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Stimulation of murine intestinal intraepithelial lymphocytes by the bacterial superantigen staphylococcal enterotoxin
M S Siebrecht1, E Hsia, C Spychalski
1Mucosal Immunology Laboratory, Massachusetts General Hospital East Charlestown 02129.
To gain insight into the specificity and function of intestinal intraepithelial lymphocytes (IEL), we have examined their response to staphylococcal enterotoxin B (SEB), a significant cause of food poisoning and a potent T cell mitogen. IEL include two populations of TCR alpha beta+ T cells. One of these resembles the T cells found in the Peyer's patch and is thymus dependent. The other subset is characterized by both TCR alpha beta and gamma delta+ IEL bearing a unique form of the CD8 molecule, expressed as an alpha alpha homodimer. CD8 alpha+ beta- IEL are thymus independent and appear to mature extrathymically in the gut epithelium. Two-color flow cytometric analysis showed that in vitro stimulation of IEL with SEB resulted in the expansion of the thymus dependent but not the thymus independent IEL; the CD8 alpha+ beta- IEL were functionally non-responsive to stimulation with SEB. 'Forbidden' self-superantigen reactive T cells present among IEL were also non-responsive to stimulation with SEB. The presence or absence of class II MHC molecules does not appear to play a role in the non-responsiveness to SEB, since CD8 alpha+ beta- IEL from class II deficient mice also failed to respond to stimulation with SEB. Depletion of CD8 beta+ and CD4+ T cells from total IEL decreased IL-2 production by IEL in response to cross-linking with anti-CD3, suggesting that the non-responsiveness of CD8 alpha+ beta- IEL extends to antigens other than SEB.
To gain insight into the specificity and function of intestinal intraepithelial lymphocytes (IEL), we have examined their response to staphylococcal enterotoxin B (SEB), a significant cause of food poisoning and a potent T cell mitogen. IEL include two populations of TCR alpha beta+ T cells. One of these resembles the T cells found in the Peyer's patch and is thymus dependent. The other subset is characterized by both TCR alpha beta and gamma delta+ IEL bearing a unique form of the CD8 molecule, expressed as an alpha alpha homodimer. CD8 alpha+ beta- IEL are thymus independent and appear to mature extrathymically in the gut epithelium. Two-color flow cytometric analysis showed that in vitro stimulation of IEL with SEB resulted in the expansion of the thymus dependent but not the thymus independent IEL; the CD8 alpha+ beta- IEL were functionally non-responsive to stimulation with SEB. 'Forbidden' self-superantigen reactive T cells present among IEL were also non-responsive to stimulation with SEB. The presence or absence of class II MHC molecules does not appear to play a role in the non-responsiveness to SEB, since CD8 alpha+ beta- IEL from class II deficient mice also failed to respond to stimulation with SEB. Depletion of CD8 beta+ and CD4+ T cells from total IEL decreased IL-2 production by IEL in response to cross-linking with anti-CD3, suggesting that the non-responsiveness of CD8 alpha+ beta- IEL extends to antigens other than SEB.