber scaffold for treatment of rheumatic arthritis models

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2012Volume 35Issue 4 Pages 318a
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DOIhttps://doi.org/10.2177/jsci.35.318a

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Objectives: Mesenchymal stem cells (MSCs) are considered as a possible tool for treatment of rheumatoid arthritis (RA) due to their immunoregulatory ability and pluripotency. Here we established an effective delivery system of MSCs on a arthritis animal model.
Methods: MSCs were seeded on poly-lactic-co-glycollic acid (PLGA) scaffold then implanted into ankles (IMP) of collagen induced arthritis (CIA) rats or simply injected intra-articularly (IA) or intra-peritoneally (IP).
Results: IMP to bilateral ankles significantly suppressed the severity of arthritis evaluated by arthritis score, hind paw thickness and body weight compared to CIA, while IA and IP showed less or no effect. Accordingly, bone destruction detected by X-ray, micro CT and infiltration of inflammatory cells, damage of cartilage and bone destruction detected histologically were reduced in IMP group but not in other groups. Furthermore, the size of the draining lymph nodes was smaller with reduced germinal center formation in the IMP group.
Conclusion: Implantation of MSCs with nano-fiber scaffold efficiently suppressed arthritis and bone destruction, suggesting a novel MSCs delivery system for future RA treatment.

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2012Volume 35Issue 4 Pages 318b
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DOIhttps://doi.org/10.2177/jsci.35.318b

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2012Volume 35Issue 4 Pages 319a
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DOIhttps://doi.org/10.2177/jsci.35.319a

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2012Volume 35Issue 4 Pages 319b
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DOIhttps://doi.org/10.2177/jsci.35.319b

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[in Japanese], John O'Shea, [in Japanese]

2012Volume 35Issue 4 Pages 320a
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DOIhttps://doi.org/10.2177/jsci.35.320a

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2012Volume 35Issue 4 Pages 320b
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2012Volume 35Issue 4 Pages 321a
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DOIhttps://doi.org/10.2177/jsci.35.321a

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2012Volume 35Issue 4 Pages 321b
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2012Volume 35Issue 4 Pages 322a
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DOIhttps://doi.org/10.2177/jsci.35.322a

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[in Japanese], [in Japanese], [in Japanese], Amit Bar-Or

2012Volume 35Issue 4 Pages 322b
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DOIhttps://doi.org/10.2177/jsci.35.322b

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[in Japanese], [in Japanese], [in Japanese], [in Japanese], Sang-Kyou ...

2012Volume 35Issue 4 Pages 323a
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DOIhttps://doi.org/10.2177/jsci.35.323a

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2012Volume 35Issue 4 Pages 323b
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DOIhttps://doi.org/10.2177/jsci.35.323b

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2012Volume 35Issue 4 Pages 327a
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2012Volume 35Issue 4 Pages 327b
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2012Volume 35Issue 4 Pages 328a
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DOIhttps://doi.org/10.2177/jsci.35.328a

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2012Volume 35Issue 4 Pages 328b
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2012Volume 35Issue 4 Pages 329a
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DOIhttps://doi.org/10.2177/jsci.35.329a

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[in Japanese], [in Japanese], [in Japanese], [in Japanese]

2012Volume 35Issue 4 Pages 329b
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2012Volume 35Issue 4 Pages 330a
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P1-008 Defective immune homeostasis mechanisms in Celiac Disease (CD), in its progression to Refractory Celiac Disease (RCD) and transformation to Enteropathy-Associated T-Cell Lymphoma (EATL type 1).

Joaquim Carreras, Rifat Hamoudi, William Howat, Anne Lavergne-Slove, S ...

2012Volume 35Issue 4 Pages 330b
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To evaluate the status of the immune regulation and homeostasis mechanisms in Celiac Disease (CD), and its progression toward Refractory Celiac Disease (RCD) and transformation to EATL type 1 focusing on FOXP3+Tregs, ITGAX+DCs, BTLA+cell, PDCD1+TFH subpopulations.
The series was comprised of 69 cases consisting on 50 samples of CD and 19 samples of EATL type 1. Protein expression was analyzed and quantified by digital image analysis. Histological compartmentalization included lamina propria, isolated lymphoid follicles and tumoral lymphoid area. In comparison to physiological conditions, CD was characterized by higher numbers of FOXP3+Tregs and ITGAX+DCs, but lower BTLA+cells and PDCD1+TFH cells. Progression from CD to RCD1, RCD2 and transformation to EATL was characterized by decreasing trends of FOXP3+Tregs and BTLA+cell. ITGAX+DCs showed a similar decreasing trend from CD to RCD stages but transformation to EATL was characterized with a striking increase. The RCD progression and EATL transformation stages show a defect in inhibitory pathways of FOXP3 and BTLA. Those results pinpoint the role of immune homeostasis and tolerance in CD and in the generation of cancer.

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2012Volume 35Issue 4 Pages 331a
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DOIhttps://doi.org/10.2177/jsci.35.331a

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2012Volume 35Issue 4 Pages 331b
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DOIhttps://doi.org/10.2177/jsci.35.331b

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2012Volume 35Issue 4 Pages 332a
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DOIhttps://doi.org/10.2177/jsci.35.332a

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2012Volume 35Issue 4 Pages 332b
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DOIhttps://doi.org/10.2177/jsci.35.332b

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2012Volume 35Issue 4 Pages 333a
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DOIhttps://doi.org/10.2177/jsci.35.333a

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2012Volume 35Issue 4 Pages 333b
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DOIhttps://doi.org/10.2177/jsci.35.333b

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