Parallel pattern of expression of CD43 and of LFA-1 on the CD45RA+ (naive) and CD45RO+ (memory) subsets of human CD4+ and CD8+ cells. Correlation with the aggregative response of the cells to CD43 monoclonal antibodies.
Human peripheral blood T cells form large aggregates when cultured in the presence of antibodies to the highly sialylated protein CD43. About 25% of the cells in such cultures do not aggregate, however, although virtually all T cells express CD43. To find out if these cells constitute a distinct subpopulation of T cells, we analysed the expression of CD43 and lymphocyte function-associated antigen-1 (LFA-1) and examined the aggregation induced by CD43 monoclonal antibodies (mAb) in CD4+ and CD8+ cells and in their CD45RA+ (naive) and CD45RO+ (memory) subsets, respectively. We found that CD43-stimulated CD8+ cells aggregated more rapidly and formed larger aggregates than CD4+ cells. Furthermore, whereas CD8+CD45RO+ cells formed compact clusters after some hours of incubation, a majority (about 75%) of the CD4+CD45RA+ cells remained as singles even after overnight culture. Flow cytometry analysis showed that the patterns of expression of CD43 and of LFA-1 on the different subsets were strikingly parallel to each other. Thus, CD4+ and CD8+ memory (CD45RO+) T cells expressed higher levels of CD43 than the corresponding naive cells, suggesting that increased levels of CD43 expression are, like LFA-1 expression, a marker of primed or recently activated cells. Immunoprecipitation and sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis of 125I-labelled subsets showed that CD8+ cells expressed about twice as much CD43 as CD4+ cells. In a particular donor where the mean size of the cells in the four subsets was close to equal, CD4+ memory cells showed a 1.4-fold and CD8+ memory cells a twofold increase in CD43 compared to their corresponding naive populations. The propensity of memory T cells to extravasate may be facilitated by high expression of CD43.
Youseffi-Etemad
R
R
Department of Immunology, Stockholm University, Sweden.
Axelsson
B
B
D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D015703:Antigens, CD; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002448:Cell Adhesion / Q000276:immunology; D004591:Electrophoresis, Polyacrylamide Gel; D005434:Flow Cytometry; D006801:Humans; D051917:Leukosialin; D008213:Lymphocyte Activation; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism*; D011233:Precipitin Tests; D012795:Sialoglycoproteins / Q000276:immunology / Q000378:metabolism*; D013601:T-Lymphocytes / Q000276:immunology*
D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D051917:Leukosialin; D016169:Lymphocyte Function-Associated Antigen-1; C465014:SPN protein, human; D012795:Sialoglycoproteins