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Distribution of cells and cytokines in the spleen of dogs naturally infected with Leishmania chagasi (117.31)
Visceral leishmaniasis is associated with architectural disorganization of the splenic tissue in human and in dogs. In this study we estimate the changes in the number of Ki-67+ (proliferating cells), CD3+ (T cells), α-CD79+ (cells B) and S100+ (follicular dendritic cells) and in the expression of C...
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Published in: | The Journal of immunology (1950) 2011-04, Vol.186 (1_Supplement), p.117-117.31 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Visceral leishmaniasis is associated with architectural disorganization of the splenic tissue in human and in dogs. In this study we estimate the changes in the number of Ki-67+ (proliferating cells), CD3+ (T cells), α-CD79+ (cells B) and S100+ (follicular dendritic cells) and in the expression of CXCL13, LTα, TNF, IFN-gamma, IL10, TGFbeta, CCR7, CCL19, CCL21 in the spleens of dogs from an endemic area of visceral leishmaniasis, with organized or disorganized splenic architecture. The number of T cells, B cells, proliferating cells and follicular dendritic cells was lower in the lymphoid follicle of the animals with disorganized splenic tissue than in animals with organized splenic tissue (P < 0.01). The number of B cells was also reduced in the MZ of animals with disorganized splenic tissue (P < 0.01). B cells (P < 0.01) and proliferating cells (P < 0.05) density was lower in the lymphoid follicles of animals with disorganized splenic tissue. CXCL13 (P < 0.02) and LT-α (P < 0.05) expressions were lower in the spleens of animals with disorganized splenic tissue than with organized splenic tissue. There is a correlation between the disorganization of the splenic tissue and abnormal cell distribution and expression of cytokines involved in architectural organization of the splenic lymphoid tissue. These alterations of the spleen may impair leukocyte cooperation against infection by ,Leishmania and other pathogens. |
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ISSN: | 0022-1767 1550-6606 |
DOI: | 10.4049/jimmunol.186.Supp.117.31 |