Analysis of the expression of CD5 by human B cells and correlation with functional activity.
B cells expressing the CD5 marker in the mouse have been suggested to be a separate lineage and a major source of autoantibody production. In man, this relationship is less clear. Studies were therefore undertaken to determine whether human CD5+ B cells represent a distinct lineage of cells that differ in patterns of antibody production from CD5- B cells. In normal B cell populations, CD5 was expressed by a mean of 24.0 +/- 2.8% (n = 10) of CD20+ B cells. Of note, an increased frequency of CD5+ B cells was not found in patients with systemic lupus erythematosus (mean of 17.9 +/- 2.8%, n = 16). Analyzing CD5+ B cells for cell membrane Ig isotype expression demonstrated similar frequencies of IgG and IgA expressing cells as were found on the CD5- B cell population, although the frequency of IgM+ cells was slightly increased. Incubation of CD20+ B cells with phorbol myristate acetate (PMA) for 72 hr increased the frequency of CD5 expressing B cells by more than threefold. CD5 expression was also increased by coculture with anti-CD3-activated T cells and most markedly by simultaneous stimulation with both PMA- and anti-CD3-activated T cells (greater than 50% positive). Analysis of CD5- B cells clearly indicated that stimulation with PMA or anti-CD3-activated T cells induced the majority to become CD5+ transiently. Functional analysis of Ig production by CD5+ and CD5- B cells stimulated with anti-CD3-activated T cells indicated that both populations in normals produced IgM and a variety of autoantibodies in comparable amounts, whereas the CD5- B cells produced greater quantities of IgG. B cells were activated with anti-CD3-stimulated T cells followed by separation into CD5+ and CD5- populations. The largest amount of Ig was produced by CD5- B cells that were induced to express CD5, although all populations produced some Ig. These data suggest that CD5 behaves as an activation marker on human B cells rather than as a marker for a distinct lineage of cells. Moreover, CD5 expression does not appear to identify a population of resting B cells with a greater capacity to produce antibodies to DNA or other autoantibodies.
Harold C. Simmons Arthritis Research Center, University of Texas Southwestern Medical Center, Dallas 75235.
L A
LA
Vernino
D S
DS
Pisetsky
P E
PE
Lipsky
D000917:Antibody Formation; D015703:Antigens, CD / Q000032:analysis*; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis; D001323:Autoantibodies / Q000096:biosynthesis*; D016175:B-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology*; D018956:CD5 Antigens; D002454:Cell Differentiation; D005434:Flow Cytometry; D006801:Humans; D066298:In Vitro Techniques; D007958:Leukocyte Count; D008213:Lymphocyte Activation
D015703:Antigens, CD; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte; D001323:Autoantibodies; D018956:CD5 Antigens