
Up‐regulated expression of Fas antigen (CD95) by peripheral naive and memory T cell subsets in patients with systemic lupus erythematosus (SLE): a possible mechanism for lymphopenia
Author(s) -
AMASAKI Y.,
KOBAYASHI S.,
TAKEDA T.,
OGURA N.,
JODO S.,
NAKABAYASHI T.,
TSUTSUMI A.,
FUJISAKU A.,
KOIKE T.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb05540.x
Subject(s) - fas receptor , antigen , immunology , t cell , il 2 receptor , medicine , cytotoxic t cell , fas ligand , biology , apoptosis , immune system , programmed cell death , in vitro , biochemistry
SUMMARY Fas antigen (CD95) is a membrane‐associated molecule that mediates apoptotic cell death and may play a role in the induction and maintenance of T cell tolerance. To elucidate the involvement of Fas antigen in human autoimmune diseases, we analysed Fas antigen expression by peripheral T cells from patients with SLE and rheumatoid arthritis (RA), using three‐colour flow cytometry. Both CD4 + and CD8 + T cell from SLE patients expressed Fas antigen in a higher density than did these cell from healthy donors and from RA patients. Enhancement of Fas antigen density was noted in Fas + CD45RO + memory T cell from SLE patients. More remarkably, a significant expression of Fas antigen was observed in CD45RO − naive T cells from SLE patients CD4 + CD45RO − T cells from SLE patients co‐expressed Fas antigen and early to intermediate activation antigens such as CD25 and CD71, and late activation antigen HLA‐DR in only Fas hi CD4 + naive T tells. Such up‐regulation of Fas antigen expression in SLE patients seems to be clinically meaningful, because mean fluorescence intensity (MFI) of Fas antigen on CD4 + T cell subsets inversely correlates with the absolute size of CD4 + T tell subsets in peripheral blood of SLE patients. These results suggest that T cells with increased Fas antigen expression may be highly susceptible to apoptotic cell death, in vivo. A putative mechanism for lymphopenia in SLE patients is discussed.