Human intestinal B‐cell blasts and plasma cells express the mucosal homing receptor integrin α4β7

IN Farstad, TS Halstensen, AI Lazarovits… - Scandinavian …, 1995 - Wiley Online Library
IN Farstad, TS Halstensen, AI Lazarovits, J Norstein, O Fausa, P Brandtzaeg
Scandinavian journal of immunology, 1995Wiley Online Library
Interactions between homing receptors on circulating leucocytes and endothelial addressins
regulate tissue‐specific cellular extravasation. Although integrin á4β7 appears to be the
main receptor for guthoming T lymphocytes, less is known about molecules mediating
mucosal B cell homing. Expression of integrin α4β7 on B lymphocytes, B cell blasts, and
plasma cells in human gut‐associated lymphoid tissue (GALT; the Peyer's patches and
appendix) and lamina propria was studied by multi‐colour immunofluorescence applied on …
Interactions between homing receptors on circulating leucocytes and endothelial addressins regulate tissue‐specific cellular extravasation. Although integrin á4β7 appears to be the main receptor for guthoming T lymphocytes, less is known about molecules mediating mucosal B cell homing. Expression of integrin α4β7 on B lymphocytes, B cell blasts, and plasma cells in human gut‐associated lymphoid tissue (GALT; the Peyer's patches and appendix) and lamina propria was studied by multi‐colour immunofluorescence applied on cryosections. Isolated mononuclear cells from the same tissue compartments were examined by flow cytometry and compared with peripheral blood B cells. Integrin α4β7 was expressed by IgA+ B cell blasts and plasma cells (CD38high) in the lamina propria, B cell blasts in GALT, and sIgD+ B lymphocytes in peripheral blood. In contrast, GALT sIgD+ B lymphocytes were negative or only weakly positive for α4β7. These results suggested that B lymphocytes down‐regulate αAβ7 upon extravasation in GALT but up‐regulate this integrin after antigen‐priming. Thus, α4β7 may be a homing receptor also for B cell blasts extravasating in the gut lamina propria, where this integrin is maintained on plasma cells, perhaps as a local retention factor.
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