Impaired antibody production in blunt trauma. Possible role for T cell dysfunction
D. I. McRitchie, M. J. Girotti, O. D. Rotstein and J. A. Teodorczyk-Injeyan
Department of Surgery, Toronto General Hospital, Ontario, Canada.
This study investigates mechanisms of impaired humoral immune response in a
well-defined population of blunt trauma patients (n = 18, Injury Severity
Score greater than or equal to 20). Spontaneous and pokeweed
mitogen-induced polyclonal immunoglobulin production were assessed in
cultures of peripheral blood mononuclear cells. The proliferative response
to alloantigen and mitogen was assessed in parallel by the mixed lymphocyte
reaction and pokeweed mitogen-induced blastogenesis, respectively. Pokeweed
mitogen-induced IgG and IgM production was significantly reduced in trauma
patients compared with controls. This effect was not reversed by depletion
of adherent cells or by the addition of indomethacin. Exogenous interleukin
2 was also ineffective. However, the addition of normal T cells or
supernatants from isoantigen-stimulated cultures of these cells to patient
B cell-enriched cultures significantly enhanced (by 1.4- to 5.1-fold) the
antibody response to pokeweed mitogen. Thus, suppression of humoral
antibody response in blunt trauma patients may be due to failure of T-cell
mediated help, resulting in insufficient secretion or activity of cytokines
required for adequate B cell activation, proliferation, or differentiation
into immunoglobulin-secreting cells.
