Fractalkine expression and CD16+monocyte accumulation in glomerular lesions: association with their severity and diversity in lupus models
| Autor: | Yoshihiko Saito, Masato Nose, Ken-ichi Samejima, Miho Terada, Kimihiko Nakatani, Shuhei Yoshimoto, Masayuki Iwano, Hitoshi Hasegawa, Hirokazu Sakan, Osamu Asai |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Mice
Inbred MRL lpr Chemokine Physiology Interleukin-1beta Kidney Glomerulus Lupus nephritis Mice SCID CD16 Transfection Polymerase Chain Reaction Severity of Illness Index Monocytes Mice L Cells CX3CR1 medicine Animals Humans RNA Messenger Receptor Cell Proliferation Hybridomas Systemic lupus erythematosus biology Chemokine CX3CL1 Tumor Necrosis Factor-alpha business.industry Monocyte Receptors IgG Endothelial Cells Fibroblasts medicine.disease Immunohistochemistry Lupus Nephritis Chemotaxis Leukocyte Disease Models Animal medicine.anatomical_structure Immunoglobulin G Immunology biology.protein business Microdissection |
| Zdroj: | American Journal of Physiology-Renal Physiology. 299:F207-F216 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.00482.2009 |
| Popis: | Fractalkine (Fkn) is expressed on injured endothelial cells and is a membrane-bound chemokine that attracts cells expressing its receptor, CX3CR1, including CD16+monocytes (CD16+Mos). To clarify the role played by Fkn in the development of glomerular lesions in lupus nephritis, we examined Fkn expression and CD16+Mo accumulation induced in experimental C.B-17/Inc-scid/scid (SCID) lupus model mice by injection of IgG3-producing hybridoma clones obtained from MRL/lpr mice. Glomerular Fkn expression and accumulation of CD16+Mos were semiquantitatively evaluated using laser capture microdissection and real-time PCR. Injection of the 2B11.3 and 7B6.8 clones induced formation of glomerular proliferative and wire-loop lesions, respectively. Immunohistological analysis of the localization of Fkn and CD16+Mos revealed that Fkn expression and CD16+Mo accumulation were markedly elevated in glomerular lesions induced by 2B11.3, whereas no elevation was detected in those induced by 7B6.8. In addition, to examine the contribution of glomerular Fkn to the development of proliferative lesions, L cells producing an Fkn antagonist (Fkn-AT) were transplanted into SCID mice exhibiting proliferative lupus nephritis (DPLN) induced by 2B11.3. Notably, transplantation of the Fkn-AT-producing cells was functionally and histologically protective against this DPLN. Taken together, our findings suggest that Fkn and CD16+Mo accumulation are partially associated with the severity and diversity of histology of lupus nephritis. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|