Journal of clinical & laboratory immunology最新文献

{"title":"Over-utilization of the J delta 3 gene-segment in Crohn's disease.","authors":"S B Landau,&nbsp;C S Probert,&nbsp;C A Stevens,&nbsp;S P Balk,&nbsp;R S Blumberg","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A majority of normal human intestinal intraepithelial lymphocytes (iIEL) are CD8+, express the alpha beta-T cell receptor (TCR) and are oligoclonal. The remainder of normal iIELs, which are also oligoclonal, express the gamma delta-TCR and preferentially utilize variable regions (V delta 1 and V delta 3) which are different from adult peripheral blood lymphocytes (V delta 2). The junctional region usage of gamma delta-TCRs in intestinal diseases is largely unknown. The aim of this study was to examine gamma delta-T cell clonality and junctional region usage of V delta 1 and V delta 3 transcripts in Crohn's Disease (CD) in comparison to several other chronic inflammatory diseases of the colon by polymerase chain reaction amplification, cloning and sequencing. As previously observed in normal subjects, all inflammatory cases examined, including CD (n = 3), ulcerative colitis (n = 1), diverticulitis (n = 1) and lymphocytic colitis (n = 1), the V delta 1 and V delta 3 transcripts contained reiterated sequences consistent with the expansion of gamma delta-T cells expressing these receptors. In 2/3 CD cases, but none of the non-CD inflammatory cases, transcripts containing J delta 3, a rarely used J delta, was observed among the V delta 1 and/or V delta 3 transcripts. Thus, in a subset of CD, gamma delta-T cells expressing J delta 3 may be expanded implicating a role for unique ligands that drive the expansion of T cells expressing these receptors.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 1","pages":"33-44"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21201570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is MS an auto-immune disease or a chronic gammaherpesvirus infection?","authors":"H S MacGregor,&nbsp;Q I Latiwonk","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The geographical-epidemiological findings of MS over the past 75 years are reviewed. Evidence concerning PR latitude-gradients, clusters, migration patterns, and enhancement-protective factors are critically reviewed and analyzed. The evidence in genetics, twin-studies and auto-immune theories are also thoroughly scrutinized as to their possible involvement as causative factors in MS- and found to be somewhat lacking. Environmental discoveries in the Faroes and Key West clusters are reviewed for possible similar environmental causes by a deadly agent. Exogenous-environmental candidate agents over the past 35 years from measles to Marek's are reviewed and analyzed. The undisputed positive laboratory findings of MDV are discussed in relation to Bray's unusually high positive findings with EBV antigen and MS serums. The important discovery of HHV-6 in oligodendrocytes of MS brains but not controls is considered and how this might relate to MDV. The conclusion is that genetics are indeed important in the natural resistance of individual immune systems to invading infectious agents (especially herpesviruses) but genetics in general have little to do with the pathogenesis of multiple sclerosis (but HHV-6, EBV, and MDV do).</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 2","pages":"45-74"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25694889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corticosteroid-induced apoptosis of eosinophils in atopic dermatitis patients.","authors":"M Matsukura,&nbsp;H Yamada,&nbsp;T Yudate,&nbsp;T Tezuka,&nbsp;J Chihara","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We examined the mechanism by which steroid administration significantly decreases the high eosinophil cell count in peripheral blood in patients with atopic dermatitis (AD). Eosinophils were isolated from the peripheral blood of patients with moderate or severe adult AD, and cultured. After steroid was added to the culture medium, we examined the changes in eosinophils, i.e., 1) the survival rates, 2) morphological changes and 3) fragmentation of DNA with respect to 2 factors, the steroid concentration and culture time. The steroid or interleukin-5 (IL-5) were added to eosinophils from patients with AD and those from non-AD patients with eosinophilia to compare serial changes in the survival rate. In eosinophils from patients with AD, the survival rate significantly decreased time-dependently and steroid concentration-dependently. Steroid administration significantly inhibited the survival rate of eosinophils from patients with AD compared to the survival rates of monocytes and neutrophils. The nuclei of eosinophils were serially reduced, and disappeared 72 hours after steroid administration. Simultaneously, cell size decreased, although the cell membrane remained intact. Granules developed in the cell membrane. In the steroid-treated group, apoptotic cells appeared earlier than in the untreated group. The number of cells showing apoptosis was increased steroid concentration-dependently. The number of DNA ladders was increased time-dependently and steroid concentration-dependently. In eosinophils derived from patients with AD and those derived from non-AD patients with eosinophilia, treatment with recombinant human (rh) IL-5 prolonged the life-span of cells. However, there were differences in the survival rates. In the presence of rhIL-5, the eosinophils from non-AD patients survived 1.4 times longer than those from AD patients at 24 hours (P < 0.05). In the presence of steroid, the eosinophils from non-AD patients survived twice as long as those from AD patients at 24 hours (P < 0.01). These findings suggest that apoptosis induced by steroids decreases the eosinophil count in vivo in patients with AD. There may be a difference in the incidence of steroid-induced apoptosis between eosinophil cells from patients with AD and those from patients with eosinophilia due to other underlying diseases.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 3","pages":"109-22"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20911583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum levels of anti-Staphylococcus aureus-specific IgE in patients with atopic dermatitis.","authors":"H Yamada,&nbsp;T Yudate,&nbsp;T Orita,&nbsp;T Tezuka","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We investigated the role of Staphylococcus aureus-specific IgE in patients with atopic dermatitis (AD). The titer of serum S. aureus-specific IgE was measured using the RAST method in 67 patients with AD and correlated with serum LDH, eosinophil count and total IgE. The titer of S. aureus-specific IgE was elevated in 41 patients but was not detected in 26 patients. The mean serum level of total IgE was higher in the positive group than in the negative group, but the eosinophil count and LDH levels were not different between the two groups. S. aureus was detected and cultured from the skin of 33/41 (80%) patients in the positive group, but only from the skin of 5/26 (19%) patients of the negative group. Our results suggest that S. aureus-specific antibody is present in patients with moderate-to-severe atopic dermatitis and may be involved in the pathogenesis of AD.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 4","pages":"167-75"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20731283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular dysmetabolism: the dark side of HIV-1 infection.","authors":"G Famularo,&nbsp;S Moretti,&nbsp;S Marcellini,&nbsp;E Alesse,&nbsp;C De Simone","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The progression to disease in subjects infected with the human immunodeficiency virus type I (HIV-1) cannot be explained solely on the basis of the infecting HIV-1 species. There is recent evidence that abnormalities in the cellular metabolism are crucial to the progression of the infection through common pathways that involve the induction of apoptosis and oxidant stress. Conversely, the low propensity of lymphocytes to undergo apoptosis, a normal redox status, and a balanced ceramide metabolism appear to predict a slow progression, or the non-progression at all, of the infection. It is likely that the ability of the host to maintain over time a balanced cellular metabolism despite the chronic infection with the virus contributes to the especially favourable outcome of an otherwise fatal infection seen in a discrete subgroup of HIV-1-infected individuals (long-term non-progressors) who might never experience any of the adverse effects of HIV-1 infection and will never demonstrate disease progression. Furthermore, this background supports the hypothesis that adjunctive therapies directed at correcting certain abnormalities of cellular metabolism seen in the infected host should be given in combination with antiretroviral drugs in order to slow the progression of the infection.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 3","pages":"123-32"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20911584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor necrosis factor production by rat Kupffer cells-regulation by lipopolysaccharide, macrophage activating factor and prostaglandin E2.","authors":"M Tanaka,&nbsp;H Ishibashi,&nbsp;Y Hirata,&nbsp;K Miki,&nbsp;J Kudo,&nbsp;Y Niho","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Tumor necrosis factor (TNF) is considered to be deeply involved in the hepatocyte damages in severe hepatitis. To delineate which mediators are involved in the production of TNF in vivo, we examined regulatory mechanisms of the production of TNF by rat Kupffer cells using a variety of mediators. Lipopolysaccharide (LPS) markedly induced TNF production by Kupffer cells. Kinetic studies revealed a rapid release of TNF within 3-4 hrs after the addition of LPS to the culture medium. Spleen cell derived-macrophage activating factor prepared from rat spleen cells did not by itself induce the production of TNF. However, the presence of a small amount of the factor during or before exposure to LPS induced higher levels of TNF, suggesting that macrophage activating factor had a priming effect. Recombinant human interferon-gamma and recombinant human granulocyte-macrophage colony stimulating factor, the natural types of which are components of the macrophage activating factor, displayed similar effects. Prostaglandin E2 (PGE2) and dexamethasone both inhibited LPS-induced TNF production in a dose dependent manner. Indomethacin, a cyclooxygenase inhibitor, increased LPS-induced TNF production. Interestingly, a combination of PGE2 and indomethacin inhibited TNF production more strongly than PGE2 alone, suggesting that the simultaneous treatment with PGE2 and indomethacin decreases liver damage in severe hepatitis rather than PGE2 alone. In addition, PGE2 pretreatment reduced the response to the newly added PGE2, suggesting the presence of a desensitization mechanism in the PGE2 receptor system. These findings suggest that spleen cell-derived macrophage activating factor and bowel-derived LPS take important parts in TNF production through the portal blood in the liver in vivo.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 1","pages":"17-31"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21201569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated plasma RANTES levels in patients with atopic dermatitis.","authors":"H Yamada,&nbsp;J Chihara,&nbsp;M Matsukura,&nbsp;H Yasuba,&nbsp;T Yudate,&nbsp;T Tezuka","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Eosinophils and T cells are involved in the pathologic process of atopic dermatitis. To further understand the role of these cells, and the possible involvement of RANTES, in the pathogenesis of atopic dermatitis, we measured the plasma level of RANTES using the sandwich ELISA. The mean plasma level of RANTES in 11 patients with atopic dermatitis was significantly higher than that of 15 normal control subjects. RANTES levels were higher in patients with severe form of atopic dermatitis than that of patients with mild disease. These findings suggest that RANTES may play a role in the recruitment and activation of eosinophils and T cells in atopic dermatitis.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 2","pages":"87-91"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25694741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adjuvant activity of diesel exhaust particulates (DEP) in production of anti-IgE and anti-IgG1 antibodies to mite allergen in mice.","authors":"T Suzuki,&nbsp;T Kanoh,&nbsp;M Ishimori,&nbsp;S Ikeda,&nbsp;H Ohkuni","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The present study indicates that diesel exhaust particulates (DEP) and pyrene contained in DEP have an adjuvant activity on IgE and IgG1 antibody productions in mice immunized intranasally with a mite allergen. The effect of pyrene on IgE and IgG1 antibody productions in mice was investigated to clarify the relation between mite allergy and adjuvancy of the chemical compounds in DEP. Der f II, one of the major allergens of house dust mite (Dermatophagoides farinae), was used as a mite allergen. Mice were grouped, and immunized with 5 micrograms of Der f II alone, 5 micrograms of Der f II plus 200 micrograms of pyrene and 5 micrograms of Der f II plus 100 micrograms of DEP intranasally seven times at two week intervals. The separate groups of mice were also immunized with 10 micrograms of Der f II plus the same dose of adjuvants in the same way. The IgE antibody responses to Der f II in mice immunized with Der f II plus pyrene or Der f II plus DEP were markedly enhanced compared with those immunized Der f II alone. The anti-Der f II IgE antibody production increased with increasing the dose of Der f II from 5 micrograms to 10 micrograms in mice immunized with Der f II plus the same dose of adjuvants. The IgG1 antibody responses to Der f II in mice immunized with 10 micrograms of Der f II plus 200 micrograms of pyrene or 10 micrograms of Der f II plus 100 micrograms of DEP were extremely higher than those immunized with 10 micrograms of Der f II alone. In addition, when the peritoneal macrophages obtained from normal mice were incubated with pyrene or DEP in vitro, an enhanced interleukin-1 alpha production of the macrophages was observed. When the spleen lymphocytes obtained from the mice immunized with 10 micrograms of Der f II plus 100 micrograms of DEP or 10 micrograms Der f II plus 200 micrograms of pyrene were stimulated with 10 micrograms of Der f II in vitro, an enhanced IL-4 production of the lymphocytes was also observed compared with those immunized with Der f II alone. These results suggest that the adjuvancy of DEP and pyrene on the production of IgE and IgG1 antibodies to Der f II may be one of the factors responsible for an incidence of asthma caused by house dust mite.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 5","pages":"187-99"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20325119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Usage of T cell receptor (TCR) V beta gene in ulcerative colitis.","authors":"M Shigematsu,&nbsp;H Masuda","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Ulcerative colitis (UC) is an inflammatory disease of unknown etiology. In this study, the expression of TCRV beta gene in UC patients was examined. The present study included 11 consecutive Japanese patients with UC. The control group comprised 10 healthy people. The usage of T Cell Receptor (TCR) V beta chain gene segments in peripheral blood was examined using RT-PCR. In addition, HLA-DR DNA typing was performed for the 11 patients with UC. The average of the positive expression rates in the UC group was 0.617 +/- 0.126, which was significantly higher than that of the control group (0.829 +/- 0.080) (p < 0.01). In the UC group, the usage of V beta chain gene in the active phase was almost same as that in the inactive phase. No specific distribution of V beta repertoire was observed in the UC group. In UC patients, no distinct correlation was found between any certain HLA-DR type and TCRV B gene usage. UC patients had a significantly lower rate of the expression of TCR V beta genes compared to normal controls. There is a possibility that the restricted usage of TCR V beta repertoire is possibly related to the existence of oligoclonal TCR repertoire in UC patients.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 5","pages":"177-86"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20325118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Murine experimental abortion by IL-2 administration is caused by activation of cytotoxic T lymphocytes and placental apoptosis.","authors":"H Shiraishi,&nbsp;S Hayakawa,&nbsp;K Satoh","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Fetal loss caused by IL-2 administration to pregnant mice is regarded as a model of human habitual abortion due to allo-immune reactions. To estimate feto-placental damages in this model, we examined apoptosis histochemically in the placenta.</p><p><strong>Methods: </strong>Four allogenic mated mice were administered intraperitoneally with 1000 IU of recombinant human IL-2 on days 3, 5 (7) after mating. We examined the presence of apoptosis in the placentae by TUNEL stain. We also examined expression of CTL specific granzyme B/perforin mRNA and usage of TCR V beta receptor segments by RT-PCR.</p><p><strong>Results: </strong>1. Allogenic pregnant mice given IL-2 revealed increased apoptotic scores in villous trophoblasts compared with control mice. Extracted DNA from IL-2 treated placentae revealed ladder formations. 2. Expression of granzyme B mRNA was increased while expression of perforin mRNA was not changed. 3. We observed increased numbers of TCR V beta gene segments in the decidua from IL-2 treated mice compared with untreated mice.</p><p><strong>Conclusion: </strong>We suggest that placental apoptosis caused by activation of maternal CTL may play important roles in the rejection of fetal allografts.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"48 3","pages":"93-108"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20911582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}