Migration of lymphocyte subpopulations towards CXCL12 was analyzed coupled to six-color flow cytometry in untreated patients in the remitting phase, during relapse, in patients with clinically isolated syndrome (CIS), and in healthy volunteers.
Migration of lymphocyte subsets across primary human brain microvascular endothelial cells was assessed in an in vitro transmigration assay.
Those cytokines will activate migration of lymphocyte cells into the ocular surface with more secretion of inflammatory cytokines, chemokines, metalloproteinases, and proangiogenic molecules that will facilitate the infiltration of pathogenic immune cells that give rise to the clinical picture [ 5].
Neutrophils migrate in response to chemoattractant gradient and chemotactic factors while the migration of lymphocytes is stimulated by specific antigens, mitogens and other non-specific factors produced by lymphocytes [ 50].
Therefore, it appears that there is tissue specificity in the migration of lymphocytes into the inflamed gingival tissues and that antigen is required for distinct tissue-specific lymphocyte traffic to occur.
Tissue-specific migration of lymphocytes is tightly regulated by a complex network of chemokines.
This was associated with a significant decrease in CD62L expression, a cell surface molecule implicated in lymphocytes homing to peripheral tissue, suggesting the migration of lymphocytes from the spleen to the periphery.
Taken together, we can postulate that there are both constitutive expression of CCL28 with mainly the antimicrobial activity and induced expression which is necessary for massive migration of lymphocytes to the gut.
These data, suggesting a potential increase in the migration of lymphocytes to the gut in the EC group, are consistent with the hypothesis of a down-regulation of CCL25 in the presence of L. fermentum and an up-regulation of the chemokine expression in the presence of E. coli.
These phenotypic changes in the S1PL−/− mature thymocyte population are consistent with a block in the migration of lymphocytes into the periphery and a concomitant accumulation of mature thymocytes in the thymus of the S1PL-deficient animals [28], [38], [39], [42], [43].
Previous studies demonstrated that the addition of Bb or a Bb-lipoprotein to cultured endothelial monolayers induces endothelial cells to produce proinflammatory cytokines, chemokines, adhesion molecules and chemotaxis activity, promoting transendothelial migration of lymphocytes and neutrophils [4], [5], [19], [31], [32].
