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At least 163 records · Page 9Linked to original sources
PubMed2004

The organ-specific extrapulmonary presentation of sarcoidosis: a frequent occurrence but a challenge to an early diagnosis. A 3-year-long prospective observational study.

BACKGROUND AND AIM: The percentage of organ-specific extrapulmonary presentation of sarcoidosis has usually been estimated on the basis of retrospective studies, with figures varying in the range of 7-22%. We have hypothesized that a prospective study could give a higher figure, and could better outline the variable pattern of extrapulmonary presentation. MATERIAL AND METHODS: A careful examination with particular interest to the possible extrapulmonary signs or symptoms of the disease, even if previously unrecognized, was carried out in 204 consecutive sarcoid patients (mean age 37 +/- 11) seen between 2000 and 2002. Some of them had already visited our clinic in previous years. Their median follow up in our clinic was 34 months, while the median duration of disease was 60 months. RESULTS: An organ-specific extrapulmonary presentation did occur in 73 patients (35.78%). The most frequent extrapulmonary presentation was due to skin lesions (different from erythema nodosum) and to peripheral lymph nodes (8% each). Less frequent were renal stones (4%), uveitis (3%) and others (12%). The extrapulmonary presentation may be a challenge to the diagnosis. In our series an early diagnosis was reached only in 38 of 73 patients. In the other 35 patients, the diagnosis was reached later, after a time interval ranging from 6 months to 20 years. The lung involvement was detected early in 33 patients with extrapulmonary presentation. In 35 other patients the pulmonary involvement appeared after a median time interval of 24 months (range 6-240, interquartiles 15-60). In 5 patients, no pulmonary changes ever appeared after a long term follow up of 20 months, 5 years (2 patients), 10 years and 29 years respectively. CONCLUSION: An organ-specific extrapulmonary presentation is common in sarcoidosis, but may go unrecognized for years.

Adolescent↗
PubMed2005

Mitogen-activated protein kinases and selected downstream targets display organ-specific responses in the hibernating ground squirrel.

The responses of mitogen-activated protein kinase (MAPK) family members, including the extracellular signal-regulated kinases (ERKs), the c-jun NH2-terminal kinases (JNKs) and p38MAPK, during mammalian hibernation were analyzed in five organs of Richardson's ground squirrels, Spermophilus richardsonii. Each kinase subfamily responded differently in torpor and each showed organ-specific patterns of response. ERK1/2 activities increased significantly in muscle and brain during hibernation but decreased in kidney and liver. JNK activity rose in four organs (except brain) during hibernation whereas active, phosphorylated p38MAPK increased only in muscle and heart. Activities of ERK-activated kinases also responded to hibernation: MAPKAPK-1 rose in muscle and brain, MAPKAPK-2 decreased in liver and kidney but rose in the other three organs, and p70S6K kinase activity decreased kidney and heart. Transcription factors, c-Jun and CREB, also showed organ-specific responses during torpor. The data suggest key roles for MAPKs in the regulation of the known organ-specific changes in gene expression and protein phosphorylation that define the hibernation phenotype.

Animals↗
PubMed2003

Differential representation of sunflower ESTs in enriched organ-specific cDNA libraries in a small scale sequencing project.

BACKGROUND: Subtractive hybridization methods are valuable tools for identifying differentially regulated genes in a given tissue avoiding redundant sequencing of clones representing the same expressed genes, maximizing detection of low abundant transcripts and thus, affecting the efficiency and cost effectiveness of small scale cDNA sequencing projects aimed to the specific identification of useful genes for breeding purposes. The objective of this work is to evaluate alternative strategies to high-throughput sequencing projects for the identification of novel genes differentially expressed in sunflower as a source of organ-specific genetic markers that can be functionally associated to important traits. RESULTS: Differential organ-specific ESTs were generated from leaf, stem, root and flower bud at two developmental stages (R1 and R4). The use of different sources of RNA as tester and driver cDNA for the construction of differential libraries was evaluated as a tool for detection of rare or low abundant transcripts. Organ-specificity ranged from 75 to 100% of non-redundant sequences in the different cDNA libraries. Sequence redundancy varied according to the target and driver cDNA used in each case. The R4 flower cDNA library was the less redundant library with 62% of unique sequences. Out of a total of 919 sequences that were edited and annotated, 318 were non-redundant sequences. Comparison against sequences in public databases showed that 60% of non-redundant sequences showed significant similarity to known sequences. The number of predicted novel genes varied among the different cDNA libraries, ranging from 56% in the R4 flower to 16 % in the R1 flower bud library. Comparison with sunflower ESTs on public databases showed that 197 of non-redundant sequences (60%) did not exhibit significant similarity to previously reported sunflower ESTs. This approach helped to successfully isolate a significant number of new reported sequences putatively related to responses to important agronomic traits and key regulatory and physiological genes. CONCLUSIONS: The application of suppressed subtracted hybridization technology not only enabled the cost effective isolation of differentially expressed sequences but it also allowed the identification of novel sequences in sunflower from a relative small number of analyzed sequences when compared to major sequencing projects.

DNA, Complementary↗
PubMed1996

Organ-specific therapy in critical illness: interfacing molecular mechanisms with physiological interventions.

Sepsis and SIRS is the outward manifestation of a generalized uncontrolled inflammatory response, which, if sustained, induces widespread endothelial damage and MODS. Immunomodulating therapies, at present, have proven ineffective in reducing morbidity and mortality, presumably because of the heterogeneous nature of sepsis and septic shock and the reciprocating and redundant nature of this inflammatory cascade. Organ-specific therapies can support life but impair both organ-specific function and remote organ function. Novel therapies aimed at minimizing further organ dysfunction may improve outcome in a cost-effective fashion by preventing both further primary organ dysfunction or remote organ dysfunction secondary to the subsequent activation of the inflammatory response.

Animals↗
PubMed1994

Regulation of gelatinase production in metastatic renal cell carcinoma by organ-specific fibroblasts.

We have recently established a human renal cell carcinoma KG-2 line that is tumorigenic in the subcutis (ectopic) and kidney (orthotopic) of nude mice but spontaneously metastasizes to the lung only after orthotopic implantation. KG-2 cells growing in the kidney (orthotopic) and lung metastases secreted higher levels of gelatinase than did cells growing in the subcutis (ectopic). We examined whether organ-specific fibroblasts play a role in the regulation of gelatinase production and invasion by renal carcinoma cells. The gelatinase level in the culture supernatants of KG-2 cells was increased by their cultivation with mouse kidney or lung fibroblasts. In contrast, cocultivation of KG-2 cells with mouse skin fibroblasts resulted in a significant reduction of gelatinase activity. Similar results were obtained by culturing KG-2 cells in the media conditioned by the different mouse fibroblasts. We, therefore, investigated effects on KG-2 cells of cytokines and growth factors known to be produced by fibroblasts of various origins. Of ten cytokines and growth factors tested, basic fibroblast growth factor, hepatocyte growth factor, and transforming growth factor-beta 1 (TGF-beta 1) stimulated gelatinase expression by the cultured KG-2 cells. Parallel immunohistochemical analyses revealed that mouse kidney and lung fibroblasts produced higher levels of TGF-beta 1 than did skin fibroblasts. These results indicate that gelatinase production by KG-2 renal cell carcinoma cells is influenced by the organ microenvironment. Specifically, organ-specific fibroblasts regulate the production of degradative enzymes by KG-2 cells and, hence, profoundly influence their invasive and metastatic capacity.

Animals↗
PubMed2001

Resolution of organ-specific complications of human immunodeficiency virus infection in children with use of highly active antiretroviral therapy.

Opportunistic infections are a major source of morbidity and mortality in children and adults infected with human immunodeficiency virus (HIV). In addition, organ-specific complications of HIV infection, such as cardiomyopathy, nephropathy, encephalopathy, and others, contribute substantially to the morbidity and mortality associated with HIV infection. Highly active antiretroviral therapy (HAART) has produced a dramatic decline in the incidence of opportunistic infections among patients with HIV infection. Nevertheless, there is very little information concerning the value of HAART for organ-specific complications of HIV infection. In this report, we describe 3 children with HIV infection in whom the dominant clinical manifestations were cardiomyopathy, red cell aplasia, and nephropathy. HAART produced a decrease in the HIV ribonucleic acid level, an increase in the CD4 cell count, and resolution of the organ-specific complications in all patients. These cases add to our knowledge concerning the benefits of HAART for children with HIV infection.

AIDS-Associated Nephropathy↗
PubMed1999

[Development and characterization of a monoclonal antibody which recognizes a new prostate-organ specific antigen].

PURPOSE: Development and characterization of monoclonal antibodies which recognizes a new prostate-organ specific antigen. METHOD: For development of monoclonal antibodies, hybrid cells were prepared by fusion of spleen cells of BALB/c mice immunized with the homogenates of surgically resected prostatic tissue and P 3 x Ag 8 U 1 (P 3 U 1) murine myeloma cells. Supernatants of hybrid clones were primarily screened using an ELISA on human prostatic cancer cell line PC-3 and human bladder cancer cell line T-24. In the secondary screening, they were tested on normal tissues by immunohistochemical staining. To characterize the antigens, biochemical analyses were performed using seminal plasma as an antigen by western blotting and gel filtration, and the reactivity of antibodies were compared with that of antibodies against prostatic acid phosphatase (PAP), prostate-specific antigen (PSA) and gamma-seminoprotein (gamma-Sm). RESULTS: A monoclonal antibody termed KP-9 was obtained and it only reacted with PC-3 and prostate tissues, but did not react with other cell lines and normal tissues. Immunohistochemical staining of prostate tissue revealed that KP-9 stained grandular epithelium and grandular exudate of normal and malignant prostatic tissues, and especially, strongly stained the apical site of grandular epithelium. Western blotting and gel filtration of seminal plasma suggested that the molecular weight of the KP-9 antigen was more than 300,000 and was different from PAP, PSA and gamma-Sm. CONCLUSION: We have developed a monoclonal antibody, KP-9 which specifically reacts with prostatic cancer as well as benign prostatic tissues. The antigen recognized by KP-9 appeared to be a new prostate-organ specific antigen and may be a useful marker for prostatic cancer such as PAP, PSA and gamma-Sm.

Animals↗
PubMed2000

Organ-specific distribution of major histocompatibility antigens in rats.

The present study systematically investigated the expression and distribution of the major histocompatibility complex (MHC) classes I and II in the rat. About 150 native tissue probes from eight adult Lewis rats were taken, representative for most organs, tissues, and the vascular system. MHC expression was analyzed by two monoclonal antibodies (mAb) generated against the non-polymorphic determinants of rat MHC class I (Ox-18) and class II (Ox-6). Immunoreactivities were compared to those of different endothelial (HIS52, TLD-3A12, Ox-43, REHA-1 antigen), histiocytic (ED1, ED2), B-cell (RLN-9D3), and T-cell (MRC Ox-52) markers. A nonspecific mAb (MR12/53) served as a negative control. Pretested concentrations on various tissues and the alkaline phosphatase-anti-alkaline phosphatase technique allowed semiquantitative evaluation of serial cryostat tissue sections. MHC class I expression was detected on most immunocompetent cells. Endothelial cells were stained heterogeneously along the vascular system and the organ-specific microcirculation. Furthermore, some organs showed staining of parenchymal cells. MHC class II was found on all immunocompetent cells positive for the B-cell marker and about 15% of cells positive for the histiocytic markers. Besides the well-known expression of MHC class II in the outer zone of the renal proximal tubule, further organ-specific cell forms were found positive. In conclusion, the present study outlines tissue-specific distribution of MHC I/ II and implies that each organ carries a variable immunologic burden that needs to be considered for any transplantation model.

Adrenal Cortex↗
PubMed1995

Organ- and non-organ-specific auto-antibodies in children with hypopituitarism on growth hormone therapy.

UNLABELLED: Serum non-organ-specific antibodies (NOSA) against nuclear, mitochondrial (AMA), smooth muscle, liver/kidney microsomal (LKM), reticulin, ribosomal, and organ-specific antibodies (OSA) against pituitary gland, gonads (testis, ovary) adrenal cortex, thyroid (thyroglobulin and microsomal), pancreas islet cells, gastric parietal cells and intestinal epithelial cells were evaluated in 45 patients with hypopituitarism (mean age 12.4 +/- 4.0 years). In 22 of them, 9 with isolated growth hormone (GH) deficiency (IGHD) and 13 with multiple pituitary hormone deficiency, MRI showed anterior pituitary hypoplasia with structural stalk abnormality and ectopic posterior pituitary. Twelve had isolated small anterior pituitary and IGHD and 11 had normal morphology of pituitary gland and IGHD. Controls were healthy age-sex-matched subjects. Thyroid antibodies were detected by a passive haemagglutination test while indirect immunofluorescence was used for the others. The auto-antibodies were found in 7/45 asymptomatic patients, a frequency not significantly different from that in controls; 5 were type NOSA and 2 type OSA. Pituitary antibodies were positive in 1 girl with IGHD and normal pituitary morphology. One girl developed hyperthyroidism during the follow up. Autoantibodies were equally distributed between the three groups and the frequency was not dissimilar from that in controls; this suggests that these patients are not at a higher risk of developing auto-immune disease, at least during the first two decades. CONCLUSION: Pituitary insufficiency in children with different MRI features seems unlikely to be secondary to an auto-immune process.

Adolescent↗
PubMed1990

Reversal of autoimmune encephalomyelitis by membranes presenting myelin basic protein-associated class II MHC molecule as an approach to immunotherapy of organ-specific autoimmune diseases.

Experimental autoimmune encephalomyelitis (EAE), a well-accepted experimental model for multiple sclerosis in humans, is a paralytic disease mediated by CD4+ T cells specific for myelin basic protein (MBP). Several approaches to immune-specific therapy of EAE as a model for other organ-specific autoimmune diseases have previously been reported. We now show that macrophages (M phi) or B cells, as antigen-presenting cells, when pulsed with MBP and intraperitoneally (but not intravenously) inoculated after the encephalitogenic challenge, are highly effective in blocking the development of EAE. Moreover, M phi pulsed with an organ tissue homogenate, mouse spinal cord homogenate, can also present the relevant target antigen, MBP, and are as effective as MBP-pulsed M phi in blocking the development of EAE. This capacity of the M phi to identify and present the relevant target antigen indicates that this approach is also applicable to organ-specific autoimmune diseases other than EAE, regardless of how much is known about their etiological agent or specific target antigen. Nonviable glutaraldehyde-fixed MBP-pulsed M phi or membranes derived from MBP-pulsed M phi retain their capacity to block the development of EAE.

Animals↗
PubMed1996

Adrenal autoantibodies and organ-specific autoimmunity in patients with Addison's disease.

OBJECTIVE: Autoimmune destruction of the adrenal gland is the major cause of Idiopathic Addison's disease, but the significance of 21-hydroxylase autoantibodies and their correlation with the presence of other autoantibodies have not so far been investigated in a larger population of patients with Addison's disease. We have now characterized a cohort of patients with idiopathic Addison's disease (n = 97) regarding the specificity of autoantibodies against the adrenal cortex and, as Addison's disease can be either an isolated condition or part of a polyendocrine disorder, we investigated the presence of organ-specific polyendocrine autoimmunity in this patient population. DESIGN: Cross-sectional study. MEASUREMENTS: Autoantibodies were analysed with indirect immunofluorescence (IF) on tissue preparations, ELISA and in Western blots using bacterially expressed proteins. RESULTS: Eighty-four per cent (81/97) of the patient sera recognized the steroid-producing cells of the adrenal cortex in indirect IF. The antigen was identified as 21-hydroxylase by 72% (70/97) of the patient sera in Western blots. Seven sera that were negative on adrenocortical IF identified 21-hydroxylase on Western blot, while eight IF-positive sera were 21-hydroxylase-negative. Five sera weakly recognized 17 alpha-hydroxylase in Western blots, but all of these were also positive for 21-hydroxylase. In 13 cases (12 women), the sera also reacted with testicular Leydig cells, and nine of these identified the side-chain cleavage (SCC) enzyme. Other clinically evident organ-specific autoimmune disorders were present in 40% of the 97 patients and abnormal titres of organ-specific antibodies were found in 60% of the patients. CONCLUSIONS: In idiopathic Addison's disease, auto-antibodies against 21-hydroxylase are found in a majority of cases and this represents an important diagnostic tool. The enzyme 17 alpha-hydroxylase does not seem to constitute a major autoantigen in Addison's disease. In a subgroup of patients with autoantibodies to gonads, antibodies to SCC are produced, often in parallel with antibodies to 21-hydroxylase. In yet another subgroup the specificity of autoantibodies giving positive immunofluorescence is still unknown. Three patients revealed a polyendocrine syndrome which clinically resembles autoimmune polyendocrine syndrome (APS) type I, but serologically corresponds to APS type II. Polyendocrine disorders are often associated with Addison's disease, and screening, including quantification of autoantibodies, may help to identify those at risk of developing associated autoimmune disorders.

Addison Disease↗
PubMedDate not supplied

Target organ specificity of cell proliferation induced by various carcinogens.

The target organ specificities of cell proliferation and histopathological lesion induction by 5 carcinogens having different target organs were evaluated using a multiorgan carcinogenesis bioassay. In Group 1, male F-344 rats aged 6 wk were sequentially treated with N-diethylnitrosamine (DEN, single 100-mg/kg ip injection, week 0), N-methyl-N-nitrosourea (MNU, 4 20-mg/kg ip injections, weeks 0-2), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN, 0.05% in drinking water, weeks 0-2), N,N'-dimethylhydrazine (DMH, 4 40-mg/kg sc injections, weeks 2-4), and dihydroxy-di-N-propylnitrosamine (DHPN, 0.1% in drinking water, weeks 2-4) during the first 4 wk. In Groups 2-6, rats were treated with only one of the above initiators, applied as in Group 1. Group 7 served as the no-treatment control. Bromouracil deoxyriboside (BUdR) labeling indices (LI) were counted in various organs at weeks 2 and 4. Numbers and areas of glutathione S-transferase placental form positive (GST-P+) liver foci were measured at weeks 2, 4, and 28. Preneoplastic or neoplastic lesion development was assessed at week 28. With regard to specific elevation of cell proliferation in target organs, BUdR LIs in the urinary bladder, liver, and colon were, respectively, increased in the BBN alone, DEN alone, and DMH alone treated groups as well as in Group 1. However, LIs of thyroid, lung, and kidney were also elevated by several carcinogens not including these organs in their carcinogenic target specificity. On the other hand, morphological lesions and GST-P+ foci were limited to Group 1 and the target organs of the corresponding carcinogen-treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)

1,2-Dimethylhydrazine↗
PubMed1981

[Organ-specific ultrastructural cellular signs of cancerous breast tumors].

The ultrastructural analysis of 40 cases of mammary carcinomas revealed two groups of cells: with ultrastructural organ specific features (differentiated cells) and without them (undifferentiated cells). Intracytoplasmic lumens, secretory granules (lipid, protein, and mixed lipid-protein), and myoepithelial cells are the main organ specific features of mammary carcinomas. The histospecific features showing the epithelial origin of the tumor cells include cell-to-cell contacts, ductules, intercytoplasmic lumens with microvilli, and fragments of basal lamina. These ultrastructural features of mammary carcinomas can facilitate the differential diagnosis of tumors of this organ.

Adenocarcinoma↗
PubMed1982

Organ specificity of neonatal methyl mercury hydroxide poisoning in the rat: effects of ornithine decarboxylase activity in developing tissues.

To determine the organ specificity of neonatal mercury hydroxide (CH3HgOH) exposure on biochemical development of its potential target tissues, effects on rat brain, liver, heart and kidney were compared utilizing the ontogenetic pattern of ornithine decarboxylase (ODC) activity, an early index of perturbation of cellular maturation. CH3HgOH was given daily beginning at birth for up to 21 days, using three dose levels (1, 2.5 or 5 mg/kg s.c.). In the brain, CH3HgOH treatment resulted in an initial reduction in ODC followed by a subsequent elevation of activity, a maturational pattern known to be associated with delayed cellular development. In contrast to the effects of CH3HgOH on brain, the pattern obtained in the liver, an initial elevation followed by a subsequent decline, is usually associated with compression of the time couse of cellular development. In the heart and kidney, CH3HgOH produced sustained elevations of ODC representing prolongation of the developmental period of rapid tissue growth and development; these patterns were associated with tissue hypertrophy which was sustained through the preweaning stage for both tissues and well into the postweaning period for the kidney. The results obtained with ODC clearly demonstrate that neonatal CH3HgOH poisoning causes organ-specific biochemical lesions which can play a role in subsequent effects on overall tissue development.

Aging↗
PubMed1974

Localization of histocompatibility and organ specific antigens on mouse spermatozoa.

Further studies on the topographic localization of histocompatibility and organ-specific antigens on mouse spermatozoa have been reported. Specific antisera to a histocompatibility antigen (H-2a) and a serum prepared by injecting male mice with syngeneic testicular homogenate were labeled with peroxidase and the antigens were located by immunoelectron microscopy. The organ-specific antigen was located on the sperm head and occasionally on the midpiece, whereas the H-2 antigen was confined to the sperm head. The observations were not quantitative, because of the obvious limitations in the examination of thin sections. The distribution of the 2 antigens may be related to the functions of the various parts of the spermatozoa, although no clear correlation could be suggested. The authors indicate several points of discussion arising from their observations. There is no general agreement at present about the presence or absence of histocompatability antigens on spermatozoa. The reported location of these antigens on spermatozoa conflicts with some earlier results. The present observations must also be considered in relation to the fluid mosaic model of cell membranes, for the localization of antigens to particular sites imples that restrictions are placed on the movement of some membrane constituents.

Biology↗
PubMed1992

The TACPyAT repeats in the chalcone synthase promoter of Petunia hybrida act as a dominant negative cis-acting module in the control of organ-specific expression.

Analysis of the expression of the GUS reporter gene driven by various regions of the Petunia hybrida chalcone synthase (chsA) promoter revealed that the developmental and organ-specific expression of the chsA gene is conferred by a TATA proximal module located between -67 and -53, previously designated as the TACPyAT repeats. Histochemical analysis of GUS reporter gene expression revealed that the organ-specific 67 bp promoter fragment directs the same cell-type specificity as a 530 bp promoter, whereas additional enhancer sequences are present within the more TATA distal region. Moreover, the region between -800 and -530 is also involved in extending the cell-type specificity to the trichomes of flower organs and of young seedlings. The mechanism by which the TACPyAT repeats modulate expression during plant development was studied by analysing the expression of the GUS gene driven by chimeric promoters consisting of the CaMV 35S enhancer (domain B, -750 to -90) fused to various chsA 5' upstream sequences. Detailed enzymatic and histochemical analysis revealed that in the presence of the TACPyAT module the CaMV 35S region only enhances GUS activity in those organs in which the chsA promoter is normally active. Furthermore, this analysis shows that enhancement in the presence of the CaMV 35S domain B is accomplished by increasing the number of cell types expressing the GUS gene within the organ, rather than enhancement of the chsA cell-type-specific expression within these organs. Deletion of the TACPyAT sequences in the chimeric promoter construct completely restores the well-documented CaMV 35S domain B cell-type specificity, showing that the TACPyAT module acts as a dominant negative cis-acting element which controls both organ and developmental regulation of the chsA promoter activity.

Acyltransferases↗
PubMed1995

Organ-specific effects and interactions of acute insulin-like growth factor I (IGF-I) and growth hormone (GH).

The acute organ-specific and metabolic actions of Insulin-like Growth Factor-I (IGF-I) and Growth Hormone (GH) were investigated in normal rats. Rats received a single subcutaneous injection of IGF-I (100 micrograms), GH (100 micrograms) or a combined treatment with IGF-I (100 micrograms) plus GH (100 micrograms) following a 2(2) factorial design. The acute treatment with IGF-I produced an increase in its plasma concentration along with a reduction in insulin levels. Plasma glucose and total cholesterol decreased in all treated groups as well as triglycerides in IGF-I treated animals as compared to controls. The rates of protein synthesis, measured by amino acid incorporation were not affected by any of these treatments in muscle or liver. However, GH treatment raised the rate of protein synthesis in the jejunum, while IGF-I treatment produced an increase in tibia protein synthesis rate. Negative interactions between GH and IGF were noted concerning tibia and jejunum protein formation. Thus, GH appeared to inhibit the response to IGF-I in bone, while IGF-I inhibited the response of the jejunum to GH administration. Also, liver cathepsin activity was reduced, while bone alkaline phosphase was increased by the GH treatment. Therefore, these results have demonstrated some acute organ-specific anabolic effects and interactions of IGF-I and GH on different aspects of metabolism in normal rats.

Acid Phosphatase↗
PubMed2000

Characterization of T cell receptor (TCR) of organ-specific autoimmune disease-inducing T cells and TCR-based immunotherapy with DNA vaccines.

Organ-specific autoimmune diseases and their animal models are characterized by the finding that the development of the diseases is closely associated with, or induced by, T cells reactive to organ-specific antigens. Therefore, the identification of T cell receptors (TCR) used by disease-inducing T cells within a short period of time is a key factor for designing TCR-based immunotherapy. The findings introduced in this article show that TCR associated with the development of multiple sclerosis and experimental autoimmune diseases including encephalomyelitis (EAE), neuritis (EAN) and carditis (EAC) are identifiable by complementarity-determining region 3 (CDR3) spectratyping analysis and subsequent sequencing of the CDR3 region of spectratype-derived TCR clones. It is also demonstrated that immunotherapy targeting disease-associated TCR using monoclonal antibodies and DNA vaccines significantly reduced the histological severity, and completely suppressed the inflammation in some animals. Since depletion or suppression of one of several types of effector cells does not significantly improve the severity of the disease, combined TCR-based immunotherapy should be considered as a primary therapy for T cell-mediated autoimmune diseases. TCR-based immunotherapy after rapid identification of autoimmune disease-associated TCR by CDR3 spectratyping can be applicable, not only to animal, but also to human autoimmune diseases whose pathomechanism is poorly understood.

Animals↗