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Kundel HL; Gefter W; Aronchick J; Miller W Jr; Hatabu H; Whitfill CH; Miller W Sr 《Radiology》1997,205(3):859
4.
CTLA-4 is required for the induction of high dose oral tolerance 总被引:5,自引:3,他引:5
Samoilova EB; Horton JL; Zhang H; Khoury SJ; Weiner HL; Chen Y 《International immunology》1998,10(4):491-498
Mucosal and systemic administrations of high dose antigens induce long-
lasting peripheral T cell tolerance. We and others have shown that high
dose peripheral T cell tolerance is mediated by anergy or deletion and is
preceded by T cell activation. Co-stimulatory molecules B7-1 (CD80)/B7-2
(CD86) and their counter-receptors CD28/CTLA-4 play pivotal roles in T cell
activation and immune regulation. In the present study, we examined the
roles of the B7 co-stimulation pathway in the generation of high dose
peripheral T cell tolerance. We found that blocking B7:CD28/CTLA-4
interaction at the time of tolerance induction partially prevented T cell
tolerance, whereas selective blockade of B7:CTLA-4 interaction completely
abrogated peripheral T cell tolerance induced by either oral or i.p.
antigens. These results suggest that CTLA-4-mediated feedback regulation
plays a crucial role in the induction of high dose peripheral T cell
tolerance.
相似文献
5.
Molecular genetic characterization of XRCC4 function 总被引:2,自引:0,他引:2
XRCC4 is a generally expressed protein of 334 amino acids that is involved
in the repair of DNA double-strand breaks and in V(D)J recombination, but
its function is unknown. In this study, we have used a mutational approach
and the yeast two-hybrid method to perform an initial characterization of
this protein. We show that the XRCC4 protein is located in the nucleus. We
also demonstrate that several potential phosphorylation sites are not
required for XRCC4 function in a transient V(D)J recombination assay. In
addition, we show that XRCC4 forms a homodimer in vivo with the
homodimerization domain being located within amino acids 115-204. Finally,
we define a core domain of XRCC4 that functions in V(D)J recombination and
comprises amino acids 18-204. Potential functions of XRCC4 are discussed.
相似文献
6.
Bofin AM Qvigstad G Waldum C Waldum HL 《APMIS : acta pathologica, microbiologica, et immunologica Scandinavica》2002,110(9):658-664
The aim of the study was to determine if, by means of tyramide signal amplification (TSA), the presence of chromogranin A (CgA)-positive tumour cells could be demonstrated in breast cancer cases found to be negative by conventional immunohistochemical staining. Sections from 44 cases of breast cancer (28 infiltrating ductal carcinomas, 2 lobular carcinomas, 4 ductal carcinomas in situ (DCIS), 7 lobular carcinomas in situ (LCIS), and 3 mucinous carcinomas) were stained for CgA by conventional immunohistochemical methods and by immunohistochemistry with TSA. The sections were also histologically graded and their oestrogen receptor (ER), progesterone receptor (PgR) and HER-2 oncogene status was recorded. Five of the tumours showed CgA-positive staining with the polyclonal antibody 430 with conventional methods. Thirty cases showed CgA-immunoreactive tumour cells after immunohistochemical staining with the polyclonal antibody 430 with TSA. However, eight of these also showed faint staining with the negative control antibody X0936 with TSA. One case showed immunopositivity for CgA using a monoclonal antibody without tyramide amplification and only a further two cases were positive when TSA was applied. The presence of CgA appears to be associated with a lower histological grade and may be more often found in oestrogen receptor-positive tumours. 相似文献
7.
Liu JQ; Bai XF; Shi FD; Xiao BG; Li HL; Levi M; Mustafa M; Wahren B; Link H 《International immunology》1998,10(8):1139-1148
Induction of mucosal tolerance by inhalation of soluble peptides with
defined T cell epitopes is receiving much attention as a means of
specifically down-regulating pathogenic T cell reactivities in autoimmune
and allergic disorders. Experimental autoimmune encephalomyelitis (EAE)
induced in the Lewis rat by immunization with myelin basic protein (MBP)
and Freund's adjuvant (CFA) is mediated by CD4+ T cells specific for the
MBP amino acid sequences 68-86 and 87-99. To further define the principles
of nasal tolerance induction, we generated three different MBP peptides
(MBP 68-86, 87-99 and the non- encephalitogenic peptide 110-128), and
evaluated whether their nasal administration on day -11, -10, -9, -8 and -7
prior to immunization with guinea pig MBP (gp-MBP) + CFA confers protection
to Lewis rat EAE. Protection was achieved with the encephalitogenic
peptides MBP 68-86 and 87-99, MBP 68-86 being more potent, but not with MBP
110-128. Neither MBP 68-86 nor 87-99 at doses used conferred complete
protection to gp-MBP-induced EAE. In contrast, nasal administration of a
mixture of MBP 68-86 and 87-99 completely blocked gp-MBP-induced EAE even
at lower dosage compared to that being used for individual peptides. Rats
tolerized with MBP 68-86 + 87-99 nasally showed decreased T cell responses
to MBP reflected by lymphocyte proliferation and IFN-gamma ELISPOT assays.
Rats tolerized with MBP 68-86 + 87-99 also had abrogated MBP-reactive
IFN-gamma and tumor necrosis factor-alpha mRNA expression in lymph node
cells compared to rats receiving MBP 110-128 nasally, while similar low
levels of MBP-reactive transforming growth factor-beta and IL-4 mRNA
expressing cells were observed in the two groups. Nasal administration of
MBP 68-86 + 87-99 only slightly inhibited guinea pig spinal cord
homogenate-induced EAE, and passive transfer of spleen mononuclear cells
from MBP 68-86 + 87-99-tolerized rats did not protect naive rats from EAE.
Finally, we show that nasal administration of MBP 68-86 + 87-99 can reverse
ongoing EAE induced with gp-MBP, although higher doses are required
compared to the dosage needed for prevention. In conclusion, nasal
administration of encephalitogenic MBP peptides can induce antigen-specific
T cell tolerance and confer incomplete protection to gp-MBP-induced EAE,
and MBP 68-86 and 87-99 have synergistic effects. Non-regulatory mechanisms
are proposed to be responsible for tolerance development after nasal
peptide administration.
相似文献
8.
Fossmark R Martinsen TC Qvigstad G Bendheim MØ Kopstad G Kashima K Waldum HL 《APMIS : acta pathologica, microbiologica, et immunologica Scandinavica》2005,113(7-8):506-512
Poorly differentiated neuroendocrine cells can be difficult to recognise. Sensitive methods are needed to label cells that have lost their ultrastructural features and have reduced concentrations of neuroendocrine markers. In gastric neoplasms, enterochromaffin-like cells might dedifferentiate and lose their characteristic granules and secretory vesicles, making detection of such cells increasingly difficult. However, chromogranin A (CgA) immunogold labelling could provide sensitive and specific detection of gastric neuroendocrine cells. We present ultrastructural findings, CgA immunogold labelling as well as conventional immunohistochemical findings of two human enterochromaffin-like cell carcinoids. Electron-dense granules of poorly differentiated cells were less intensely labelled than granules in well-differentiated cells. Granules with atypical shape as well as punctuate granules previously found in neuroendocrine neoplasms were also CgA labelled. The CgA labelling efficacy after antigen retrieval in an alkaline solution was higher after heating in an autoclave at 135 degrees C compared to a microwave at 100 degrees C for both granules and secretory vesicles without significant deterioration of the ultrastructure. In conclusion, the use of CgA immunogold labelling could ensure a specific classification of cells with neuroendocrine granules and be a supplement to immunohistochemical examination of poorly differentiated tumours. 相似文献
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10.
Background Duodenogastric reflux is known to cause an increased frequency of cancer in the glandular portion of the stomach in rats. Furthermore, it is debated whether inhibition of gastric acid secretion may promote gastric carcinogenesis. In the present study we examined the combined effect of gastroduodenal reflux and acid inhibition with respect to the development of gastric carcinoma in the rat.Methods Following the construction of a gastrojejunostomy in male Wistar rats, half of them were given the proton pump inhibitor lanzoprazole for 1 year. The rats were then killed and the pH in the stomach and gastrin in blood were measured. The stomach was examined macroscopically as well as histologically.Results Gastrin levels at autopsy were significantly increased in treated rats compared to the control group, confirming an effect of lanzoprazole on gastric acid secretion. Body weight was significantly reduced in the treated rats. Thirty of 79 rats developed gastric cancer, and they were all adenocarcinomas of the Lauren intestinal type. Gastric cancers occurred significantly more often in lanzoprazole-treated rats (50%) compared with controls (27%).Conclusion Lanzoprazole given orally enhances the carcinogenic effect of duodenogastric reflux in rats. 相似文献