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HLA class I expression on erythrocytes and platelets from patients with systemic lupus erythematosus, rheumatoid arthritis and from normal subjects
Author(s) -
Botto Marina,
So Alex K.L.,
Giles Carolyn M.,
Mason Philip D.,
Walport Mark J.
Publication year - 1990
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1990.tb02624.x
Subject(s) - rheumatoid arthritis , immunology , human leukocyte antigen , medicine , platelet , percoll , lupus erythematosus , endocrinology , antibody , gastroenterology , antigen , biology , in vitro , biochemistry
Summary It has previously been shown, by a haemagglutination assay, that patients with systemic lupus erythematosus (SLE) express increased levels of HLA class I on erythrocytes compared with normal subjects and patients with rheumatoid arthritis (RA). A radioligand‐binding assay, using monoclonal antibody W6/32, was devised to quantify HLA class I expression on erythrocytes and platelets. An increased number of class I molecules was expressed on erythrocytes from 45 patients with SLE (mean = 354 molecules per cell, median = 255 molecules, range = 30–1270 molecules per cell), compared with cells from 46 normal subjects (mean = 132, median = 78, range = 40–550) and 31 RA patients (mean = 132, median = 89, range = 26–497). The presence of HLA‐B7 correlated with increased class I expression on erythrocytes from both normal subjects and patients with SLE. Levels of HLA class I in serum were measured. All subjects with HLA‐A9 (A23, 24) showed higher levels of serum class I than their A9‐negative counterparts, and there was no difference in levels between SLE patients and normal subjects. There were no correlations between class I levels in serum and on erythrocytes amongst SLE patients or normal subjects. Red cells were fractionated, according to their age in vivo , on Percoll gradients. Class I levels fell with increasing erythrocyte age in all individuals, but were higher in all fractions from SLE patients compared with age‐matched fractions from normal subjects. HLA‐B7‐positive erythrocytes also expressed higher class I levels in each Percoll fraction, compared with their HLA‐B7‐negative counterparts, suggesting that enhanced B7 expression is not due to greater structural stability of this class I allotype. These data are compatible with the hypothesis that class I is expressed as an intrinsic protein of erythrocyte membranes and that expression is increased amongst patients with SLE.