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T lymphocytes from normal human controls and sickle cell disease (SCD) patients were isolated from peripheral blood and cultured for 72 hours following addition of phytohemagglutinin. The ratio for the fraction of cells in DNA synthesis (S phase) over the fraction in G2 phase (S/G2) was significantly higher in SCD patients in comparison to the controls (mean +/- SD) (4.01 +/- 0.78 vs. 2.78 +/- 0.76, P less than 0.02). Following in vivo zinc supplementation to two subjects, the S/G2 ratio was normalized. We conclude that the distribution of T lymphocytes in cell cycle is altered in SCD patients and that this effect may be zinc-dependent.

In this study, we evaluated lymphocyte subpopulations in 23 adults with SCA. When compared to controls, SCA patients had higher lymphocyte counts with normal numbers of T101+ cells (T-lymphocytes) and T4+ cells. T8+ cells were significantly increased in SCA patients in comparison to controls (1684 +/- 243 vs 980 +/- 367, p less than .001). This increment was largely dependent on a T101-, T8+ cell population. The SCA patients as a group had significantly decreased T4/T8 ratio (p less than .0001). The SCA patients with history of blood transfusions had higher T4+ cells numbers and higher T4/T8 ratio, but no other significant differences from nontransfused patients were noted. Our results are different from those reported for nontransfused children with SCA who showed normal T4/T8 ratio. Thus, a distinct pattern of abnormalities is seen in the lymphocyte subpopulations of adult SCA patients, unrelated to their exposure to blood transfusions.

Type-specific IgM and IgG antibody responses to a polyvalent influenza vaccine were evaluated in 16 adults with sickle cell anemia, with the use of an enzyme-linked immunosorbent assay. When compared to healthy controls, 8 out of the 16 patients had decreased or undetectable postvaccination anti-influenza IgM antibody levels. These patients were found to have significantly lower serum IgM levels and nondetectable splenic tissue (by 99Tc scans), as compared to those with normal IgM responses. Impaired IgM antibody primary immune responses may play a role in the pathogenesis of infectious complications seen in adult patients with sickle cell anemia.