Extrathymic derivation of gut lymphocytes in parabiotic mice.
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In adult mice, c-kit+ stem cells have recently been found in their liver, intestine and appendix, where extrathymic T cells are generated. A major population of such thymus-independent subsets among intraepithelial lymphocytes is T-cell receptor (TCR)gamma delta+ CD4- CD8alpha alpha+(beta-) cells, but the origins of other lymphocyte subsets are still controversial. In this study, we examined what type of lymphocyte subsets were produced in situ by such stem cells in the small intestine, large intestine and appendix. To investigate this subject, we used parabiotic B6.Ly5.1 and B5.Ly5. 2 mice which shared the same circulation by day 3. The origin of lymphocytes was identified by anti-Ly5.1 and anti-Ly5.2 monoclonal antibodies in conjunction with immunofluorescence tests. Lymphocytes in Peyer's patches and lamina propria lymphocytes (especially B cells and CD4+ T cells) in the small intestine became a half-and-half mixture of Ly5.1+ and Ly5.2+ cells in each individual of parabiotic pairs of mice by day 14. However, the mixture was low in CD8alpha alpha+, CD8alpha beta+ and gamma delta T cells in the small and large intestines and in CD3+ CD8+ B220+ cells in the appendix. These cells might be of the in situ origin. When one individual of a pair was irradiated before parabiosis, the mixture of partner cells was accelerated. However, a low-mixture group always continued to show a lower mixture pattern than did a high-mixture group. The present results suggest that extrathymic T cells in the digestive tract may arise from their own pre-existing precursor cells and remain longer at the corresponding sites. (+info)
Studies on the role of suppressor cells in specific unresponsiveness to DNCB.
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Lymph nodes--and to a lesser extent spleen cells--from guinea-pigs tolerant to DNCB contact sensitivity, when injected into normal syngeneic guinea-pigs, decrease the ability of the recipients to become sensitized to contact with DNCB. The difference between the complete tolerance transferred by parabiosis with tolerant partners and the partial tolerance induced by transfer of tolerant cells can be explained by the different numbers of cells homing in the recipients. The tolergen does not play any role in the transfer of tolerance. (+info)
The effect of nephrectomy on the incidence of breast carcinoma in irradiated parabiosed rats.
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The incidence of carsinoma the breast in parabiosed female NEDH rats is 2.5%. When one member of such a pair is irradiated, the incidence rises to 11% in the irradiated partner and 10% in the nonirradiated partner. If in such a pair of rats one kidney is removed from each partner, the incidence of breast carcinoma rises fivefold in the nonirradiated partner. The factors involved in such an increase probably have to do with alteration in retention, interchange, and feedback of the pituitary and ovarian hormones. (+info)
Rationale for the existence of additional adipostatic hormones.
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Parabiosis studies with obese rodents demonstrated that circulating factors are involved in the long-term control of food intake and energy balance. More than 40 years ago it was hypothesized that rats made obese by hypothalamic or dietary means, as well as genetically obese fa/fa rats and db/db mice, produce a circulating factor that either inhibits food intake or acts metabolically to reduce the fat content of non-obese ad libitum-fed partners. However, none of these obese rodents showed a significant change in weight when parabiosed to a normal animal. It was therefore postulated that these obese rodents produced a circulating lipostatic factor but were unable to respond to it. In contrast, genetically obese ob/ob mice were thought to be deficient in the circulating signal, as they lost weight when parabiosed to lean or obese db/db mice. The discovery of leptin suggested that the circulating lipostatic signal had been identified. However, a closer look at the outcome of the parabiotic studies reveals that leptin alone does not explain all of the findings of the parabiotic experiments. Another (or more than one) as yet unidentified factor(s) may be involved in energy balance regulation. The evidence for the existence of further leptin-like hormones comes from observations in which the direct effect of leptin has been eliminated or can be excluded. (+info)
CXCL13 is required for B1 cell homing, natural antibody production, and body cavity immunity.
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B1 cells are a predominant cell type in body cavities and an important source of natural antibody. Here we report that in mice lacking the chemokine, CXCL13, B1 cells are deficient in peritoneal and pleural cavities but not in spleen. CXCL13 is produced by cells in the omentum and by peritoneal macrophages, and in adoptive transfers, B1 cells home to the omentum and the peritoneal cavity in a CXCL13-dependent manner. CXCL13(-/-) mice are deficient in preexisting phosphorylcholine (PC)-specific antibodies and in their ability to mount an anti-PC response to peritoneal streptococcal antigen. These findings provide insight into the mechanism of B1 cell homing and establish a critical role for B1 cell compartmentalization in the production of natural antibodies and for body cavity immunity. (+info)
Little evidence for developmental plasticity of adult hematopoietic stem cells.
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To rigorously test the in vivo cell fate specificity of bone marrow (BM) hematopoietic stem cells (HSCs), we generated chimeric animals by transplantation of a single green fluorescent protein (GFP)-marked HSC into lethally irradiated nontransgenic recipients. Single HSCs robustly reconstituted peripheral blood leukocytes in these animals, but did not contribute appreciably to nonhematopoietic tissues, including brain, kidney, gut, liver, and muscle. Similarly, in GFP+:GFP- parabiotic mice, we found substantial chimerism of hematopoietic but not nonhematopoietic cells. These data indicate that "transdifferentiation" of circulating HSCs and/or their progeny is an extremely rare event, if it occurs at all. (+info)
Stomach and upper intestine of the rat in the regulation of food intake.
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The role of the upper intestine in the regulation of food intake and gastric emptying has been studied in normal, gastrectomized, and "crossover" rats, parabiotic rats with a common visceral cavity in which the proximal duodenum of each parabiont is anastomosed to the pylorus of the stomach of the partner. One rat of "crossover" pairs eats and the partner eats little or nothing. Normal rats fed a raw soybean (RS) diet ate less and gastric evacuation proceeded more slowly than in normal rats fed a heated soybean (HS) diet. It is postulated that RS contains a heat-labile intestinal irritant. The upper intestine of gastrectomized rats regulates food intake and prevents overloading of the intestine. Force feeding of excessive amounts of the RS diet elicited the secretion of much more solids and nitrogen into the upper intestine than did similar amounts of the HS diet. The upper intestines of "crossover" rats lose all control over entry of gastric contents into their duodena. Fed ad libitum, the parabiont whose stomach emptied first, ate continuously, while the recipient partner showed diarrhea. It is postulated that the control of food intake traditionally assigned to the stomach resides, rather, in the upper intestine. (+info)
Systemic alteration induced in mice by ultraviolet light irradiation and its relationship to ultraviolet carcinogenesis. 1977.
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Chronic irradiation of mice with ultraviolet (UV) light produces a systemic alteration of an immunologic nature. This alteration is detectable in mice long before primary skin cancers induced by UV light begin to appear. The alteration results in the failure of UV-irradiated mice to reject highly antigenic, transplanted UV-induced tumors that are rejected by unirradiated syngeneic recipients. The immunologic aspect of this systemic alteration was demonstrated by transferring lymphoid cells from UV-irradiated mice to lethally x-irradiated recipients. These recipients were unable to resist a later challenge with a syngeneic UV-induced tumor, whereas those given lymphoid cells from normal donors were resistant to tumor growth. Parabiosis of normal mice with UV-irradiated mice, followed by tumor challenge of both parabionts with a UV-induced tumor, resulted in the growth of the challenge tumors in both WV-irradiated and unirradiated mice. Splenic lymphocytes from tumor-implanted UV-treated mice were not cytotoxic in vitro against UV-induced tumors, whereas under identical conditions cells from tumor-implanted, unirradiated mice were highly cytotoxic. Our findings suggest that repeated UV irradiation can circumvent an immunologic mechanism that might otherwise destroy nascent UV-induced primary tumors that are strongly antigenic. (+info)