The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Analysis of adhesion molecules involved in leukocyte homing into the basolateral pockets of mouse Peyer's patch M cells.

The basolateral membranes of intestinal M cells are invaginated to form large intraepithelial "pockets" that are populated by specific sub-sets of mucosal leukocytes, including CD4+ T cells, memory and naïve B cells, and occasional dendritic cells. The adhesion molecules involved in leukocyte trafficking and/or retention within this unique immunological niche are unknown. In this study, we used immunofluorescence microscopy and a battery of monoclonal antibodies to identify the adhesion molecules expressed by leukocytes situated within the intracellular pockets of mouse Peyer's patch (PP) M cells. M cell associated leukocytes (MAL) consistently stained positive for integrin alpha4beta7, and integrin LFA-1 (CD11a/CD18), but were rarely positive for L-selectin (CD62L) or the mucosal integrin alphaEbeta7. However, neither the alpha4beta7 ligands MadCAM-1 or VCAM-1, nor the LFA-1 ligand ICAM-1, were detected on M cell basolateral membranes. To determine whether integrins alpha4beta7 or LFA-1 play a functional role leukocyte homing to M cell pockets, we examined M cells in mice deficient in integrin beta7 or CD11a/CD18. Although PP from CD18 or integrin beta7 mice were reduced in number and size as compared to age-matched controls, we identified M cells in both strains of mice. However, mice lacking CD18 (but not integrin beta7) had significantly fewer leukocytes within M cell pockets as compared to control animals, suggesting LFA-1 (but not alpha4beta7) may contribute, in part, to leukocyte trafficking into and/or retention within this unique immunological niche.[1]

References

 
WikiGenes - Universities